Antisperm Antibody Production Research Articles

Human Papillomavirus and Male Infertility: What Do We Know?

In recent years, increasing attention has been paid to understanding the causes of infertility, which is being recognized as a growing health problem affecting large numbers of couples worldwide. Male infertility is a contributing factor in approximately 30-40% of cases, and one of its etiological causes is sexually transmitted infections (STIs). Among sexually transmitted pathogens, human papillomavirus (HPV) can contribute in various ways to the failure of spontaneous and assisted reproduction, acting in the different phases of conception, especially in the early ones. In particular, HPV infection can affect sperm DNA integrity, sperm motility, count, viability, and morphology and can induce the production of anti-sperm antibodies (ASAs). In this narrative review, we aimed to provide an overview of existing research on the potential adverse effects of HPV infection on male reproductive health. Furthermore, we analyzed how limiting the spread of the infection, particularly with gender-neutral vaccination, could be a possible therapeutic tool to counteract male and female fertility problems.

Psychosomatic mechanisms of idiopathic infertility: clinical observations

In the occurrence of idiopathic infertility, psychological factors and mechanisms of transformation of the mental into the somatic play an important role. The psychotherapeutic view of the problem of idiopathic infertility consists in recognizing the fact that at a particular moment of life a person is in a state of intrapsychic or interpersonal conflict, which at an unconscious level blocks the possibility of having a child. Women with idiopathic infertility compared with fertile women are characterized by a more pronounced manifestation of such unconscious mechanisms in the implementation of their reproductive function. The reproductive function is blocked by the central nervous system, as a result of which ovarian dysfunction with the formation of cysts, ovulation disorders, lack of hormone production by the corpus luteum, spasm of the fallopian tubes, increased production of antisperm antibodies can be observed. The article presents three clinical observations that describe different variants of intrapersonal conflicts that led to infertility through their somatization. The ways of overcoming infertility with the help of psychotherapy through the awareness of psychological obstacles are shown.

Idiopathic infertility is an important problem in the modern world

Infertility, defined as the inability to conceive after one year of unprotected intercourse, is a serious societal problem that causes significant psychological, economic and social problems for married couples. The problems of female infertility have been relevant and remain so for many centuries and years. The high level of modern medicine is not always able to help and answer a woman's question: "Why does pregnancy not occur?" In the last decade, these problems have been actively studied in psychology and psychotherapy, which made it possible to identify not only the psychological consequences of reproductive health disorders in women, but also the psychological causes of these disorders. The article investigates that psychological factors and mechanisms of mental to somatic transformation play a major role in the occurrence of idiopathic infertility.The psychotherapeutic approach to the problem of idiopathic infertility consists in recognizing the fact that at a specific moment in life, a person is in a state of intrapsychic or interpersonal conflict, which at an unconscious level blocks the possibility of having a child. Compared to fertile women, women with idiopathic infertility are characterized by a more pronounced manifestation of such unconscious mechanisms of realizing their reproductive function. The reproductive function is blocked by the central nervous system, as a result of which ovarian dysfunction with the formation of cysts, ovulation disorders, lack of production of hormones by the corpus luteum, spasm of fallopian tubes, increased production of antisperm antibodies can be observed.

Assessing Antisperm Antibody Changes after Testicular Sperm Extraction in Patients Referring to Ali ibn Abi Talib Hospital

