American Journal of Reproductive Immunology最新文献

{"title":"2025 American Society for Reproductive Immunology Guidelines for the Treatment of Recurrent Pregnancy Losses: Practice Recommendations From the ASRI Clinical Reproductive Immunology Fellowship","authors":"Marcelo Borges Cavalcante,&nbsp;Conor Harrity,&nbsp;Thanh Luu,&nbsp;Joy Fatunbi,&nbsp;Koji Nakagawa,&nbsp;Yuan Zhang,&nbsp;Tao Zhang,&nbsp;Hallah Alanazi,&nbsp;Li Wu,&nbsp;Sungki Lee,&nbsp;Ricardo Barini,&nbsp;Joanne Kwak-Kim","doi":"10.1111/aji.70099","DOIUrl":"https://doi.org/10.1111/aji.70099","url":null,"abstract":"<div>\u0000 \u0000 <p>Various immunomodulatory treatments have been applied to women with recurrent pregnancy losses since a significant proportion of them have cellular and autoimmune abnormalities. However, immunomodulatory treatments are often considered controversial for their efficacies. Often, they are provided to unselected patients without investigating potential etiologies by healthcare providers without appropriate reproductive immunology training and qualifications. To eliminate these concerns, the American Society for Reproductive Immunology (ASRI) established the Clinical Reproductive Immunology Fellowship and has been certifying reproductive immunologists. The approach to RPL from a reproductive immunology perspective requires a detailed understanding of underlying immunopathology, advanced knowledge of clinical and basic science and translational research, and the capability to evaluate the available evidence. The immunotherapy guideline development group, composed of clinical reproductive immunology fellows, ASRI, reviewed the currently available data and developed the clinical guidelines for immunotherapy.</p>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"93 6","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intermediate Signaling Mechanisms Regulating Human Fetal Membrane Responses to Gram-Positive Bacterial Peptidoglycan","authors":"Hanah M. Georges,&nbsp;Abigail C. Fischer,&nbsp;Vikki M. Abrahams","doi":"10.1111/aji.70090","DOIUrl":"https://doi.org/10.1111/aji.70090","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problem</h3>\u0000 \u0000 <p>Chorioamnionitis and preterm birth are leading causes of neonatal morbidity and mortality. Despite ongoing research, the signaling pathways involved in the pathogenesis of chorioamnionitis—inflammation of the fetal membranes (FM)—are not well understood. Previously, we reported that FMs utilize miR-146a-3p as an endogenously produced danger signal to sequentially activate Toll-like receptor (TLR) 8 and subsequent inflammation following lipopolysaccharide stimulation of TLR4. In this current study, following stimulation of fetal membrane explants by the TLR2 agonist peptidoglycan (PDG), we investigated sequential microRNA-activation of TLR8, intermediate signaling pathways NFκB and MAPK (p38, ERK), and their effects on inflammation and mediators of membrane weakening.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method of Study</h3>\u0000 \u0000 <p>Human FMs explants were treated with or without PDG in the presence or absence of inhibitors to TLR7, TLR8, p65 NFκB, p38 MAPK, or ERK. Culture supernatants were measured for secreted factors by ELISA, tissue RNA was measured for TLR7/8-activating miRs by RT-qPCR, and tissue protein was measured for phosphorylated proteins by Western blot.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>PDG-treated FMs produced elevated levels of TLR8-activating miR-146a-3p in a p65 NFκB-dependent manner. PDG-treated FMs produced elevated levels of the pro-inflammatory cytokine IL-1β, the neutrophil recruiting chemokine IL-8, and membrane weakening MMP1, MMP9, and PGE₂ in a TLR8-dependent manner. Except for MMP9, this inflammatory and membrane weakening response to PDG was dependent upon p65 NFκB, p38 MAPK, and ERK signaling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study gives new insight into the molecular mechanisms involved in FM responses to Gram-positive bacteria and into the pathogenesis of chorioamnionitis.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"93 6","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of TRIM47 Overcomes Paclitaxel Resistance in Ovarian Cancer by Suppressing the TGF-β Pathway via PPM1A","authors":"Hezhu Wang,&nbsp;Shengjun Chen,&nbsp;Feifei Xu,&nbsp;Xiaojing Chen","doi":"10.1111/aji.70102","DOIUrl":"https://doi.org/10.1111/aji.70102","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Objective&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;We investigated the role of tripartite motif 47 (&lt;i&gt;TRIM47&lt;/i&gt;) in paclitaxel resistance in ovarian cancer, focusing on its regulation of protein phosphatase magnesium-dependent 1A (&lt;i&gt;PPM1A&lt;/i&gt;), transforming growth factor-β (TGF-β) pathway activation, and methyltransferase-like 3 (&lt;i&gt;METTL3&lt;/i&gt;)-mediated N6-methyladenosine (m6A) modification.