Search Results (68)

Background/Objectives: The role of the endometrial microbiome in reproductive failure remains incompletely understood. This study aimed to describe the composition of the endometrial microbiome in women evaluated for infertility or recurrent miscarriage. Methods: In this single-center descriptive study, endometrial samples were collected from women evaluated for infertility or recurrent miscarriage. Microbiome profiling was performed using 16S rRNA gene next-generation sequencing. Samples were classified as Lactobacillus-dominant when Lactobacillus spp. accounted for ≥90% of the total bacterial community. Alpha diversity was assessed using the Shannon and Simpson indices, while beta diversity was evaluated using Bray–Curtis dissimilarity, principal coordinates analysis (PCoA), PERMANOVA, and PERMDISP. Results: Of the 60 samples, 20 (33.3%) were Lactobacillus-dominant and 40 (66.7%) were non-Lactobacillus-dominant. Across all samples, Firmicutes was the predominant phylum (76.6%). Non-Lactobacillus-dominant samples showed significantly higher alpha diversity than Lactobacillus-dominant samples for both the Shannon and Simpson indices (p = 1.19 × 10⁻⁶ and p = 1.51 × 10⁻⁶, respectively), as well as higher observed taxa richness (p = 0.000017). PCoA based on Bray–Curtis dissimilarity demonstrated clear separation between microbiome profiles, supported by PERMANOVA (pseudo-F = 13.87, R² = 0.193, p = 0.001). PERMDISP showed significantly greater dispersion among non-Lactobacillus-dominant samples (F = 566.94, p < 0.001). Non-Lactobacillus-dominant samples showed greater representation of Enterococcus and Prevotella. Conclusions: In this cohort non-Lactobacillus-dominant communities were more frequent with greater diversity, richness, and compositional heterogeneity than Lactobacillus-dominant communities. These findings highlight the need for larger, standardized studies with appropriate control populations to clarify their clinical significance. Full article

The aim of this study was to investigate the association between the endometrial microbiome and local immune cell composition during the implantation window. We conducted a single-center prospective observational study including endometrial samples from 58 women without endometrial pathology. All samples were obtained during the mid-secretory phase (day 5 post-ovulation). Endometrial stromal CD3⁺ T cells, CD4⁺ T helpers, CD56⁺ NK cells and CD68⁺ macrophages were identified by immunohistochemistry and quantified as a percentage of stromal cells using HALO image analysis software. Microbiome composition was assessed by 16S rRNA gene sequencing (V4–V5 region). Lactobacillus dominance (LD) was defined as the genus with the highest centered log-ratio value within each sample. Endometrial immune cell composition showed a median 2.28% CD3⁺ T cells of stromal cells, 1.75% CD56⁺ NK cells, 1.44% CD68⁺ macrophages and 0.29% CD4⁺ T helpers. Lactobacillus-dominated microbiota was identified in 51.7% (30/58) of samples. Correlation analysis showed that Lactobacillus-related taxa were negatively associated with NK/T ratios and positively with T helper-related ratios. LD samples exhibited reduced NK cell abundance (1.17% vs. 2.12%, p = 0.006, q = 0.023) and a lower NK/T ratio (0.52 vs. 1.05, p = 0.004, q = 0.023) compared to non-LD samples. This study provides evidence for a link between microbial composition and local immune regulation in the endometrium. Full article

Endometriosis is a chronic, estrogen-dependent inflammatory disorder characterized by the ectopic implantation and persistence of endometrial-like tissue outside the uterine cavity. Despite its high prevalence and significant impact on quality of life, the pathogenesis of endometriosis remains incompletely understood and involves a complex interplay between hormonal dysregulation, immune dysfunction, and chronic inflammation. In recent years, growing evidence has highlighted the role of the microbiota as a potential modulator of these interconnected pathways. This review proposes an integrative framework in which the microbiota acts as a central modulator of immune–endocrine interactions in endometriosis, while synthesizing current evidence on underlying biological mechanisms. We discuss how alterations in the gut, vaginal, and endometrial microbiota contribute to disease pathophysiology through multiple mechanisms, including disruption of intestinal barrier integrity, activation of pro-inflammatory signaling pathways, immune dysregulation, and modulation of estrogen metabolism via the estrobolome. Microbial β-glucuronidase activity and enterohepatic recirculation of estrogens are explored as key processes linking gut dysbiosis to the hyperestrogenic environment characteristic of endometriosis. Furthermore, we review current pharmacological treatments and highlight their limitations, emphasizing the need for novel therapeutic strategies targeting upstream disease mechanisms. Emerging approaches, including probiotics, postbiotics, short-chain fatty acids, and dietary interventions, are discussed as promising adjunctive therapies capable of modulating inflammation, immune responses, and metabolic pathways. Although current evidence remains heterogeneous and largely derived from preclinical and observational studies, the microbiota emerges not only as a potential therapeutic target but as a key integrative node linking endocrine, immune, and metabolic pathways in endometriosis. Future research should focus on well-designed clinical trials to validate microbiome-based interventions and to define their role in personalized management strategies for endometriosis. Full article