Background and Objective: Testicular sperm can be successfully recovered by testicular sperm extraction (TESE) and used for intracytoplasmic sperm injection. Disturbance in the testicular blood barrier can lead to the production of anti-sperm antibodies (ASA). This prospective study aimed to determine changes in the level of anti-sperm antibodies in TSTE surgery. Materials and Methods: In this prospective longitudinal study, 20 patients undergoing TESE surgery were included via purpose-based and accessible sampling. Patients were operated on according to the same surgical procedure. Firstly, demographic data, such as age, were recorded. The amount of anti-sperm antibodies was checked before surgery, and the patients were followed up for one month, and this amount was measured again after the end of one month. The changes in antibodies were investigated before and after one month. In addition, the relationship of the level of antibodies with demographic data and the type of disease was investigated. Anti-sperm antibodies in this study was investigated using Mixed Antiglobulin Reaction (MAR) and Immunobead Test (IBT) methods, and the type of antibody measured was IgG type. The abnormal level of IgG anti-sperm antibody was considered greater than or equal to 10%, signifying that more than or equal to 10% of the sperms are covered by IgG. Finally, the obtained results were analyzed in SPSS software. Results: The findings of this research pointed out that the levels of abnormal antisperm antibody 5% and 20% before and after TESE surgery, respectively. Based on the results of the chi-square test, these changes were significant. In addition, age and body mass index had no significant relationship with the level of anti-sperm antibody. Conclusion: As evidenced by the obtained results, the TESE surgery can increase serum ASA levels; nonetheless, it is suggested to assess this issue in future studies in a higher statistical population. One of the limitations of the present study was the lack of examination of the sexual partners of the study subjects. It is suggested to measure the ASA level in couples before and after the intervention due to the importance of the study in the fertility chances of the subjects and examine the correlation of ASA changes with semen analysis parameters.

Antisperm Antibody Testing: A Comprehensive Review of Its Role in the Management of Immunological Male Infertility and Results of a Global Survey of Clinical Practices.

Antisperm antibodies (ASA), as a cause of male infertility, have been detected in infertile males as early as 1954. Multiple causes of ASA production have been identified, and they are due to an abnormal exposure of mature germ cells to the immune system. ASA testing (with mixed anti-globulin reaction, and immunobead binding test) was described in the WHO manual 5th edition and is most recently listed among the extended semen tests in the WHO manual 6th edition. The relationship between ASA and infertility is somewhat complex. The presence of sperm agglutination, while insufficient to diagnose immunological infertility, may indicate the presence of ASA. However, ASA can also be present in the absence of any sperm agglutination. The andrological management of ASA depends on the etiology and individual practices of clinicians. In this article, we provide a comprehensive review of the causes of ASA production, its role in immunological male infertility, clinical indications of ASA testing, and the available therapeutic options. We also provide the details of laboratory procedures for assessment of ASA together with important measures for quality control. Additionally, laboratory and clinical scenarios are presented to guide the reader in the management of ASA and immunological male infertility. Furthermore, we report the results of a recent worldwide survey, conducted to gather information about clinical practices in the management of immunological male infertility.

Sex difference in anti-sperm antibodies.

BackgroundSome diseases have sex differences. There have been no reports on the relationship between anti‐sperm antibodies (ASA) and sex differences.MethodsASA are detected by sperm‐immobilization test using patients' sera in women. In men, the ASA testing is generally performed by direct‐immunobead test.Main findingsSperm‐immobilizing antibodies in women inhibit sperm migration in their genital tract and exert inhibitory effects on fertilization. ASA bound to sperm surface in men also show inhibitory effect on sperm passage through cervical mucus. The fertilization rate of IVF significantly decreased when sperm were coated with higher numbers of ASA. For women with the antibodies, it is important to assess individual patients' SI50 titers. In patients with continuously high SI50 titers, pregnancy can be obtained only by IVF. For men with abnormal fertilizing ability by ASA, it is necessary to select intracytoplasmic sperm injection. Production of sperm‐immobilizing antibodies is likely to occur in women with particular HLA after exposure to sperm. The risk factors for ASA production in men are still controversial.ConclusionAttention to sex differences in specimens, test methods and the diagnosis of ASA should be paid. For patients with ASA, treatment strategies have been established by considering sex difference for each.

Varicocele-Mediated Male Infertility: From the Perspective of Testicular Immunity and Inflammation.

