1. No category

Vijay Prabha et al., Androl Gynecol: Curr Res 2014, 2:1
http://dx.doi.org/10.4172/2327-4360.1000118
Andrology & Gynecology:
Current Research
Review Article
Association of Antisperm
Antibodies with Bacterial
Infection: An Insight to
Infertility
Deepali Thaper1, Harpreet Vander1 and Vijay Prabha1*
Abstract
Among other factors, immunological predictors associated with
humoral immunity against sperm antigens can be a reason for
human infertility. A hypothesis for the induction of antisperm
antibodies (ASA) is the cross-reactivity of spermatozoa antigens
and exogenous antigens. Common antigenicity has been
established between spermatozoa and bacteria, viruses, fungi
and allergens. Recent evidence suggests that many antigens
shared among unrelated cell types are surface membrane or lipid
conjugate complex carbohydrates. Although the complex pattern of
cellular glycosylation is tissue specific, the expression of specific
carbohydrate sequences may occur on several unrelated cell types
eg. blood leucocytes, kidney, deciduas, endometrium, tonsil, skin,
lung, liver, adrenal gland, brain and ovary. Thus, epitope specific
monoclonal antibodies (mAbs) rose against the components of one
cell type might be expected to recognize these rather universal
glycosylated antigenic determinants on other cells. In fact, certain
mAbs specifically those which react to immunodominant (often
heavily glycosylated) determinants, show varying degrees of
cross-reactivity with seemingly unrelated tissues depending on
the epitope recognized by the mAb and the degree of structural
similarity with the epitope. Cross-reactivity between certain
epitopes on the bacterial surface and spermatozoa, particularly
involving carbohydrate determinants might be one potential
triggering mechanism for induction of antisperm antibodies in males
and females.
Keywords
Antisperm antibodies; Human infertility; Glycosylation
Introduction
Infertility, the inability to conceive after twelve months of
contraceptive-free unprotected intercourse, is considered as a
worldwide problem which affects approximately 15% of all couples
[1]. Earlier only physiological causes of infertility were taken
into consideration but gradually the focus shifted towards the
immunological reasons behind it. For instance, the blood-testis barrier
shelters the antigenic spermatozoa from the circulating immune
cells. However, autoantigenic germ cells migrate through bloodtestis barrier and are exposed to circulating immune cells leading to
*Corresponding author: Vijay Prabha, Department of Microbiology, Panjab
University, Chandigarh 160014, India, Tel: 91-172-2534140; Fax: 91-1722541770; E-mail: satishvijay11@yahoo.com
Received: June 26, 2013 Accepted: January 30, 2014 Published: February
05, 2014
International Publisher of Science,
Technology and Medicine
a SciTechnol journal
production of antisperm antibodies, thereby reducing the ejaculate
quality and hence fertility [2]. The prevalence of such autoantibodies
in general population ranges from 0-2%, but, it is greatly increased
in infertile men, ranging from 7-26%. Although several risk factors
for ASA development have been defined (testicular torsion, variocele,
cryptorchidism, vasectomy and genital tract infections) but there are
no specific indications [3]. Morever, the presence of ‘natural’ antisperm antibodies in virgin girls [4] and boys before puberty [5] still
remains unanswered. Therefore, without losing focus, researchers
gave a new dimension in terms of molecular mimicry existing between
spermatozoa and microorganisms which might be playing a hidden
role in production of ASAs. Several reports suggested the presence of
cross-reactive antigens between spermatozoa and bacteria, Escherichia
coli, Salmonella typhi [6,7] and Helicobacter pylori [8]. Equils et al.
[9] have shown an amazing analogy between the chlamydial heat
shock proteins and human proteins. Also, increased ASA levels have
been reported among patients suffering from ulcerative colitis [10].
Witkin and Toth [11] explored the relationships between Ureaplasma
urealyticum infection, antisperm antibodies, and infertility. The
discovery of heterogeneous antigens, similar to the specific antigens
of the spermatozoa, in microorganisms not only helps to elucidate
the mechanisms of development of sterility on the basis of crossed
immunologic reactions, but also opens the way for the practical use
of harmless bacterial “spermovaccines”, essential for fertility control
in man and animals.
This review summarizes the results of several studies which
have been undertaken to analyse a potential relation of antisperm
antibodies in serum or semen with microbial findings.