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Bioinformatics analysis using Gene Expression Profiling Interactive Analysis (GEPIA), Kaplan–Meier plotter (KM plot), Linkedomics, and sequence-based RNA adenosine methylation site predictor (SRAMP) databases identified &lt;i&gt;TRIM47&lt;/i&gt; and &lt;i&gt;PPM1A&lt;/i&gt; expression patterns, prognostic significance, co-expression networks, and m6A modification sites. Paclitaxel-resistant ovarian cancer cell lines were generated. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blot analyzed gene and protein expression. Co-immunoprecipitation (Co-IP) and GST pull-down assays assessed TRIM47-PPM1A interaction, while cycloheximide (CHX) chase, and IP assays examined PPM1A stability and ubiquitination. RNA immunoprecipitation (RIP) and dual-luciferase assays determined &lt;i&gt;METTL3&lt;/i&gt;’s effect on &lt;i&gt;TRIM47&lt;/i&gt; m6A modification. Functional assays (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, and flow cytometry) evaluated proliferation, apoptosis, and drug response. An in vivo xenograft model confirmed &lt;i&gt;TRIM47&lt;/i&gt;’s role in chemoresistance.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Bioinformatics analysis showed that &lt;i&gt;TRIM47&lt;/i&gt; was overexpressed in ovarian cancer and negatively correlated with the expression of &lt;i&gt;PPM1A&lt;/i&gt;. Kaplan–Meier analysis showed that high &lt;i&gt;TRIM47&lt;/i&gt; and low &lt;i&gt;PPM1A&lt;/i&gt; expression were correlated with poor prognosis. &lt;i&gt;TRIM47&lt;/i&gt; was upregulated in paclitaxel-resistant ovarian cancer cells. The knockdown of &lt;i&gt;TRIM47&lt;/i&gt; restored drug sensitivity, inhibited cell proliferation, and induced cell apoptosis. Mechanistically, TRIM47 functioned as an E3 ubiquitin ligase, targeting PPM1A for degradation, leading to sustained TGF-β signaling and enhanced chemoresistance. CHX chase assays demonstrated reduced PPM1A stability in the presence of TRIM47, while IP-WB confirmed increased PPM1A ubiquitination. &lt;i&gt;METTL3&lt;/i&gt;-mediated m6A modification enhanced &lt;i&gt;TRIM47&lt;/i&gt; mRNA stability, further promoting its oncogenic role. In vivo, &lt;i&gt;TRIM47&lt;/i&gt; knockdown reduced tumor growth and improved paclitaxel efficacy, reinforcing its role in resistance.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;&lt;i&gt;TRIM47&lt;/i&gt; promoted paclitaxel resistance ","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"93 6","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144171242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal Relationship Between Polycystic Ovary Syndrome and Autoimmune Diseases: A Two-Sample Mendelian Randomization Study","authors":"Xiuye Xing,&nbsp;Dachao Wei,&nbsp;Qun Lu","doi":"10.1111/aji.70083","DOIUrl":"https://doi.org/10.1111/aji.70083","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problem</h3>\u0000 \u0000 <p>Polycystic ovary syndrome (PCOS) is known to be associated with immune response dysregulation, resembling autoimmune diseases. However, the causal relationship between PCOS and autoimmune diseases remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A two-sample bidirectional Mendelian randomization (MR) analysis was conducted using publicly available genome-wide association study (GWAS) data. The primary causal effects were estimated using the inverse-variance weighted (IVW) method, complemented by the weighted median, weighted mode, and MR-Egger regression approaches. Horizontal pleiotropy was assessed using MR-Egger regression and the MR pleiotropy residual sum and outlier (MR-PRESSO) method. Additionally, bidirectional MR analysis was performed to determine the directionality of causal relationships.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>IVW analysis revealed no causal inference of PCOS on autoimmune diseases (odds ratios [OR]: 0.93–1.19, <i>p</i> &gt; 0.05), and no evidence of a causal relationship was observed between autoimmune diseases and PCOS (OR 0.98–1.11, <i>p</i> &gt; 0.05). These findings were further supported by the weighted median and mode methods. However, MR-Egger analysis suggested potential causal associations between rheumatoid arthritis (RA), Crohn's disease (CD), and inflammatory bowel disease (IBD) with PCOS (OR: 0.87–1.08, <i>p</i> &lt; 0.05), though horizontal pleiotropy was detected for RA and IBD, indicating potential bias.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Genetically predicted PCOS was not causally linked to autoimmune diseases. Although potential associations between RA, CD, and IBD with PCOS were identified, these results should be interpreted cautiously due to possible pleiotropy. Future studies with larger sample sizes and advanced MR methodologies are warranted to validate these findings.