BackgroundVaricocele (VC) is present in 35 - 40% of men with infertility. However, current surgical and antioxidant treatments are not completely effective. In addition to oxidative stress, it is likely that other factors such as testicular immune microenvironment disorder contribute to irreversible testicular. Evidence suggests that VC is associated with anti-sperm antibodies (ASAs), spermatogenesis and testosterone secretion abnormalities, and testicular cytokine production. Moreover, inhibition of inflammation can alleviate VC-mediated pathogenesis. The normal function of the testis depends on its immune tolerance mechanism. Testicular immune regulation is complex, and many infectious or non-infectious diseases may damage this precision system.ResultsThe testicular immune microenvironment is composed of common immune cells and other cells involved in testicular immunity. The former includes testicular macrophages, T cells, dendritic cells (DCs), and mast cells, whereas the latter include Leydig cells and Sertoli cells (SCs). In animal models and in patients with VC, most studies have revealed an abnormal increase in the levels of ASAs and pro-inflammatory cytokines such as interleukin (IL)-1 and tumor necrosis factor (TNF)-alpha in the seminal plasma, testicular tissue, and even peripheral blood. It is also involved in the activation of potential inflammatory pathways, such as the nucleotide-binding oligomerization domain-like receptor family pyrin domain containing (NLRP)-3 pathway. Finally, the development of VC-mediated infertility (VMI) may be facilitated by abnormal permeability of proteins, such as claudin-11, that constitute the blood-testis barrier (BTB).ConclusionsThe testicular immune response, including the production of ASAs and inflammatory factors, activation of inflammatory pathways, and destruction of the BTB may be involved in the pathogenesis of VMI it is necessary to further explore how patient outcomes can be improved through immunotherapy.

Neisseria Gonorrheae: A Cause of Male Infertility

Background: Gonorrhoea is a sexually transmitted infection that is commonly related to male infertility. The infection affects sperm transport through the urinary tract and subsequent damage of the testicular tubes. The infection also impair sperm production as the infection is rarely asymptomatic and can be difficult to diagnose, it is possible that its contribution to male infertility is underestimated. Infection of the genitals results in a purulent (pus-like) discharge from the genitals which may be foul smelling, inflammation, redness, swelling, dysuria, and a burning sensation during urination. As with Chlamydia, it is possible to have a Gonorrhea infection without noticeable symptoms, and which can cause permanent scarring and blockage in the sperm production duct. Gonorrhoea is a bacterial infection and is treatable with antibiotics. Laboratory studies reveal that N. gonorrhoeae infection can impair motility, viability and spermatogenesis; increase anti-sperm antibodies are associated with a decrease in semen parameters as a result of the production of anti-sperm antibodies in the genital tract. Aim: The study aimed at reviewing the possible role of gonorrhoea in male infertility. Method: Research publications such as Pubmed, Scopus, Medline etc. Results: over 115 journals of international repute were obtained, out of which 50 were found to be closely relevant such as; the implication of N. gonorrheae in male infertility, complication of N. gonorrhea infection, N. gonorrhea e and male infertility and were reviewed. Conclusion: N. gonorrhoae was found implicative in male infertility and the need for comprehensive modern laboratory methods for the diagnosis of the infection and also to included routine laboratory tests.

Relationship Between Post-Pubertal Mumps Infection In Males With Infertilityand Its Effect on The Result of Seminal Fluid Analysis and Occurrence of Immunological Infertility