Chlamydia trachomatis
Chlamydia trachomatis infection has become the most
commonly prevalent and most damaging genital tract infection
in the world. The common manifestations of C. trachomatis as
salpingitis [12] and pelvic inflammatory disease [13] are well
accredited in women with infertility problems [14]. Because of the
alterations it causes in the epithelium and mucus composition, and
by the presence of inflammatory cells, it has been cited as a major
cause of tubal obstructions, lacerations and ectopic pregnancy, and
can result in pelvic inflammatory disease (PID), adnexitis, local or
diffuse peritonitis, and formation of adhesions which may disrupt the
passing of oocytes through the tubes. So, the fact that this infection
interferes seriously with human reproduction, which may preclude
the couples from having a reproductive future, has put this infection
under spotlight. Regarding this, several authors have reported the
presence of circulating antibodies to C. trachomatis in women. To cite
a few: Moore et al. [15] have focussed on the presence of circulating
antibodies to C. trachomatis in women with signs of tubal damage as
compared to none in a group of controls with normal fallopian. On
the similar grounds, Gump et al. [16] reported a 64% incidence of
chlamydial antibodies in women with residual inflammatory adnexal
lesions, compared to 28% in women with normal adnexae. Genital
infections such as Chlamydia may elicit an adjuvant like effect and
inadvertent humoral immunity to inseminated spermatozoa [17].
Another study has shown an amazing analogy between the 10 kDa
and 57 kDa chlamydial HSP (cHSP10 and cHSP57/60, respectively)
All articles published in Andrology & Gynecology: Current Research are the property of SciTechnol, and is protected by
copyright laws. Copyright © 2014, SciTechnol, All Rights Reserved.
Citation: Deepali T, Vander H, Vijay P (2014) Association of Antisperm Antibodies with Bacterial Infection: An Insight to Infertility. Androl Gynecol: Curr Res
2:1.
doi:http://dx.doi.org/10.4172/2327-4360.1000118
and human proteins. This suggests that at molecular level, there
should be cross-reactivity between the human HSP60 and cHSP60,
which leads to the formation of antibodies against the HSP60 in the
serum and follicular fluid of women exposed to C. trachomatis; these
antibodies seem to have a negative impact on embryonal growth,
and increase the probability of adverse pregnancy outcomes. Also,
HSP57/60 has been found to play an important role in inducing
trophoblast apoptosis by stimulating the toll-like receptor 4 (TLR4),
which naturally mediates immune responses in placenta [9]. A
greater probability of tubal scaring and ectopic pregnancy has been
speculated in women with serum antibodies against cHSP60 and
positive for C. trachomatis as compared to only seronegative women.
[18]. There also seems to be a cross-reactivity between HSP10 and
an embryonic protein, the early pregnancy factor (EPF), and this
may cause abortions [19]. The cHSP10, too, probably correlates
to the severity of the disease in females and with the presence of
tubal factor infertility; HSP60 has consequently been proposed as a
prognostic criterion for the assessment of chlamydial infections in
women and, together with other humoral parameters, as a means for
priori diagnosis of tubal factor infertility [20]. Since this organism
has a predilection for inducing inflammatory changes of deep pelvic
organs in the female and many men were also found positive for antichlamydial antibodies in semen but not in serum [21], this raised a
curiosity so as to check its relevant pathological significance in males
as well, speculating that the significance of the organism in men may
lie in their capacity to retain a reservoir of bacteria in their sex glands
which can inoculate the female partner repeatedly. Over time, such
a chronic infection in the female may cause tubal or endometrial
pathology. This presumably explains the higher incidence of active
chlamydial infection in the male partners of women with tubal
pathology [22,23].
With focus shifting towards the male partner, it was observed
that C. trachomatis is capable of attaching to sperm [24] and seems
to impair sperm motility, and cause premature death, perhaps as
an effect of the chlamydial lipopolysaccharide [25]. Toth et al. [26]
worked on the same lines and noted that the incidence of vaginitis,
salpingitis, herpes and urinary tract infection in 1350 infertile couples
was generally higher in women whose husbands had reported a
previous history of genitourinary infection.
Several early reports have suggested a relationship between a
genital infection and the production of sperm autoantibodies. ASA’s
are produced in both women [27] and men [28] and may be found
systemically (in the blood and lymph) and in local secretions (in
seminal or cervico-vaginal fluids). Antibodies in the blood and lymph
belong predominantly to the immunoglobulin G (IgG) isotype, while
those found in the external secretions are predominantly of the IgA
isotype [29,30]. Studies conducted by Fjallbrant and Obrant [31] and
Quesada et al. [32] showed that in contrast to men without antisperm
antibodies, the frequency of prostatovesiculitis was significantly
higher in men with antibodies against spermatozoa. Furthermore,
Shahmanesh et al. [33] reported the correlation between the presence of
an organism causing a sexually transmitted disease and predisposition
of men to the development of sperm antibodies. As reported by Witkin
and Toth [11], a marked increase in the incidence of sperm antibodies
(47 vs 5%) was observed in non-symptomatic men (under fertility
investigation) with a previous history of prostatitis or urethritis.