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"93 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence for Complement Activation in Preeclampsia Placenta and Its Presence in Circulation","authors":"Shibin Cheng,&nbsp;Wendy Norris,&nbsp;Satyan Kalkunte,&nbsp;Sukanta Jash,&nbsp;Lauren R. Richardson,&nbsp;Surendra Sharma","doi":"10.1111/aji.70076","DOIUrl":"https://doi.org/10.1111/aji.70076","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Problem&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Preeclampsia (PE) is a severe pregnancy disorder caused by a multitude of dysregulated events, including placental insufficiency, inflammation, anti-angiogenic factors, and cellular stress signals. Inflammatory activation of the complement cascade has also been thought to be a contributory factor to PE pathophysiology. However, the placental and circulating presence of activated complement factors and their precise impact on gestational age-dependent trophoblast health remain inadequately addressed.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Method of Study&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Complement activation was assessed in placental tissue samples from women with normal pregnancy (NP) and PE. Immunofluorescent staining was employed to detect the membrane attack complex (MAC) deposition in placental tissues. This approach was also used in placenta-derived human extravillous trophoblast cells derived from the third trimester (TCL1) and first trimester (HTR-8) and term primary human cytotrophoblasts. Dual staining with Propidium Iodide (PI) and annexin V antibody was conducted to assess cell viability in TCL-1 cells, HTR-8 cells, and freshly isolated term primary human trophoblasts when exposed to serum samples from NP (NPS), PE (PES), and PES after complement inactivation by heating, heparin treatment, or blockade with antibodies. The expression levels of complement regulatory proteins, specifically decay-accelerating factor (CD55), protectin (CD59), and membrane cofactor protein (CD46), on trophoblasts were quantified using Fluorescence-activated cell sorting and immunohistochemistry.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Substantial MAC deposition and a notable reduction in CD55 expression in the PE placenta compared to that from NP was observed, indicating heightened complement activation and impaired complement regulation in PE. Exposure to a significant subpopulation of PES (41%, &lt;i&gt;n&lt;/i&gt; = 41) induced cell death exclusively in TCL-1 cells, not in HTR-8 cells and primary human trophoblasts. Remarkably, complement inactivation in PES abolished MAC deposition and rescued TCL-1 cells from death, unequivocally implicating complement activity in trophoblast cell demise. Flow cytometry analysis disclosed lower levels of CD55 and CD59 expression in TCL-1 cells in contrast to HTR-8 cells and primary human trophoblasts. Blockade of CD55 and CD59 in HTR-8 cells enhanced their susceptibility to PES-induced cell death.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;These findings underscore the significance of amplified complement activation, compromised complement inhibitory regulation, and consequent trophoblast cell death ","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"93 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144091807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering the Molecular Crosstalk of Endoplasmic Reticulum Stress and Immune Infiltration in Endometriosis","authors":"Yuan Ma,&nbsp;Chunfang Ha,&nbsp;Ruyue Li,&nbsp;Ruiqi Zhang,&nbsp;Min Li","doi":"10.1111/aji.70092","DOIUrl":"https://doi.org/10.1111/aji.70092","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Endometriosis (EMs), characterized by ectopic endometrial growth causing infertility. Endoplasmic reticulum stress (ERS) is an important cellular defense mechanism. However, the correlation between ERS and EMs remains unclear. We aimed to investigate the relationship between them, identify biomarkers, and offer new insights into the treatment of EMs.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Two RNA expression datasets (GSE120103 and GSE25628) related to EMs in <i>Homo sapiens</i> were used to identify ERS-differentially expressed genes (ERS-DEGs). Protein–protein interaction (PPI) networks and CytoHubba (Cytoscape) identified ERS-associated HUB genes, with receiver operating characteristic curves (ROC) evaluating diagnostic value. Constructed mRNA-microRNA (miRNA)/RNA-transcription factor (TF) interaction networks and performed ssGSEA to compare immune infiltration between EMs patients and controls. Real-time quantitative polymerase chain reaction (RT-qPCR), western blotting (WB), and immunohistochemistry (IHC) were performed to assess potential biomarker levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Thirty-three ERS-DEGs were identified, with nine HUB genes (<i>HSPA5, XBP1, HSP90B1, DNAJC3, PDIA3, PDIA6, PDIA4, HERPUD1</i>, and <i>MANF</i>) demonstrating diagnostic efficacy (AUC &gt; 0.7). Furthermore, immune infiltration revealed a significant relationship between immune cell abundance and HUB gene expression. Experimental validation confirmed the consistency of four biomarkers (<i>HSPA5, HSP90B1, PDIA6</i>, and <i>HERPUD1</i>). Regulatory network analysis identified 62 miRNAs and 44 TFs interacting with HUB genes, suggesting a multifactorial immunometabolic axis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We identified four biomarkers (<i>HSPA5, HSP90B1, PDIA6</i>, and <i>HERPUD1</i>) associated with ERS that offer new insights into the detection and treatment of EMs. Our findings indicate an abnormal response to ERS and immune system infiltration contribute to the progression of EMs.