Background: Mumps caused by paramyxovirus in the same group as parainfluenza and Newcastle disease virus, orchitis is the widely recognized complication in post-pubertal males. Approximately 50% of patients with orchitis have some degree of testicular atrophy, but sterility is rare. Objective: To demonstrate the effect of the post-pubertal mumps infection on the result of seminal fluid analysis and to know if infection by mumps after puberty can lead to immunological infertility and production of anti-sperm antibodies. Patients and Methods: Cross-sectional study in which 300 infertile males attending microbiology laboratory in Rizgary teaching hospital in Erbil city in Iraqi Kurdistan from November 2017- September 2018. Questionnaire was prepared for each male which included: name, age, occupation, history of mumps infection after puberty. Seminal fluid collected from each patient after 3 days of abstinence and analyzed according to WHO guidelines. Seminal fluid and serum obtained from each infertile male for the detection of anti-sperm antibodies by ELISA (enzyme-linked immunosorbent assay). Results: The mean age of the participant in the study was (32.805 year) with the maximum and minimum age was (50, 18) years respectively. The incidence of post-pubertal mumps was (13.3%) and the incidence of abnormal seminal fluid analysis was (10%) and the highest abnormal seminal fluid variables among infertile males with post-pubertal mumps was oligoasthenozoospermia (43%) and the anti-sperm antibodies in the semen of infertile males with post-pubertal mumps infection was (60%) while the frequency of anti-sperm antibodies in the serum in infertile males with a history of post-pubertal mumps was (40%) which was higher than those with no history of post-pubertal mumps with highly significant relation statistically. Conclusion: Abnormal seminal fluid analysis result may be due to post-pubertal mumps and it can lead to (Asthenozoospermia, Oligospermia, and Teratozoospermia). The highest percentage of abnormal seminal fluid variables was Oligoasthenozoospermia the occurrence of anti-sperm antibodies can be the sequence of post-pubertal mumps and by itself can lead to abnormality in the seminal fluid analysis. Mumps can lead to male infertility by affecting the seminal fluid parameters and also by the production of anti-sperm antibodies which can lead to subfertility in adult males. Keywords: Paramyxovirus, post-pubertal mumps, anti-sperm antibodies

Human MOSPD2: A bacterial Lmb mimicked auto-antigen is involved in immune infertility

Autoantibody production is one of the leading factors of immune infertility, an autoimmune disease of the male reproductive system. The potential involvement of MHC-class II derived self-peptides against bacterial proteins in the antisperm antibody (ASA) production has been reported previously. Apparently, Streptococcus agalactiae has been considered as an important pathogen to impart infection-induced infertility in a bacteriospermia associated leukocytospermia (LCS/BS) state. Hence, the present study attempts to confirm S. agalactiae specific Laminin binding protein (Lmb) derived self-peptide (‘KDSYTKKAKAFKKEA’) namely human Motile Sperm domain-containing protein 2 (MOSPD2) as an auto-antigen in LCS/BS condition. Semen samples were collected from infertile men with LCS/BS (n ​= ​17) and their fertile counterparts (n ​= ​10). Gram-positive bacteria were predominantly identified in the entire 17 LCS samples using culture method followed by 16S rDNA sequencing technique. TLRs 2 and 4 expression used as markers of immune response in spermatozoa and sperm dysfunction were elevated in the LCS/BS spermatozoa as compared to their fertile counterparts. A significant increase in oxidative stress indices i.e., protein carbonylation, lipid peroxidation and acridine orange test (AOT), was also observed in the LCS/BS spermatozoa. Spermatozoa lysate (both auto and heterologous), bacterial lysate (control) and synthesized MOSPD2 self-peptide were used to test their antigenicity against the autoantibodies by rocket immunoelectrophoresis (RIEP) assay. Seminal plasma from LCS/BS patients with S. agalactiae was used as the source of autoantibodies. Spermatozoa and bacteria lysate; and MOSPD2 self-peptide were able to bind autoantibodies in the seminal plasma. Besides, the self-peptide showed a dose dependent increase in the precipitation of antibody. T-cell epitope mapping of 48 Enterococcus faecalis and 91Staphylococcus aureus surface proteins confirmed MOSPD2 as a global auto-antigen. Thus, augmentation of TLR expression in LCS/BS spermatozoa inferred MOSPD2 to be a putative immunogen. Altogether, these findings will delineate the significance of MOSPD2 auto-antigen in a bacteria derived immune infertility condition.

