Journal of Innate Immunity最新文献

{"title":"Inhalation of N-Chlorotaurine Is an Effective Treatment of <italic>Aspergillus fumigatus</italic> Pneumonia in Mice.","authors":"Cornelia Speth, Günter Rambach, Andrea Windisch, Nadine Falbesoner, Christoph Schatz, Georg Schäfer, Markus Nagl","doi":"10.1159/000550140","DOIUrl":"10.1159/000550140","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;N-chlorotaurine (NCT), a long-lived oxidant of human granulocytes, can be used topically as anti-infective in different body regions. The aim of the present study was to demonstrate the efficacy and tolerability of inhaled NCT in a mouse model of Aspergillus fumigatus pneumonia.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Specific pathogen-free female C57BL/6JRj mice were immune-suppressed with cyclophosphamide or cortisone acetate. After 7 days, they were inoculated intranasally with 6.5 × 106 spores of A. fumigatus. Treatment with aerosolized (&lt;5 µm) aqueous 0.1%, 0.5%, 1.0%, or 2.0% NCT solution or 0.9% sodium chloride as placebo three times daily for 10 min was started 1 h after inoculation and ended after 14-16 days. Prophylactic treatment exclusively for 2 days before infection was investigated additionally. Main parameters of evaluation were survival and fungal load in the lung homogenate, secondary ones clinical (body weight, organ weights, body temperature) and blood inflammation parameters, bronchoalveolar lavage fluid analysis, and histology of organs.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Pneumonia occurred in all mice, but the survival was much higher in animals treated with NCT compared to placebo. In placebo groups, 8/9 mice observed for 15 days died from the infection during this time, while 0/9 to 1/9 died in groups treated with 0.5%, 1.0%, and 2.0% NCT (p &lt; 0.01 for each concentration versus saline). There was no difference between the two ways of immune-suppression. With 0.1% NCT, 4/9 mice died (p = 0.029 versus 0.5% and 2.0% NCT; p = 0.0035 versus control). The fungal load came to 5.28 log&lt;sub&gt;10&lt;/sub&gt; (4.46; 5.70; median, quartiles) colony-forming units per ml lung homogenate in the control group and to 1.3 log&lt;sub&gt;10&lt;/sub&gt; (median; maximum 2.45) in the 1% NCT group in mice immune-suppressed with cyclophosphamide (p = 0.0004). Values were similar in cortisone groups (p = 0.0023). Of note, the prophylactic inhalations with 1% NCT were equally effective. Loss of body weight was significantly higher in the control animals compared to the test ones. Organ weights of the lung, brain, and kidney were significantly higher in the control groups than in the test groups, while the opposite was found for the spleen weight with more lymphatic hyperplasia in the test animals. Mice treated with 2.0% NCT had a breath sound for a few minutes after inhalation, but no further hints for incompatibility or discomfort could be detected.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Early treatment with inhaled NCT as well as prophylactic treatment demonstrated a highly significant beneficial efficacy in Aspergillus pneumonia. A concentration around 1% NCT appears to be optimal taking into account both tolerability and efficacy, which is in agreement with previous studies and case experiences in humans. Inhalation with NCT as an antiseptic and anti-infective product of granulocytes is highly promising in infections of the lower airways and sh","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"35-51"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145781421","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":"Prior Exposure of Airway Epithelial Cells to Mycobacteria Reduces Subsequent <italic>Mycobacterium tuberculosis</italic> Infection and Resulting Inflammation.","authors":"Amy M Barclay, Dennis K Ninaber, Kimberley V Walburg, Pieter S Hiemstra, Tom H M Ottenhoff, Anne M van der Does, Simone A Joosten","doi":"10.1159/000550118","DOIUrl":"10.1159/000550118","url":null,"abstract":"<p><strong>Introduction: </strong>Repeated exposures to Mycobacterium tuberculosis (Mtb) and related species may influence host responses, which in turn may affect vaccine efficacy and could even render the host less or more susceptible to progression to active tuberculosis (TB) disease.</p><p><strong>Methods: </strong>Using well-differentiated primary human bronchial epithelial cells (PBEC), we investigated the effect of a prior exposure of the epithelium to Mtb and Mycobacterium bovis vaccine strain Bacille Calmette-Guerin (BCG) on the intracellular infection efficiency of Mtb and Mycobacterium avium (Mav) during a second exposure and measured cytokine and antimicrobial peptide secretion.</p><p><strong>Results: </strong>PBEC that were first exposed to BCG were significantly more resistant to subsequent infection with Mtb. A similar trend was observed in PBEC that were previously exposed to Mtb, although to a lesser magnitude compared to BCG pre-exposure. Furthermore, while the first exposure to mycobacteria induced inflammatory cytokine secretion by PBEC, cytokine secretion was dampened upon a secondary exposure to Mtb, most strongly in previously BCG-exposed cells. Secretion of the antimicrobial peptide hBD-2 was not affected by sequential exposures.</p><p><strong>Conclusion: </strong>Repeated exposure of differentiated airway epithelial cells to mycobacteria reduced intracellular infection and inflammation.