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"93 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/aji.70092","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143949986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and Validation of Potential Immune-Related Genes for Endometriosis","authors":"Yi Zhang,&nbsp;Lulu Wu,&nbsp;Wanjing Yuan,&nbsp;Zhen Ren,&nbsp;Li Tang,&nbsp;Jilin Kuang,&nbsp;Lin Li,&nbsp;Yingying Liang","doi":"10.1111/aji.70091","DOIUrl":"https://doi.org/10.1111/aji.70091","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aimed to identify and validate potential immune-related genes in endometriosis (Ems) through comprehensive bioinformatics analysis and immunohistochemistry (IHC) verification.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Design</h3>\u0000 \u0000 <p>Using data from the GEO database, single-cell RNA sequencing (scRNA) data and traditional bulk RNA sequencing data were analyzed to identify differentially expressed genes related to the immune system. Immunological analysis confirmed alterations in immune cells associated with Ems. Machine learning techniques were employed to identify characteristic immune genes of eutopic and ectopic endometria, which were then validated through IHC experiments.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Main Outcome Measures</h3>\u0000 \u0000 <p>Immunological analysis revealed distinct variations in the enrichment of macrophages and NK cells in Ems. Functional enrichment analysis revealed a decrease in NK cell toxicity in both ectopic and eutopic endometria, activation of M2 macrophages in the ectopic endometrium supporting the survival of ectopic endothelial cells, and the presence of lipid antigens and signaling between immune cells facilitating the development of Ems. Machine learning algorithms revealed that TGFBR1 is a characteristic immune gene associated with the eutopic endometrium and that GIMAP4 is associated with the ectopic endometrium; this conclusion was also confirmed by IHC.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Macrophage and NK cell enrichment was significantly increased in endometria from patients with Ems. TGFBR1 is a characteristic immune gene associated with the eutopic endometrium, whereas GIMAP4 is associated with the ectopic endometrium.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings provide new insights for the clinical diagnosis and selection of immune-related targets for Ems.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"93 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143950143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anhedonia Symptoms and High Sensitivity C-Reactive Protein (hs-CRP) Several Years Postpartum","authors":"Jennifer M. Nicoloro-SantaBarbara,&nbsp;Judith E. Carroll,&nbsp;Margo Minissian,&nbsp;Sarah J. Kilpatrick,&nbsp;C. Noel Bairey Merz,&nbsp;Eynav E. Accortt","doi":"10.1111/aji.70095","DOIUrl":"https://doi.org/10.1111/aji.70095","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problem</h3>\u0000 \u0000 <p>Despite adverse maternal and child consequences, postpartum depression 1.6–3 years post-delivery remains poorly understood, particularly anhedonia (lack of interest or pleasure), which can harm maternal–child relationships. Understanding the biological pathways underlying maternal depression and identifying biomarkers that contribute to its diverse symptoms is essential.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method of Study</h3>\u0000 \u0000 <p>This study investigated relations between hs-CRP levels and symptoms of depression in mothers 1.6–3 years post-delivery (<i>N</i> = 49), and examined associations between specific symptoms of depression and hs-CRP.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Clinically elevated symptoms of depression were present in 14.2%. Symptoms of depression were not significantly associated with maternal characteristics but were associated with having a Neonatal Intensive Care Unit (NICU) admission, maternal age, and a recent history of mental illness. Greater depression and anhedonia symptoms were associated with greater levels of hs-CRP (<i>r</i> = 0.308, <i>p</i> &lt; 0.05; <i>r</i> = 0.314, <i>p</i> &lt; 0.05, respectively). Adjusting for maternal age, BMI, months postpartum, and pregnancy status, elevated depression (not anhedonia) remained associated with higher levels of hs-CRP (<i>β</i> = 0.342, <i>p</i> &lt; 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Women with clinically elevated symptoms of depression had significantly higher levels of hs-CRP, suggesting that it may be an important inflammatory biomarker for symptoms of depression 1–3 years post-delivery and helps identify those in need of follow up.