Homology between cattle bull sperm and bacterial antigenic proteins viz a viz possible role in immunological infertility

This study was carried out to investigate the possible presence of identical sperm and bacterial antigens which may cause similar antisperm antibody production leading to lower fertility. Cross-reactive antigens of cattle bull spermatozoa and different bacteria including Escherichia coli (E.coli), Bacillus sp., and Staphylococcus sp. were characterized by immunoblotting and mass fingerprinting. Significant cross-reactivity was obtained for 75, 72, 44, 40, 33, 30, 25, 18, 14kDa proteins with purified IgG of calves, heifers and cows between spermatozoa and the studied bacteria. Significantly (p<0.05) matched cross-reactive 40/33/30kDa sperm, 33kDa Staphylococcus sp/Bacillus sp and 40/25kDa E.coli proteins were analyzed. Mass fingerprinting of 40/33/30kDa (spermatozoa); 40/25kDa (E.coli) and 33kDa (Bacillus/Staphylococcus) proteins revealed their matching with vitellogenin-1-like/mitochondrial malate dehydrogenase 2, NAD/acrosin-binding protein isoform XI; outer membrane insertion signal domain/spore coat protein and glyceraldehyde-3-phosphate dehydrogenase, respectively. Acrosin-binding protein isoform X1 and mitochondrial malate dehydrogenase 2, NAD contributes to the capacitation of spermatozoa. Spore coat protein; glyceraldehyde-3-phosphate dehydrogenase of E.coli; Bacillus/Staphylococcus are 37.6% and 39.01% identical to acrosin-binding protein isoform X1; mitochondrial malate dehydrogenase 2, NAD of cattle bull spermatozoa. It can be interpreted from these observations that cross-reacting antibodies developed against 33/30kDa sperm proteins and 25, 33kDa bacterial proteins in cows may affect the functional activity of spermatozoa leading to delayed fertility in heifers and cows.

Antisperm antibodies as a factor of male infertility. Relevance, modern methods of diagnosis and treatment

According to WHO statistics 40 % of childless marriage is due to factors of male infertility. One of them is the presence of antisperm antibodies in the male organism, which may be in blood serum, on the surface of spermatozoids and seminal plasma. Aim. Оn the grounds of specialized literature analysis, to show the relevance of this problem in Reproductive Medicine, to descript Basic methods of Modern treatment and diagnosis of this pathology in the body of infertile males. The most common methods of antisperm antibodies identifying are: MAR-test sample Shuvarskiy–Sims–Hyuner, Kurtsrok–Miller test, the method of latex agglutination, solid-phase immunoenzymatic blood test. Indications for antisperm antibodies determining are: modified indices, deviations in post-coital test, a negative test of sperm and cervical mucus interaction in vitro, unexplained infertility in the married couples, failure or low indices during IVF ( in vitro fertilization) and of course, the exclusion of other causes of infertility. When antisperm antibodies are detected, the strategy of treatment may be destined to reduction of their titer for further pregnancy. Such types of therapy can be used: contraceptive (long-term use contraception barrier to reduce antisperm antibodies titer in women), plasmapheresis, artificial insemination with pretreated from antisperm antibodies husband's sperm, methods of assisted reproductive technologies. Conclusoins. The formation of antisperm antibodies leads to infertility of immunological genesis (in 20 % of couples with unexplained infertility). To confirm their presence in the male body it is necessary to perform the MAR-test, Shuvarsky test, other tests and, of course, the exclusion of other causes of infertility. Men of reproductive age with an immunological factor of infertility provides for a comprehensive treatment, including elimination of all possible causative and contributing factors of infertility (infection of the male reproductive system, varicocele etc.), decreased production and removal of spermatozoa-associated antisperm antibodies and assisted reproductive technologies – intrauterine insemination and in vitro fertilization.

Sleep Deprivation and Late Bedtime Impair Sperm Health Through Increasing Antisperm Antibody Production: A Prospective Study of 981 Healthy Men.