Moreover, similar study conducted by Soffer et al. [34] reported a
highly significant increase (14 vs 1.2%) in the number of ASA in the
seminal plasma of men with mycoplasmal or chlamydial infections
Volume 2 • Issue 1 • 1000118
as compared to the non-infected controls. This could be speculated
that a previous exposure to C. trachomatis, as determined by serum
antibody, could be related to the presence of sperm agglutinating
antibodies [35]. There could be two possible mechanisms responsible
for this induction of antibodies: (a) inflammation might have led to
the migration of immune cells into the genital tract where they might
have then reacted with spermatozoa; (b) antibodies may be formed to
common antigens between the bacteria and spermatozoa. The second
possibility opened new horizons, thus paving the way for molecular
mimicry between bacteria and spermatozoa to be considered as the
next challenge. Marconi et al. [36] evaluated chronic inflammatory
and infectious diseases of the male genital tract analyzing common
bacteria including C. trachomatis and Neisseria gonorrhea, yeasts
and Mycoplasma and established that there is no association between
these diseases of the male genital tract and the presence of ASA in
semen. The disagreement in earlier studies may have occurred due
to use of different detecting methods employed to screen ASA and
also different studies have taken various cut off levels for ASA as the
significant level. Subsequent studies focussing on the cross reactivity
between certain epitopes on the bacterial surface and spermatozoa,
particularly involving carbohydrate determinants were carried out.
Witkin [37] found a significant correlation between C. trachomatis
antibody titres in serum from infertile women and antisperm
antibodies on ejaculated spermatozoa of their partners. Similar
results have been reported by Hirano et al. [38] wherein they have
observed a significantly high titers of sperm immobilizing antibodies
in infertile women with past C. trachomatis infection in contrast to
those without any past record of C. trachomatis infection.
Possible underlying mechanism could be: Since C. trachomatis
has been associated with an increased concentration of seminal
T-cells bearing γδ T-cell receptor, hence leading to release of
proinflammatory cytokines which further activates macrophages.
The inflammatory response, so produced, causes the production of
antibodies against microbial antigens and spermatozoa accounting
for the mimicry between the two at the molecular level [39-42]. Heat
Shock Proteins serve as important antigens of infectious agents,
and are among the most conserved molecules in phylogeny. Since
bacterial and human HSP share ~50% amino acid homology [43], so,
a prolonged exposure of immune system to cHSP60 and simultaneous
exposure to both cHSP60 and hHSP60 may lead to autoantibody
formation [44]. Pospisil et al. [45] have found demonstrable
amounts of antisperm antibodies in 80% of the rabbits inoculated
intratesticularly with a strain of C. psittaci. Also, after successful
processing of statistical data and graphic presentation, they could
zero down upon a close similarity between the dynamics of antiChlamydia and antisperm antibodies. These results are of significant
contribution to the knowledge of formation of antisperm antibodies
as a result of a previous testicular Chlamydia infection.
Helicobacter pylori
Helicobacter pylori are well acknowledged to cause various
gastrointestinal disorders varying from chronic gastritis to gastric
adenocarcinoma and lymphoma. Besides, it might also be associated
with extraintestinal conditions and may also play a significant role in
development of autoimmune disease [46]. From the time when the
role of common antigenicity was seen in some organisms, few studies
have been done to link infertility and H. pylori on similar grounds of
molecular mimicry.
Perez-Perez et al. [47] showed the presence of serum anti-H.
• Page 2 of 6 •
Citation: Deepali T, Vander H, Vijay P (2014) Association of Antisperm Antibodies with Bacterial Infection: An Insight to Infertility. Androl Gynecol: Curr Res
2:1.
doi:http://dx.doi.org/10.4172/2327-4360.1000118
pylori antibodies in 17% of 277 couples attending an infertility centre
and whereas both the partners were seropositive only in 6.6% cases.
Figura et al. [8] while exploring the involvement of H. pylori infections
in infertility found that the infection was more prevalent in tests than
controls. The infected individuals showed the presence of anti H. pylori
antibodies that could cross-react with spermatozoa. These antibodies
were present in semen and follicular fluids. Moreover, they found
that the sera to H. pylori whole antigens and Vacoulating cytotoxin
A (VacA) could react with the tails and the pericentriolar area of
human spermatozoa (which are rich in tubulin); a linear homology
was also observed at amino acid level between β-tubulin and three
H. pylori proteins, flagellin, VacA and cytotoxin-associated gene A
(CagA). They set forth an explanation that being the only flagellated
human cells, spermatozoa may share homology with bacterial flagella
(structures endowed with the same function are normally highly
conserved during their evolution), and therefore may cross-react with
antibodies produced against flagellated organisms, such as H. pylori.
Collodel et al. [48] in their study showed that the sperm quality
of patients infected by CagA-positive strains was significantly
reduced compared to that of CagA-negative patients: motility and the
fertility index were diminished, while the frequency of apoptosis and
necrosis was increased. The presence of antisperm antibodies was also
observed by Ambrosini et al. [49]. The concentration of anti-H. pylori
antibodies in the cervical mucus of women during the ovulatory
period in their study correlated with the serum concentration. In
positive samples, the slide test showed abnormal penetration of
spermatozoa through the semen–mucus interface. They further
established that these anti-H. pylori antibodies in cervical mucus may
be considered a new local factor in female infertility.