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"93 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143938825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Injectable Contraceptives Differentially Affect Select CD4+ HIV-1 Target Cells in the Genital Tract but Not Systemically: Implications for HIV-1 Acquisition","authors":"Chanel Avenant,&nbsp;Alexis J. Bick,&nbsp;Johnson M. Moliki,&nbsp;Sigcinile Dlamini,&nbsp;Michele Tomasicchio,&nbsp;G. Justus Hofmeyr,&nbsp;Charles Morrison,&nbsp;Pai-Lien Chen,&nbsp;Janet P. Hapgood","doi":"10.1111/aji.70093","DOIUrl":"https://doi.org/10.1111/aji.70093","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problem</h3>\u0000 \u0000 <p>Observational data suggest lower HIV susceptibility in women using the injectable contraceptive norethisterone enanthate (NET-EN) versus intramuscular depo medroxyprogesterone acetate (DMPA-IM). Clinical data investigating the effects of injectables on HIV target cells are inconsistent or limited. No data on HIV target cells are available from head-to-head randomized trials comparing DMPA-IM and NET-EN, nor at peak progestin concentrations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method of Study</h3>\u0000 \u0000 <p>The women's health, injectable contraception, and HIV (WHICH) trial randomized women to DMPA-IM or NET-EN at two South African sites (2018–2019). Cells from blood and cytobrushes from women at one site, taken at baseline and 1 week post the 24-week injection (at peak progestin levels), were analyzed by flow cytometry for select HIV-1 target cells (CD4⁺ cells expressing HIV-1 co-receptors, an integrin and/or activation markers).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Systemically, DMPA-IM and NET-EN similarly reduced the frequency and number of some CD4⁺ cells and expression of some CD4⁺ cell surface markers. In contrast, female genital tract (FGT) results showed significantly different cell numbers between contraceptives for most cell populations; DMPA-IM tended to increase, but NET-EN tended to decrease cell numbers. Excluding for non-study progestin use revealed significant increases in frequency and/or number of several FGT cell populations from baseline to 25 weeks, within the DMPA-IM arm.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Both contraceptives exert minimal effects on systemic CD4⁺ cells but have differential effects in the FGT. The changes in frequency and numbers of HIV-1 target cells investigated, particularly after exclusion for non-study progestin use, suggest that DMPA-IM use may increase HIV-1 acquisition in the FGT compared to NET-EN use.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"93 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/aji.70093","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143938824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Chronic Endometritis on Prognosis and Reproductive Outcomes in Infertile Women With Endometrial Hyperplasia","authors":"Xiaotong Dong,&nbsp;Yang Zhang,&nbsp;Shuai Liu,&nbsp;Yanbo Du,&nbsp;Linlin Cui,&nbsp;Wen Liu,&nbsp;Lei Yan","doi":"10.1111/aji.70075","DOIUrl":"https://doi.org/10.1111/aji.70075","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Problem</h3>\u0000 \u0000 <p>Chronic endometritis has been shown to cause infertility, and chronic inflammation has been confirmed to be associated with the development of cancer. However, the effect of chronic endometritis on endometrial hyperplasia (EH) among infertile women has not been studied. So, we aim to investigate whether chronic endometritis affects the prognosis and reproductive outcome in infertile women with EH who had preserved fertility therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>This study employed a retrospective design. Infertile women who underwent hysteroscopic biopsy and were diagnosed as EH were enrolled. We used CD138 immunohistochemical staining in endometrium paraffin sections of EH patients. The patients were divided into two groups according to whether they were diagnosed as chronic endometritis or not, and the disease outcome and reproductive outcome were analyzed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Result</h3>\u0000 \u0000 <p>The results showed that after progesterone therapy, women with a persistent chronic endometritis exhibited a lower rate of complete response (<i>p </i>= 0.002) of EH, along with an increased incidence of miscarriage after embryo transfer (<i>p </i>= 0.005).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our study indicates a high prevalence rate of chronic endometritis in infertile women with EH, with potential implications for prognosis and subsequent reproductive outcomes, whether antibiotics should be added to the treatment of patients with EH combined with chronic endometritis deserves further investigation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":7665,"journal":{"name":"American Journal of Reproductive Immunology","volume":"93 5","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143938917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}