BackgroundThe aim of this study was to investigate the effects of sleep duration and bedtime on sperm health, and the possible mechanism involved.Material/MethodsWe randomly divided 981 healthy Chinese men into groups according to research-set bedtimes (A=8–10 PM, B=after 10 PM, and C=after midnight) and sleep durations: group 1=<6.0 h (short), group 2=7.0–8.0 h (average), and group 3=>9.0 h (long). Sperm morphology, count, survival, and motility were examined according to sleep patterns. Antisperm antibody (ASA) production in semen was determined.ResultsSperm counts and their survival rates were lower in the short sleepers as compared to others within each group (all P<0.01). The lower counts and survival rates were observed in different bedtimes, with significant differences found between measurements of C1 vs. A1 and C2 vs. A2 or B2 (all P<0.05 or 0.01). Semen motility was lower in the short sleepers as compared to the average and long sleepers (all P<0.01). There were differences in the bedtime-related results between measurements of C1 vs. A1 or B1 (P<0.05 or 0.01). Additionally, the population proportion for the ASA-positive participates and incidence of the ASA-expressed population obviously increased in the short sleepers as compared to others within each group (all P<0.05).ConclusionsShort and long sleep durations and late bedtime were associated with impaired sperm health in the study cohort, partly through increasing ASA production in the semen.

Hemospermia is not associated with the production of antisperm antibody

Objective To investigate whether hemospermia is involved in the production of antisperm antibodies (ASA). Methods A total of 40 males with hemospermia were enrolled in this study. These males were divided into 3 groups according to their fertile status: 18 cases were patients who visited the infertility clinic (group A), 8 had fertility (group B), and 14 did not know their fertile status (group C). Semen samples were collected and ASA levels were detected by the direct immunobead test (D-IBT). Leukocytes in semen were assessed by the peroxidase assay. Results None of these males with hemospermia were found to display significant levels of ASA in the 3 groups. The number of cases who had increased levels of leukocytes in the semen samples of groups A, B and C were 15 (83.3%), 6 (75.0%) and 12 (85.7%), respectively. Conclusion Hemospermia is not associated with the production of ASA. It is worth noting that the leukocyte levels are increased in semen of males with hemospermia.

Spermatocele in a South African Boerboel Dog

A 2-year-old intact male South African Boerboel presented for semen cryopreservation and was discovered to be azoospermic. The dog had excellent libido and had sired litters within 6 months, so a further investigation of why his collection lacked sperm was warranted. On further examination of his scrotal contents, his right epididymis had an enlarged area with a hard texture. Ultrasonography revealed that the enlarged area of the right epididymis was fluid filled. A sample of the fluid was aspirated for aerobic culture. No bacteria showed growth. Although the culture was negative, it was suspected that this dog had an epididymitis or epididymal abscess, and treatment with enrofloxacin at 10mg/kg orally was initiated for 4 weeks. The abnormal texture and fluid-filled cavity in the right epididymis persisted, despite antibiotic therapy. Cytology of a repeat aspiration of the fluid-filled area after antibiotic therapy revealed a mixture of red blood cells and sperm. Owing to the potential for blood-testis barrier disruption, a unilateral orchiectomy of the right testicle was performed, as an attempt to protect future sperm production of the remaining testicle. A spermatocele was confirmed on histopathology. After another month, an excellent-quality semen sample was collected, with 90% progressive motility, good concentration, and few morphologic abnormalities. A subsequent collection was acquired and was successfully cryopreserved for future breeding. In dogs with spermatoceles, semen quality can be preserved with aggressive treatment to remove the affected testicle. The disruption of the blood-testis barrier in spermatoceles may result in antisperm antibody production and eventual infertility; however, cryopreservation can result in long-term options for owners seeking to continue using an animal in their breeding program.

HLA antigens and anti-sperm antibody production in Iranian vasectomized men

HLA antigens and anti-sperm antibody production in Iranian vasectomized men

Antisperm antibodies and testicular blood flow after inguinal hernia mesh repair.