Objectives: To evaluate the presence and dominance of Lactobacillus in the endometrial microbiome and their age-related associations in a large group of Bulgarian patients with recurrent implantation failure (RIF) and recurrent pregnancy loss (RPL) who attend our clinic. Methods: This retrospective study included 199 patients (mean age: 35.69 ± 5.16) with RIF (n = 103) and RPL (n = 96) who visited our fertility clinic between October 2019 and November 2022. Endometrial samples were analyzed using real-time PCR for target DNA sequences. Results: Overall, 62.8% (n = 125) exhibited an absence of Lactobacilli in their endometrial samples, with 63.1% (n = 65) of the RIF group and 62.5% (n = 60) of the RPL group showing a lack of Lactobacilli, with no statistically significant difference between the groups (p = 0.926). A Lactobacillus-dominant microbiome was found in 23.6% of the entire cohort (n = 47), 25.2% of the RIF group (n = 26) and 21.9% of the RPL group (n = 21). A reduced abundance of Lactobacilli was identified in 13.5% of the cohort (n = 27), though to differing degrees. There was no significant relationship between the abundance of Lactobacilli and belonging to the RIF or RPL group. A statistically significant difference was found in the mean age of two groups in cases with a Lactobacillus-dominant microbiome (mean age of 36.4 ± 4.8 years in the RIF group and 32.5 ± 3.5 years in the RPL group) (p = 0.004). Conclusions: Our findings demonstrate a high prevalence of non-Lactobacillus-dominant microbiomes in a large group of Bulgarian patients with RIF and RPL and significant age-related Lactobacillus changes in the microbiome of patients with RPL. These results point to the potential role of the uterine microbiome and support the need for further prospective studies, especially in cases of advanced maternal age. Full article

Background: Endometriosis is traditionally conceptualized as a localized gynecological disorder characterized by the presence of ectopic endometrial tissue. However, high recurrence rates following apparently complete surgical excision challenge this lesion-based paradigm and suggest the existence of underlying biological mechanisms that extend beyond residual disease. Increasing evidence indicates that endometriotic cells exhibit persistent molecular alterations, including dysregulated gene expression, epigenetic modifications, and immune dysfunction, which may contribute to disease maintenance and recurrence. Objective: This study aims to critically examine whether endometriosis can be considered a molecularly reprogrammed disease, characterized by persistent cellular and microenvironmental alterations that are not reversed by surgical removal of visible lesions. Methods: A narrative review of the literature was conducted using PubMed, Scopus, and Web of Science databases including studies published from January 2016 to March 2026. Studies investigating molecular, genetic, epigenetic, and immunological mechanisms of endometriosis persistence and recurrence were included. Particular attention was given to pathways involved in cellular survival, inflammation, hormone resistance, and epigenetic regulation. Results: Endometriotic cells demonstrate stable alterations in gene expression profiles, including pathways related to estrogen signaling, progesterone resistance, inflammation, and cellular proliferation. Epigenetic mechanisms, such as aberrant DNA methylation and histone modifications, appear to sustain these changes over time, contributing to a form of “molecular memory.” In parallel, the peritoneal microenvironment is characterized by chronic inflammation, immune tolerance, and impaired clearance of ectopic cells. These factors collectively support lesion persistence and may explain recurrence even after complete surgical excision. Emerging evidence also highlights the role of systemic factors, including endocrine–immune interactions and microbiome-related pathways, reinforcing the concept of endometriosis as a systemic rather than purely localized condition. Conclusions: Endometriosis may be more accurately defined as a persistent, molecularly reprogrammed disease driven by stable alterations in cellular behavior and the surrounding microenvironment. This paradigm shift has important clinical implications, suggesting that surgical treatment alone may be insufficient and that future therapeutic strategies should target the underlying molecular and immunological mechanisms responsible for disease persistence. Full article