Ureaplasma urealyticum
The male reproductive tract is known to be colonized by four
different species of mycoplasmas namely, M. hominis, Ureaplasma
urealyticum, M. fermentans and M. genitalium [50], out of which,
U. urealyticum extracts the major attention as a facultative pathogen
in male urogenital tract infections, associated with nonspecific
urethritis and prostatitis [51] but in cases of non-bacterial prostatitis,
it has been reported as a cause of the inflammation in 11-15% of the
cases [52,53]. U. urealyticum lacks a cell wall, has a unique ability to
hydrolyze urea and is one of the smallest self-replicating prokaryotes.
Because U. urealyticum is an inhabitant of the human lower genital
tract, infections are considered to be sexually transmitted and occur
more frequently during fertile ages. Although the contributory role
of U. urealyticum in infertility has yet to be conclusively established,
considerable data have been compiled to support the theory that
U. urealyticum can cause infertility [54-57]. Hass [58] and Witkin
[59] showed that U. urealyticum could break down the bloodtestis or blood-excurrent duct barrier, resulting in inoculation with
spermatozoa antigens. Earlier reports have implicated its role as
an aetiological agent in male infertility since this microorganism
can attach firmly to the spermatozoa [60], causing reduced sperm
motility and poor sperm morphology [61-63]. Bacterial survival
within the host depends on its ability to evade the immune responses
to infection. For pathogenic mycoplasmas, the phenomena of
phenotypic plasticity and molecular mimicry are responsible for
improper or inefficient recognition of bacteria by the immune system
of host. Witkin and Toth [11] explored the possible relationships
between U. urealyticum infection, antisperm antibodies, and
infertility. They found that the incidence of antisperm antibodies in
men with U. urealyticum infection was significantly higher than that
Volume 2 • Issue 1 • 1000118
in the control subjects. Similar findings were reported by Quesada
et al. [32], who also noted that fertility in men with U. urealyticum
infection was improved only after antibiotic therapy, whereas little
improvement was seen in a group of men with infection plus antisperm
antibodies. Since U. urealyticum adheres to the sperm surface, hence
the possibility of sperm damage by the metabolic products released
by this microorganism cannot be ignored. In this regard, it could
be postulated that the bacterium causes membrane changes which
result in the exposure of spermatozoa antigens to the immune system
leading to autoantibodies against sperm and hence causing infertility
related problems [34]. Ye et al. [64] first reported the existence of
cross-reactive antigens between U. urealyticum and human sperm.
Cole [65] and Shibata et al. [66] in their respective studies have
reported that mAb gainst HLA-B27 antigens show cross-reactivity
with several microbial ureases including those of U. urealyticum
and U. parvum. Furthermore, UreC subunit of ureaplasmal urease
shares some sequence homology with the synthetic immunogen used
to raise the mAb to HLA-B27. This feature suggests that molecular
mimicry between microbial urease and HLA-B27 could account for
autoimmune responses, including antisperm antibodies [67]. Wu
et al. [68] reported similar results, which provided some new clues
as to the potential mechanism(s) of how U. urealyticum caused the
production of antisperm antibodies leading to infertility. Recently Shi
et al. [69] have confirmed the existence of cross-reactive antigens (61,
50 and 25 kDa) between U. urealyticum and hSMP (human sperm
membrane protein). This is the first systematic study on cross-reactive
antigens between U. urealyticum and hSMP. The N-terminal amino
acids of the U. urealyticum 25-kDa protein were sequenced to be
MKRPLIIGVG and database analysis showed identity with UreG of U.
urealyticum. Further, they identified a common pentapeptide between
UreG and NASP (nuclear autoantigenic sperm protein), one of the
human sperm proteins. This pentapeptide, IERLT, corresponded to
published amino acids 21 to 25 in UreG and amino acids 398 to 402 in
human NASP. The results provide strong evidence for the underlying
cause of infertility in men infected with U. urealyticum and displayed
positive anti-sperm antibodies in their serum and/or semen. UreG
is a Ni2+ binding GTPase involved in the regulation of expression
and the maturation of urease and hydrogenase. NASP encodes a H1
histone-binding protein (778 amino acids, 86 kDa) that is involved in
transporting histones into the nucleus of dividing cells [70]. Multiple
isoforms are encoded by transcript variants of this gene. The somatic
form is expressed in all mitotic cells, is localized to the nucleus,
and is coupled to the cell cycle. The testicular form is expressed in
embryonic tissues, tumor cells, and the testis. In male germ cells,
this protein is localized to the cytoplasm of primary spermatocytes
and the periacrosomal region of mature spermatozoa [71]. Recently,
Al-Daghistani and Fram [41] have also recorded that women with
infertility related to autoantibodies directed towards reproductive
tissue (testis and ovaries) showed a significantly higher prevalence of
M. hominis (19.2% and 7.3% respectively) and U. urealyticum (13.7%
and 9.8%) compared with women without autoantibody-related
infertility and compared with fertile women. Repeated exposure
to Mycoplasma infection may be one of the stimulators that lead to
the formation of autoantibodies as a result of some antigenic crossreactivity between bacteria and human spermatozoa.