Testicular flow studies after hernia mesh repair mostly showed different outcomes. The reason of infertility in some men after hernia repair is immunological factors. Aim of the study was to investigate the influence of mesh hernia repair on antisperm antibodies production and testicular blood flow and a connection among these parameters. A prospective interventional longitudinal cohort study was made on 82 male patients without exclusion criteria who had an inguinal hernia. Patients underwent laparoscopic TAPP or open tension-free hernia repair. Vascular ultrasound and antisperm antibodies were measured in the preoperative and postoperative periods. Main outcome measures were resistive index (RI), peak systolic velocity (PSV) cm/s, and end-diastolic velocity (EDV) cm/s in testicular blood flow measurement and the quantitative value of antisperm antibodies (ASA) in serum (IU/ml). ASA significantly increased postoperatively only in patients who underwent open tension-free hernia repair (p < 0.001). ASA stayed in normal range in all patients except the one with postoperative complication. Friedman analysis showed significant change of the RI only on intratesticular (p < 0.001) and capsular artery level (0.02) in patients who underwent laparoscopic technique. PSV significantly changed on intratesticular (p < 0.001) and capsular artery level (p = 0.015) in the laparoscopic hernia repair. PSV showed significant change on intratesticular (p < 0.001) and testicular artery levels (p < 0.001) in the open tension-free hernia repair. EDV showed significant change only on testicular artery level (p = 0.032) in the patients who had open tension-free hernia repair. These blood flow parameters significantly increased in the early postoperative period and returned on basal value in the late postoperative period. Parameters of flow did not show any significant correlation with ASA. Mesh hernia repairs without complication caused only a transitory change in testicular blood flow and no clinical significant autoimmune reaction.

Does Bone Marrow–derived Mesenchymal Stem Cell Transfusion Prevent Antisperm Antibody Production After Traumatic Testis Rupture?

To determine whether transfusion of mesenchymal stem cells (MSCs) could prevent humoral immune response and autoimmunization against sperms after traumatic testis rupture. Immunomodulatory properties of MSCs have been evaluated by a prospective cohort on 50 adult BALB/c mice. In each interventional arms of study, controlled testis rupture and surgical repair were exerted. In addition to tissue repair, single dose of 5×10(5) MSCs labeled by green fluorescent protein was delivered intravenously to 20 cases (cell therapy group). After euthanizing, seroconversion of antisperm antibody (ASA) was compared between 2 interventional groups as response of humoral immune system. Lung and testis tissues were examined for green fluorescent protein-positive cells to assess whether presence of stem cells is correlated with seroconversion rates. Six cases had been lost during the study. Fourteen of 16 mice in cell therapy control group formed ASA (87.5%) but 6 of 18 mice (33.3%) in cell therapy group were immunized and formed ASA (P=.002). Transplanted cells were traced in lungs of 55% (n=10) of cell therapy group and none were found in trauma site. Small volume of mice blood was our main limitation to trace seroconversion or quantitative measurement of ASA in each case. In this in vivo model of autoimmune infertility, bone marrow-derived MSC transfusion showed immunosuppressive effects on antibody production. Considering immunomodulatory properties of MSCs even in allogeneic settings, novel clinical application should be investigated further.

Effect of P/E-selectin blockage on antisperm antibody development and histopathological alterations in experimental orchitis