Successful embryo implantation requires dynamic, bidirectional communication between a developmentally competent blastocyst and a receptive endometrium, integrating hormonal, molecular, and immunologic signals. Increasing evidence indicates that endometrial receptivity is critically dependent on a specialized immune microenvironment that supports trophoblast invasion while maintaining maternal tolerance. This review synthesizes current knowledge on the immunologic regulation of implantation, with emphasis on uterine natural killer (uNK) cells, regulatory T cells (Tregs), macrophages, dendritic cells, and cytokine networks. We further examine intracellular signaling pathways—including JAK/STAT, PI3K/AKT, NF-κB, and MAPK—that integrate immune and decidual responses. The bidirectional embryo–endometrium dialogue is explored through embryo-derived mediators such as human chorionic gonadotropin (hCG), cytokines, growth factors, and extracellular vesicles. The endometrium is increasingly recognized as a biosensor of embryo quality, selectively supporting viable embryos. Disruption of this complex communication network is implicated in recurrent implantation failure and early pregnancy loss. Despite substantial mechanistic advances, clinical translation remains limited. Emerging strategies, including immune profiling, microbiome modulation, and extracellular vesicle-based diagnostics, hold promise for precision reproductive medicine. Full article

Polycystic ovary syndrome (PCOS) is increasingly recognized as a complex, multi-system disorder involving interactions among metabolic dysfunction, chronic low-grade inflammation, and neuroendocrine dysregulation, rather than a condition confined to the ovary. While current management strategies primarily target symptomatic manifestations, such as menstrual irregularity, hyperandrogenism, and insulin resistance, they do not directly address the underlying integrative pathways linking the gut microbiome, cellular energy sensing, and hypothalamic reproductive control. This review proposes a mechanistic framework in which algae-derived bioactives modulate a gut–SIRT1–kisspeptin axis, thereby offering a systems-level perspective on PCOS pathophysiology and intervention. Gut dysbiosis in PCOS contributes to altered bile acid signaling, disrupted microbial metabolite profiles, and increased inflammatory tone, all of which may impair both metabolic and reproductive functions. Concurrently, reduced activity of the NAD⁺-dependent deacetylase SIRT1 has been documented across ovarian, endometrial, and metabolic tissues, linking energy imbalance to oxidative stress, inflammation, and impaired steroidogenesis. At the neuroendocrine level, dysregulated kisspeptin signaling contributes to abnormal gonadotropin-releasing hormone pulsatility and luteinizing hormone hypersecretion, key features of PCOS. Algae-derived compounds, including polysaccharides, phlorotannins, fucoidan, fucoxanthin, and microalgae bioactives, exhibit prebiotic, anti-inflammatory, and metabolic regulatory properties that intersect with these pathways, particularly through modulation of gut microbiota and activation of AMPK/SIRT1 signaling. The central proposition of this review is that algae-derived bioactives may act across interconnected biological layers: reshaping gut microbial ecology, restoring SIRT1-mediated metabolic balance, and retuning kisspeptin-driven neuroendocrine activity. While individual components of this axis are supported by substantial evidence, direct experimental validation of the complete pathway remains limited. Therefore, this framework is positioned as a translationally grounded but hypothesis-driven model that integrates currently fragmented findings into a coherent and testable paradigm. Future research should prioritize multi-level experimental and clinical studies that simultaneously assess microbiota composition, metabolic signaling, and reproductive neuroendocrine outcomes to establish the therapeutic potential of algae-based interventions in PCOS. Full article