Gastrointestinal flora
Inflammatory bowel diseases (IBD) are an outcome of an
exaggerated and inappropriate mucosal immune response to
normal constituents of the mucosal microflora. These are chronic
• Page 3 of 6 •
Citation: Deepali T, Vander H, Vijay P (2014) Association of Antisperm Antibodies with Bacterial Infection: An Insight to Infertility. Androl Gynecol: Curr Res
2:1.
doi:http://dx.doi.org/10.4172/2327-4360.1000118
inflammatory and relapsing diseases of the gastrointestinal tract
which cause impairment of gastrointestinal structure and function.
IBD comprises of both Crohn’s disease and ulcerative colitis (UC).
A pathologic activation of the mucosal immune system in response
to antigens serves as a key factor in the pathogenesis of IBD
[72]. Since there is a loss of integrity of the mucosal membrane,
absorption studies have shown an increased permeability of intestine
to macromolecules in patients with IBD. Knoflach et al. [73] have
observed the elevated titers of serum antibodies against different
dietary antigens. The possible explanation to the observation that
there is an increased intestinal permeability in patients with IBD
could be that there might be some sharing between common epitopes
between alimentary antigens or antigens of the common intestinal
flora and human spermatozoa.
Earlier reports have suggested that there exists some similarity
between antigens of E. coli and human spermatozoa. The studies
conducted by Popivanov et al. [74] have suggested that E. coli cells of
serotypes 08, 09 and 086 contain heterogenetic antigens similar to the
cellular antigens of human spermatozoa and represented mainly on
the surface of the bacteria and spermatozoa. These antigens cannot be
classed with the heterogeneous antigens similar to the group antigens
of ABO system, for the former could not be detected in the chosen
strains by the method of absorption of specific sera against A, B and
O antigens. The possibility evidently cannot be ruled out that these
antigens may belong to the mannans of the bacterial cell walls, which
have been shown to be similar to the cellular carbohydrates of the
human spermatozoa.
Following the similar path, a study was carried out in our
laboratory, which showed that Fluorescein Isothiocyanate
(FITC) labelled sperm immobilization factor (SIF) isolated from
Staphylococcus aureus not only binds to spermatozoa but to various
gram positive and gram negative bacteria viz. Escherichia coli,
Pseudomonas aeruginosa, Salmonella enterica typhi, Shigella flexneri,
Enterococcus faecalis, Bacillus cereus and Proteus mirabilis. Therefore
it could be hypothesized that there is a common SIF binding motif
on spermatozoa and bacteria. Moreover, the co-incubation along
with SIF receptor isolated and purified from spermatozoa completely
inhibited binding of SIF to all the bacteria tested. These results further
provide an evidence for common antigenicity between bacteria and
spermatozoa [75].
Whatever the mechanisms, molecular mimicry has remained
an attractive connection between infection and infertility and is
of utmost importance to justify the increased interest of research
community, because the convincing identification of shared epitopes
would open promising opportunities for development of effective
contraceptives as well as treatment of infertility.
References
1. Irvine DS (1998) Epidemiology and aetiology of male infertility. Hum Reprod
13: 33-44.
2. Skau PA, Folstad I (2003) Do bacterial infections cause reduced ejaculate
quality? A meta-analysis of antibiotic treatment of male infertility. Behav Ecol
14: 40-47.
3. Heidenreich A, Bonfig R, Wilbert DM, Strohmaier WL, Engelmann UH (1994)
Risk factors for antisperm antibodies in infertile men. Am J Reprod Immunol
31: 69-76.
4. Eggert-Kruse W, Huber K, Rohr G, Runnebaum B (1993) Determination
of antisperm antibodies in serum samples by means of enzyme-linked
immunosorbent assay – a procedure to be recommended during infertility
investigation? Hum Reprod 8: 1405-1413.
Volume 2 • Issue 1 • 1000118
5. Lenzi A, Gandini L, Lombardo F, Cappa M, Nardini P, et al. (1991) Antisperm
antibodies in young boys. Andrologia 23: 233-235.
6. Tung KS (1975) Human sperm antigens and antisperm antibodies I. Studies
on vasectomy patients. Clin Exp Immunol 20: 93-104.
7. Kurpisz M, Alexander NJ (1995) Carbohydrate moieties on sperm surface:
physiological relevance. Fertil Steril 63: 158-165.
8. Figura N, Piomboni P, Ponzetto A, Gambera L, Lenzi C, et al. (2002)
Helicobacter pylori infection and infertility. Eur J Gastroenterol Hepatol 14:
663-669.
9. Equils O, Lu D, Gatter M, Witkin SS, Bertolotto C, et al. (2006) Chlamydia
heat shock protein 60 induces trophoblast apoptosis through TLR4. J
Immunol 177: 1257-1263.