AimThis study aimed to evaluate the effect of P/E-selectin blockage on antisperm antibody (ASA) development and histopathological alterations in experimental orchitis. Materials and MethodsThirty-six Wistar albino-type male rats weighing 100–150g were included in the study. Rats were allocated into six groups (n=6) including control (CG), sham (SG), orchitis (OG), antimicrobial treatment (AG), P/E-selectin blockage (PESG), and both antimicrobial and P/E-selectin treatment (TG) groups. In CG, serum samples were taken from the tail vein prior to the procedure and followed by extraction of both testes. In SG, 1ml of saline solution was injected in testicular parenchyma. OG was obtained by injecting 0.1ml 106cfu/ml Escherichia coli (0:6 strain) and 1ml saline solution into the right testes. AG received ciprofloxacin (50mg/kg/day) twice a day through gastrogavage 24hours after generating orchitis. In PESG, P/E-selectin antibody (100μg) was administered intravenously via the tail vein 24hours after the induction of orchitis. Finally, both ciprofloxacin and P/E-selectin antibody were administered in TG 24hours after the induction of orchitis for 14days. At the end of treatment, 1ml of serum sample was obtained to evaluate the ASA, P-selectin and E-selectin levels. In order to evaluate spermatogenesis (Johnsen score) and testicular injury (Cosentino score), both testes were extracted at the end of the 14th day. ResultsIn orchitis-induced groups (OG, ATG, PSEG, TG), ASA levels were significantly increased at the 14th day when compared to SG (p<0.05). In TG, ASA levels were decreased when compared to AG. However, similar alteration in ASA levels was not detected in PSEG (p>0.05). In OG and AG, P-selectin levels were decreased at the 14th day when compared to levels observed on 0 day (p<0.05). E-selectin levels on 0 day showed that each group had higher levels of E-selectin when compared to CG (p>0.05). There was no significant difference regarding E-selectin when compared to CG (p>0.05). No significant differences regarding E-selectin levels were detected on the 0th and 14th days between AG and CG (p>0.05). When the Cosentino and Johnsen scores were compared among groups, TG and PSEG has decreased scores of Cosentino than OG on the right testicle (p<0.05). In contrast, an increased Johnsen score was detected in TG and PSEG when compared to OG (p<0/05). No significant difference was detected for both Cosentino and Johnsen scores on the left testicle (p>0.05). There was no difference with regard to the right and left testicular injury in TG. In P/E-blocked groups, decreased histopathological alterations were observed in the contralateral testis. ConclusionP/E-selectin blockage may reduce ASA production after orchitis when combined with antimicrobial treatment. P/E-selectin blockage not only has a protective effect on blood–testis barrier but also decreases the histopathological alterations in both the affected and contralateral testis. Histopathological parameters of spermatogenesis may also be prevented by P/E-selectin blockage in experimental orchitis.

Les anticorps anti-spermatozoïdes chez l’homme : de la physiopathologie à la thérapeutique

Immunoinfertility is an important problem, involving a significant number of infertile men. According to the literature many factors can induce the development of antisperm antibodies (ASA) in the male serum of genital fluids such as genital trauma, history of genital infections, varicoceles and vasectomy. Antisperm antibodies can impair the fertilizing capacity of spermatozoa by decreasing the semen parameters, mucus penetration and by inhibiting sperm–oocyte interaction. Moreover, ASA may have a deleterious effect on embryo development and implantation. Various methods have been proposed to reduce ASA production and to treat this class of infertility. In the present review, we note the different physiopathological mechanisms responsible for the production of ASA in humans, various detection techniques ASA, their involvement in the couple's infertility and the different therapeutic methods to propose in the case of the immune infertility. Les anticorps anti-spermatozoïdes (ASA) forment une catégorie de glycoprotéines fréquemment rencontrée chez les hommes infertiles. Les facteurs physiopathologiques à l’origine du développement de cette auto-immunité sont à nos jours mal définis. Cependant, les traumatismes testiculaires, les antécédents d’infections urogénitales, les cures de varicocèle, la vasectomie ainsi que les pratiques homosexuelles sont toujours évoqués dans les cas d’une infertilité immunologique. Cette catégorie d’anticorps est à l’origine d’une altération de la capacité du spermatozoïde à franchir le mucus cervical et à interagir avec l’ovocyte. De plus, les ASA peuvent altérer le développement embryonnaire et son implantation au niveau de l’endomètre de la femme. Plusieurs stratégies ont été proposées soit pour réduire les taux de ces ASA dans le sperme ou le sérum de l’homme ou encore pour traiter les couples souffrant d’une telle infertilité. Dans cette présente revue, nous relevons les différents mécanismes physiopathologiques à l’origine de la production des ASA chez l’homme, les différentes techniques de mise en évidence des ASA, leur implication dans l’infertilité du couple ainsi que les différents moyens thérapeutiques à proposer dans le cadre de cette infertilité d’origine immunologique.