Background: Chronic endometritis (CE) is a subtle, often asymptomatic endometrial inflammation marked by CD138⁺ plasma cell infiltration and linked to recurrent implantation failure (RIF), recurrent pregnancy loss (RPL), and unexplained infertility. Emerging evidence implicates endometrial microbiome dysbiosis in CE. Objective: To systematically review and conduct meta-analysis on the association between CE and endometrial microbiome alterations and their reproductive implications. Methods: We searched MEDLINE, Embase, Web of Science, Scopus, Cochrane CENTRAL, and Google Scholar for studies diagnosing CE via CD138 immunostaining, assessing microbiota with molecular techniques. Data extraction, quality assessment, and meta-analysis were performed. Results: Twenty-two studies including 4022 women were analyzed. CE was associated with reduced prevalence of Lactobacillus-dominated microbiota and increased detection of non-Lactobacillus species, particularly Streptococcus spp., Enterococcus spp., Escherichia coli, Staphylococcus spp., Ureaplasma spp., and Gardnerella vaginalis. In the meta-analysis (2947 women), Enterococcus spp. and Ureaplasma spp. were significantly more prevalent in women with CE, whereas Streptococcus spp., E. coli, Staphylococcus spp. and G. vaginalis showed non-significant trends. Only E. coli and Streptococcus spp. showed significant heterogeneity between-studies. Conclusions: CE is linked to microbial dysbiosis with reduced Lactobacillus dominance and enrichment of potentially pathogenic taxa, notably Enterococcus and Ureaplasma spp. These findings suggest that the endometrial microbiome contributes to chronic inflammation and adverse reproductive outcomes, yet heterogeneity and limited evidence call for standardized diagnostics and robust trials before clinical implementation. Full article

Anti-β2GPI/HLA-DR antibody, chronic endometritis (CE), and endometrial dysbiosis are likely to be associated with the etiologies of recurrent pregnancy loss (RPL). This prospective cohort study aimed to investigate these new risk factors together with conventional causes for RPL, and to evaluate pregnancy outcomes in women individually treated. A total of 87 women with RPL underwent conventional assessment together with anti-β2GPI/HLA-DR antibody measurements, CD138 immunohistochemistry for CE, and 16S rRNA sequence analysis for endometrial microbiome. Women with anti-β2GPI/HLA-DR antibody, CE, and endometrial dysbiosis received low-dose aspirin and heparin, antibiotics, and probiotics, respectively. Pregnancy outcomes of the participants were assessed. Anti-β2GPI/HLA-DR antibody, CE, non-Lactobacillus-dominant microbiome (NLDM)-1 (Lactobacillus + Bifidobacterium < 80%), and NLDM-2 (Lactobacillus without iners + Bifidobacterium < 80%) were detected in 16 (18.4%), 22 (25.3%), 27 (31.0%), and 46 (52.8%) women, respectively. Based on conventional assessment, 65.5% of women with RPL were classified as unexplained etiology; however, the percentage reduced to 16.1% when these new tests were assessed together. All 9 pregnancies with anti-β2GPI/HLA-DR antibody, 13 (92.9%) of 14 pregnancies with CE, and 24 (92.3%) of 26 pregnancies with NLDM-2 resulted in live birth. Assessment of these new tests may be clinically useful for reducing the proportion of unexplained RPL, and for providing high live birth rates if women receive relevant treatments. Full article

Background/Objectives: Pregnancy loss is a common and multifactorial complication of human reproduction, traditionally attributed to fetal chromosomal abnormalities, maternal anatomical and endocrine disorders, and immune dysfunction. Growing evidence now indicates that the maternal microbiome, particularly within the reproductive tract, plays a critical role in implantation, placental development, and the maintenance of immune tolerance during early pregnancy. Importantly, the influence of the microbiome on miscarriage appears to be strongly modulated by host genetic background and immune regulation. Methods: This narrative review summarizes current evidence linking alterations in the vaginal, endometrial, placental, and gut microbiomes to miscarriage, with a specific focus on host genetics and immune–microbial interactions. Results: We discuss how genetic variation in innate and adaptive immune pathways, inflammatory signaling, and mucosal barrier function may shape host responses to microbial communities, thereby influencing susceptibility to PL. In addition, we highlight emerging data on microbiome-driven regulation of gene expression and epigenetic modifications in the endometrium and decidua, emphasizing the role of microbial metabolites in immune tolerance and placental function. Conclusions: By integrating findings from microbiome research, host genomics, immunology, and epigenetics, this review proposes a framework in which miscarriage is viewed as a consequence of disrupted host–microbe crosstalk rather than isolated pathology. Finally, we address key methodological challenges and outline future research directions aimed at advancing mechanistic understanding and translational applications. Full article