10.Dimitrova D, Kalaydjiev S, Mendizova A, Piryova E, Nakov L (2005)
Circulating antibodies to human spermatozoa in patients with ulcerative
colitis. Fertil Steril 84: 1533-1535.
11.Witkin SS, Toth A (1983) Relationship between genital tract infections, sperm
antibodies in seminal fluid, and infertility. Fertil Steril 40: 805-808.
12.Mårdh PA, Ripa T, Svensson L, Weström L (1977) Chilamydia trachomatis
infection in patients with acute salpingitis. N Engl J Med 296: 1377-1379.
13.Weström L (1975) Effect of acute pelvic inflammatory disease on fertility. Am
J Obstet Gynecol 121: 707-713.
14.Paavonen JA, Saikku P, Vesterinen E, Lehtovirta P (1979) Infertility and
cervical Chlamydia trachomatis infections. Acta Obstet Gynecol Scand 58:
301-303.
15.Moore DE, Spadoni LR, Foy HM, Wang SP, Daling JR, et al. (1982) Increased
frequency of serum antibodies to Chlamydia trachomatis in infertility due to
distal tubal disease. Lancet 2: 574-577.
16.Gump DW, Gibson M, Ashikaga T (1983) Evidence of prior pelvic
inflammatory disease and its relationship to Chlamydia trachomatis antibody
and intrauterine contraceptive device use in infertile women. Am J Obstet
Gynecol 146: 153-159.
17.Barratt CL, Pockley AG (1998) Sperm survival in the female reproductive
tract: presence of immunosuppression or absence of recognition? Mol Hum
Reprod 4: 309-313.
18.LaVerda D, Albanese LN, Ruther PE, Morrison SG, Morrison RP, et al. (2000)
Seroreactivity to Chlamydia trachomatis Hsp10 correlates with severity of
human genital tract disease. Infect Immun 68: 303-309.
19.Betsou F, Borrego MJ, Guillaume N, Catry MA, Romão S, et al. (2003) Crossreactivity between Chlamydia trachomatis heat shock protein 10 and early
pregnancy factor. Clin Diagn Lab Immunol 10: 446-450.
20.Tiitinen A, Surcel HM, Halttunen M, Birkelund S, Bloigu A, et al. (2006)
Chlamydia trachomatis and chlamydial heat shock protein 60-specific
antibody and cell-mediated responses predict tubal factor infertility. Hum
Reprod 21: 1533-1538.
21.Ibadin KO, Enabulele OI, Eghafona NO, Aziken ME (2010) Seroevidence
of Chlamydia trachomatis antibody in infertile women in University of Benin
Teaching Hospital (Ubth) Benin City, Nigeria. Malays J Microbiol 6: 91-93.
22.Nagy B, Corradi G, Vajda Z, Gimes R, Csömör S (1989) The occurrence
of Chlamydia trachomatis in the semen of men participating in an IVF
programme. Hum Reprod 4: 54-56.
23.Eggert-Kruse W, Gerhard I, Näher H, Tilgen W, Runnebaum B (1990)
Chlamydial infection--a female and/or male infertility factor? Fertil Steril 53:
1037-1043.
24.Wølner-Hanssen P, Mårdh PA (1984) In vitro tests of the adherence of
Chlamydia trachomatis to human spermatozoa. Fertil Steril 42: 102-107.
25.Eley A, Pacey AA, Galdiero M, Galdiero M, Galdiero F (2005) Can Chlamydia
trachomatis directly damage your sperm? Lancet Infect Dis 5: 53-57.
26.Toth A, Lesser ML, Labriola D (1984) The development of infections of the
genitourinary tract in the wives of infertile males and the possible role of
spermatozoa in the development of salpingitis. Surg Gynecol Obstet 159:
565-569.
27.Shibahara H, Koriyama J, Shiraishi Y, Hirano Y, Suzuki M, et al. (2009)
Diagnosis and treatment of immunologically infertile women with sperm-
• Page 4 of 6 •
Citation: Deepali T, Vander H, Vijay P (2014) Association of Antisperm Antibodies with Bacterial Infection: An Insight to Infertility. Androl Gynecol: Curr Res
2:1.
doi:http://dx.doi.org/10.4172/2327-4360.1000118
immobilizing antibodies in their sera. J Reprod Immunol 83: 139-144.
28.Shibahara H, Shiraishi Y, Suzuki M (2005) Diagnosis and treatment of
immunologically infertile males with antisperm antibodies. Reprod Med Biol
4: 133-141.
29.Mazumdar S, Levine AS (1998) Antisperm antibodies: etiology, pathogenesis,
diagnosis, and treatment. Fertil Steril 70: 799-810.
30.Marshburn PB, Kutteh WH (1994) The role of antisperm antibodies in
infertility. Fertil Steril 61: 799-811.
50.Taylor-Robinson D, McCormack WM (1980) The genital mycoplasmas (first
of two parts). N Engl J Med 302: 1003-1010.
51.Weidner W, Brunner H, Krause W (1980) Quantitative culture of ureaplasma
urealyticum in patients with chronic prostatitis or prostatosis. J Urol 124: 622625.