The human microbiota is increasingly recognized as a key component of women’s reproductive health. This narrative review examines the vaginal, endometrial, and gut microbiota and their roles in the pathogenesis of gynecologic and obstetric disorders, aiming to integrate current evidence into a clinically relevant framework. We review intrinsic (genetic, hormonal, and immunological) and extrinsic (environmental, lifestyle, and pharmacological) factors shaping microbial composition, with particular focus on dysbiosis and the role of the gut estrobolome within the microbiome in estrogen metabolism. The review synthesizes data on microbiota alterations associated with endometriosis, adenomyosis, uterine fibroids, endometrial polyps and hyperplasia, gynecologic malignancies, pelvic inflammatory disease, bacterial vaginosis, infertility, and adverse obstetric outcomes, including preterm birth and fetal growth restriction. Methodological approaches used to characterize the reproductive tract microbiota, such as vaginal swabs, endometrial sampling, and fecal analysis, are critically discussed, together with limitations related to low-biomass environments and contamination risk. Evidence regarding therapeutic modulation of the microbiota, including antibiotics, probiotics, hormonal therapies, and emerging microbiota-based interventions, is summarized, alongside the impact of gynecologic surgery on microbial translocation and long-term microbial balance. Overall, the available literature supports an association between microbiota alterations and multiple reproductive conditions, although causality remains incompletely established. Further standardized and longitudinal studies are needed to clarify mechanisms and guide microbiota-informed diagnostic and therapeutic strategies. Full article

The human endometrium, previously considered a sterile environment, is now recognized as a low-biomass but biologically active microbial niche critical to reproductive health. Advances in sequencing technologies, particularly shotgun metagenomics, have provided unprecedented insights into the taxonomic and functional complexity of the endometrial microbiome. While 16S rRNA sequencing has delineated the distinction between Lactobacillus-dominant and non-dominant microbial communities, shotgun metagenomics has revealed additional diversity at the species and strain level, uncovering microbial signatures that remain undetected by amplicon-based approaches. Current evidence supports the association of Lactobacillus dominance with endometrial homeostasis and favorable reproductive outcomes. Dysbiosis, characterized by increased microbial diversity and enrichment of anaerobic taxa such as Gardnerella, Atopobium, Prevotella, and Streptococcus, is linked to chronic endometritis, implantation failure, and adverse IVF results. Beyond compositional differences, the endometrial microbiome interacts with the host through immunological, metabolic, and epigenetic mechanisms. These interactions modulate cytokine signaling, epithelial barrier integrity, and receptivity-associated gene expression, ultimately influencing embryo implantation. However, discrepancies between published studies reflect the lack of standardized protocols for sampling, DNA extraction, and bioinformatic analysis, as well as the inherent challenges of studying low-biomass environments. Factors such as geography, ethnicity, hormonal status, and antibiotic exposure further contribute to interindividual variability. Culturomics approaches complement sequencing by enabling the isolation of viable bacterial strains, offering perspectives for microbiome-based biotherapeutics. Emerging 3D endometrial models provide additional tools to dissect microbiome–host interactions under controlled conditions. Taken together, the growing body of data highlights the potential of endometrial microbiome profiling as a biomarker for reproductive success and as a target for personalized interventions. Future research should focus on integrating multi-omics approaches and functional analyses to establish causal relationships and translate findings into clinical practice. This review gives a new insight into current knowledge on the uterine microbiome and its impact on implantation success, analyzed through the lenses of microbiology, immunology, and oxidative stress. Full article

Objective: The primary objective of this systematic review is to present current knowledge about the oncobiome of gynecological cancers. Methods: Our systematic review contains data about the oncobiome of uterine corpus cancer, ovarian cancer and cervical cancer. Articles about other gynecological cancers were excluded. Results: A total of 72 articles were included in our systematic review. In uterine corpus cancer, cervical cancer and ovarian cancer, representatives of bacteria, fungi, viruses and parasites can be found. The oncobiome of ovarian cancer is connected with the oncobiome of head and neck cancers. Our systematic review proved that the human papilloma virus is connected with ovarian and cervical cancer. Gut dysbiosis can be used as a marker of ovarian cancer. In cervical cancer, we found the difference between the microbiota of healthy patients and patients with cervical cancer. Methylobacter, Robignitomaculum, Klebsiella, Micromonospora and Microbispora have an impact on overall survival. The microbiome of uterine corpus cancer is more differentiated than in cancer-free samples. Chronic endometrial inflammation has an impact on endometrial microbiome. Discussion: Treatment of gynecological cancers is changing permanently. Chemotherapy, as a systematic treatment, is being left in the past. Modern methods of therapy are addressed to specific genes. In the past, researchers claimed that tumors are sterile. However, the newest research indicates that malignancies were found to have genetic fragments of pathogens, which can be used as vectors for medications or as markers for the detection of a specific malignancy. Three most common gynecological cancers are as follows: endometrial cancer, ovarian cancer and cervical cancer. Each of these has their specific microbiome, which can be used for oncological treatment. These discoveries create possibilities for new, efficient methods of treatment. This systematic review analyzes publications about the composition of the gynecological tumor microenvironment, correlation between microbiomes of different organs, the female reproductive tract and the microbiome of the female reproductive tract during malignancy. Moreover, we provide information on the influence of some pathogens on the treatment. Full article

Antimicrobial therapy is a mainstay for treating reproductive diseases, including endometritis. Ceftiofur, a third-generation cephalosporin, is a common antibiotic used to treat equine bacterial endometritis. It is also routinely given empirically as an intra-uterine (IU) infusion in broodmare practice. We hypothesized that ceftiofur IU would disrupt the resident microbial community within the healthy uterus of mares. To test our hypothesis, eight university-owned mares were selected for characterization of the estrual uterine microbiome before and after IU ceftiofur. Double-guarded swabs of the estrual endometrium were taken before and 3 days after both IU saline and ceftiofur in a crossover design. Isolation of DNA from endometrial swabs was performed, followed by amplification of the V4 region of the 16S rRNA gene by Illumina Miseq sequencing to examine core bacterial communities present before and after ceftiofur. The uterine microbial composition of sham and ceftiofur-treated mares was not significantly different as measured by beta diversity. The only notable difference was a lower abundance of Christensenellaceae_R-7_group after ceftiofur (0.14 ± 1.05% vs. 2.89 ± 1.07% control; p = 0.0428). In conclusion, three-day treatment of ceftiofur did not change the microbial composition acutely within the mare uterus when sampled directly after treatment. Ceftiofur may have a long-term effect on the uterine microbiome, which may require sampling several weeks post treatment. In conclusion, ceftiofur does not change the healthy uterine microbiome acutely during estrus and but should still be used judiciously. Full article

Sexually transmitted infections (STIs) are a significant global health concern, affecting millions of people worldwide, particularly sexually active adolescents and young adults. These infections, caused by various pathogens, including bacteria, viruses, parasites, and fungi, can have profound implications for women’s reproductive health and fertility. This review explores the role of vaginal and uterine infections in women’s infertility, focusing on the most common pathogens and their impact on reproductive outcomes. Bacterial infections, such as those caused by intracellular bacteria (Mycoplasma, Ureaplasma, and Chlamydia), Neisseria gonorrhoeae, and bacterial vaginosis, are among the most prevalent causes of infertility in women. Studies have shown that these infections can lead to pelvic inflammatory disease, tubal occlusion, and endometrial damage, all of which can impair fertility. Mycobacterium tuberculosis, in particular, is a significant cause of genital tuberculosis and infertility in high-incidence countries. Viral infections, such as Human papillomavirus (HPV) and Herpes simplex virus (HSV), can also affect women’s fertility. While the exact role of HPV in female infertility remains unclear, studies suggest that it may increase the risk of endometrial implantation issues and miscarriage. HSV may be associated with unexplained infertility. Parasitic infections, such as trichomoniasis and schistosomiasis, can directly impact the female reproductive system, leading to infertility, ectopic pregnancy, and other complications. Fungal infections, such as candidiasis, are common but rarely have serious outcomes related to fertility. The vaginal microbiome plays a crucial role in maintaining reproductive health, and alterations in the microbial balance can increase susceptibility to STIs and infertility. Probiotics have been proposed as a potential therapeutic strategy to restore the vaginal ecosystem and improve fertility outcomes, although further research is needed to establish their efficacy. In conclusion, vaginal and uterine infections contribute significantly to women’s infertility, with various pathogens affecting the reproductive system through different mechanisms. Early diagnosis, appropriate treatment, and preventive measures are essential to mitigate the impact of these infections on women’s reproductive health and fertility. Full article