52.Meseguer MA, Martinez-Ferrer M, De Rafael L, Galvez M, Baquero F (1984)
Differential counts of Ureaplasma urealyticum in male urologic patients. J
Infect Dis 149: 657-658.
31.Fjällbrant B, Obrant O (1968) Clinical and seminal findings in men with sperm
antibodies. Acta Obstet Gynecol Scand 47: 451-468.
53.Weidner W, Krause W, Schiefer HG, Brunner H, Friedrich HJ (1985)
Ureaplasmal infections of the male urogenital tract, in particular prostatitis,
and semen quality. Urol Int 40: 5-9.
32.Quesada EM, Dukes CD, Deen GH, Franklin RR (1968) Genital infection and
sperm agglutinating antibodies in infertile men. J Urol 99: 106-108.
54.Gnarpe H, Friberg J (1973) T-mycoplasmas as a possible cause for
reproductive failure. Nature 242: 120-121.
33.Shahmanesh M, Stedronska J, Hendry WF (1986) Antispermatozoal
antibodies in men with urethritis. Fertil Steril 46: 308-311.
55.Friberg J, Gnarpe H (1974) Mycoplasmas in semen from fertile and infertile
men. Andrologia 6: 45-52.
34.Soffer Y, Ron-El R, Golan A, Herman A, Caspi E, et al. (1990) Male genital
mycoplasmas and Chlamydia trachomatis culture: its relationship with
accessory gland function, sperm quality, and autoimmunity. Fertil Steril 53:
331-336.
56.Xu C, Wang YF, Zhang ZH, Shi QX (1994) Pathogenic mechanisms of male
infertility cause by Ureaplasma urealyticum infection—the effect on sperm
penetrating capability. Reprod Contract 67-71.
35.Close CE, Wang SP, Roberts PL, Berger RE (1987) The relationship of
infection with Chlamydia trachomatis to the parameters of male fertility and
sperm autoimmunity. Fertil Steril 48: 880-883.
36.Marconi M, Pilatz A, Wagenlehner F, Diemer T, Weidner W (2009) Are
antisperm antibodies really associated with proven chronic inflammatory and
infectious diseases of the male reproductive tract? Eur Urol 56: 708-715.
57.Xu C, Sun GF, Zhu YF, Wang YF (1997) The correlation of Ureaplasma
urealyticum infection with infertility. Andrologia 29: 219-226.
58.Haas GG Jr (1987) Antibody-mediated causes of male infertility. Urol Clin
North Am 14: 539-550.
59.Witkin SS (1988) Mechanisms of active suppression of the immune response
to spermatozoa. Am J Reprod Immunol Microbiol 17: 61-64.
37.Witkin SS (1996) Circulating antibodies to Chlamydia trachomatis in women:
relationship to antisperm and antichlamydial antibodies in semen of male
partners. Hum Reprod 11: 1635-1637.
60.Fowlkes DM, Dooher GB, O’Leary WM (1975) Evidence by scanning electron
microscopy for an association between spermatozoa and T-mycoplasmas in
men of infertile marriage. Fertil Steril 26: 1203-1211.
38.Hirano Y, Shibahara H, Koriyama J, Tokunaga M, Shimada K, et al. (2011)
Incidence of sperm-immobilizing antibodies in infertile women with past
Chlamydia trachomatis infection. Am J Reprod Immunol 65: 127-132.
61.Swenson CE, Toth A, O’Leary WM (1979) Ureaplasma urealyticum and
human infertility: the effect of antibiotic therapy on semen quality. Fertil Steril
31: 660-665.
39.Akande V (2002) Tubal pelvic damage: prediction and prognosis. Hum Fertil
(Camb) 5: S15-20.
62.Aparicio NJ, Muchinik G, Levalle O, Tropea L, Guitelman A, et al. (1980)
The effect of a treatment with doxycycline on semen of asthenozoospermic
patients with T-Mycoplasma genital infection. Andrologia 12: 521-524.
40.de Barbeyrac B, Papaxanthos-Roche A, Mathieu C, Germain C, Brun JL, et
al. (2006) Chlamydia trachomatis in subfertile couples undergoing an in vitro
fertilization program: a prospective study. Eur J Obstet Gynecol Reprod Biol
129: 46-53.
41.Al-Daghistani HI, Fram KM (2009) Incidence of anti-zona pellucida and
anti-sperm antibodies among infertile Jordanian women and its relation to
mycoplasmas. East Mediterr Health J 15: 1263-1271.
42.de Jesús De Haro-Cruz M, Deleón-Rodriguez I, Escobedo-Guerra MR,
López-Hurtado M, Arteaga-Troncoso G, et al. (2011) Genotyping of
Chlamydia trachomatis from endocervical specimens of infertile Mexican
women. Enferm Infecc Microbiol Clin 29: 102-108.
63.Toth A, Lesser ML (1982) Ureaplasma urealyticum and infertility: the effect
of different antibiotic regimens on the semen quality. J Urol 128: 705-707.
64.Ye YK, Lu DY, Zhu YF, Peng W, Wang YF (1994) Study on the common
antigen between human sperm and Ureaplasma urealyticum. J Androl 8: 1-4.
65.Cole BC (1996) Mycoplasma interactions with the immune system:
implications for disease pathology. ASM News 62: 471-475.
66.Shibata K, Sasaki T, Watanabe T (1995) AIDS-associated mycoplasmas
possess phospholipases C in the membrane. Infect Immun 63: 4174-4177.
43.Shinnick TM (1991) Heat shock proteins as antigens of bacterial and parasitic
pathogens. Curr Top Microbiol Immunol 167: 145-160.
67.Diaz Garcia FJ, Medina SF, Cerezo SG (2010) Impaired function of the
spermatozoa: Links with Mycoplasmal and Chlamydial infections. In: Human
spermatozoa: Maturation, capacitation, Nova Science publishers Inc.
44.Witkin SS, Neuer A, Giraldo P, Jeremias J, Tolbert V, et al. (1997) Chlamydia
trachomatis Infection, Immunity, and Pregnancy Outcome. Infect Dis Obstet
Gynecol 5: 128-132.
68.Wu AW, Huang GL, Lin TF, Shen JL (1996) Analyses of common antigen
between the membrane protein of sperm and Ureaplasma ureolyticum. J
Androl 10: 203-205.
45.Posposil L, Diblikova I, Venzik Z, Zraly Z, Horova I, Budikova M (2000)
Production of antisperm antibodies associated with genital Chlamydial
infection in rabbits. Vet Met Czech 45: 163-170.
69.Shi J, Yang Z, Wang M, Cheng G, Li D, et al. (2007) Screening of an antigen
target for immunocontraceptives from cross-reactive antigens between
human sperm and Ureaplasma urealyticum. Infect Immun 75: 2004-2011.
46.Franceschi F, Gasbarrini A (2007) Helicobacter pylori and extragastric
diseases. Best Pract Res Clin Gastroenterol 21: 325-334.
70.Batova I, O’Rand MG (1996) Histone-binding domains in a human nuclear
autoantigenic sperm protein. Biol Reprod 54: 1238-1244.
47.Perez-Perez GI, Witkin SS, Decker MD, Blaser MJ (1991) Seroprevalence of
helicobacter pylori infection in couples. J Clin Microbiol 29: 642-644.
71.Lee YH, O’Rand MG (1993) Ultrastructural localization of a nuclear
autoantigenic sperm protein in spermatogenic cells and spermatozoa. Anat
Rec 236: 442-448.
48.Collodel G, Moretti E, Campagna MS, Capitani S, Lenzi C, et al. (2010)
Infection by CagA-positive Helicobacter pylori strains may contribute to alter
the sperm quality of men with fertility disorders and increase the systemic
levels of TNF-alpha. Dig Dis Sci 55: 94-100.
49.Ambrosini G, Andrisani A, Fiore C, Faggian D, D’Antona D, et al. (2011) AntiHelicobacter pylori antibodies in cervical mucus: a new cause of infertility. Eur
J Obstet Gynecol Reprod Biol 155: 157-160.
Volume 2 • Issue 1 • 1000118
72.Neurath MF, Schürmann G (2000) Immunopathogenesis of inflammatory
bowel diseases. Chirurg 71: 30-40.
73.Knoflach P, Park BH, Cunningham R, Weiser MM, Albini B (1987) Serum
antibodies to cow’s milk proteins in ulcerative colitis and Crohn’s disease.
Gastroenterology 92: 479-485.
74.Popivanov RP, Zhukov-Verezhnikov NN, Bulanov ID, Podoplelov II,
Mishchenko BA (1981) [Heterogenetic antigens of E. coli similar to human
• Page 5 of 6 •
Citation: Deepali T, Vander H, Vijay P (2014) Association of Antisperm Antibodies with Bacterial Infection: An Insight to Infertility. Androl Gynecol: Curr Res
2:1.
doi:http://dx.doi.org/10.4172/2327-4360.1000118
sperm antigens]. Biull Eksp Biol Med 92: 316-317.
bacteria: A fluorescent microscopy study. Current Microscopy Contributions
to Advances in Science and Technology, Méndez-Vilas, Formatex Research
Center, Spain, 112-118.
75.Prabha V, Vander H (2012) Molecular similarities between spermatozoa and
Author Affiliations
1
Top
Department of Microbiology, Panjab University, Chandigarh, India
Submit your next manuscript and get advantages of SciTechnol
submissions
™™
™™
™™
™™
™™
™™
50 Journals
21 Day rapid review process
1000 Editorial team
2 Million readers
Publication immediately after acceptance
Quality and quick editorial, review processing
Submit your next manuscript at ● www.scitechnol.com/submission
Volume 2 • Issue 1 • 1000118
• Page 6 of 6 •