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"52-67"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12880847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145878423","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":"Increased Bacterial Load per Neutrophil Reduces Intracellular Killing Capacity.","authors":"Louise V Duebel, Simon O Dekker, Suzanne H Bongers, Corneli van Aalst, Eva Mulder, Falco Hietbrink, Leo Koenderman, Nienke Vrisekoop","doi":"10.1159/000551415","DOIUrl":"10.1159/000551415","url":null,"abstract":"<p><strong>Introduction: </strong>Neutrophils are the most abundant innate immune cells in the peripheral blood and eliminate bacteria through phagocytosis and antimicrobial mechanisms. Early in infection, they often encounter high bacterial loads before full recruitment. Individual neutrophils can ingest many bacteria, but it remains unclear how high bacterial loads per neutrophil affect intracellular killing.</p><p><strong>Methods: </strong>Neutrophils were isolated from healthy donor blood by fluorescence-activated cell sorting. Intracellular bacterial load was quantified using imaging flow cytometry to measure spot counts and green fluorescent protein (GFP) intensity after exposure to GFP-expressing Staphylococcus aureus. A single-cell killing assay assessed intracellular killing across bacterial load categories by sorting individual GFP+ neutrophils into 384-well plates and counting wells with outgrowth after 100 h. Phagolysosomal acidification was measured using dual-labeled (pH-sensitive pHrodo and pH-insensitive PromoFluor 520 LSS NHS ester [PF520]) S. aureus bioparticles.</p><p><strong>Results: </strong>Bacterial uptake by neutrophils was highly heterogeneous in vivo and in vitro. GFP spot counts strongly correlated with GFP intensity (R2 = 0.66), allowing stratification into GFP fluorescence intensity categories. In the single-cell killing assay, higher bacterial loads per neutrophil were associated with reduced intracellular killing (χ2(4) = 11.72, p = 0.0003). Higher bacterial loads per neutrophil corresponded with diminished phagolysosomal acidification capacity (χ2(4) = 24.00, p < 0.0001).</p><p><strong>Conclusion: </strong>Neutrophils ingesting higher bacterial loads exhibit reduced intracellular killing, likely due to decreased phagolysosomal acidification. These findings highlight how bacterial load per neutrophil shapes antimicrobial capacity and early infection control.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"156-168"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13105470/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147443776","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":"Macrophages in Ulcerative Colitis: Immunomodulatory Roles, Phenotypic Switching, and Therapeutic Targeting.","authors":"Maojun Zhao, Shaochen Yu, Mengjie Zhang, Yuting Huang, Ziyue Dou, Beibei Tian, Langlang Yang, Jian Lu","doi":"10.1159/000550397","DOIUrl":"10.1159/000550397","url":null,"abstract":"<p><strong>Background: </strong>Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by dysregulated immune responses in the gut. Macrophages, as key innate immune cells in the intestinal mucosa, play a central role in both maintaining homeostasis and driving pathology in UC.</p><p><strong>Summary: </strong>Under physiological conditions, intestinal macrophages exhibit a unique \"inflammatory anergy\" phenotype, supporting epithelial integrity and immune tolerance. In UC, however, persistent inflammatory signals promote monocyte recruitment and their polarization into pro-inflammatory M1-like macrophages. These cells secrete cytokines such as TNF-α, IL-1β, IL-6, and IL-12/23, produce reactive oxygen species and reactive nitrogen species, and release matrix metalloproteinases, collectively driving epithelial barrier disruption, tissue damage, and sustained inflammation. This review comprehensively discusses the origin, heterogeneity, and functional plasticity of intestinal macrophages, their dynamic interactions with other cells, and key regulatory signaling pathways - such as NF-κB, JAK-STAT, and the NLRP3 inflammasome - in UC.</p><p><strong>Key messages: </strong>We evaluate current and emerging macrophage-targeted therapies, including cytokine blockade, chemokine receptor antagonism, phenotypic reprogramming, nanomedicine, and cell-based interventions. Furthermore, we highlight the limitations of the M1/M2 dichotomy and emphasize the need for single-cell and spatial transcriptomic approaches to better define macrophage subsets in human disease. Advancing the understanding of macrophage biology in UC will facilitate the development of precise immunomodulatory strategies and biomarker-based diagnostics, ultimately aiming to bridge the gap between mechanistic discovery and improved patient care.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"85-103"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12923256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145966109","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":"Neutrophil Plasticity in Airway Disease: Balancing Damage and Repair.","authors":"Sabina M Janciauskiene, Joanna Chorostowska-Wynimko, Beata Olejnicka, Sabine Wrenger","doi":"10.1159/000549824","DOIUrl":"10.1159/000549824","url":null,"abstract":"<p><strong>Background: </strong>Neutrophils, previously viewed as short-lived microbial killers, are now recognized as highly adaptable regulators of innate immunity. Advances in transcriptomic, metabolic, and epigenetic profiling reveal their remarkable heterogeneity and ability to adopt microenvironment-specific phenotypes. In the lung, this plasticity gives neutrophils a double role: they fight infection but can also cause long-lasting inflammation, tissue damage, and scarring.</p><p><strong>Summary: </strong>We review how neutrophils are activated, move, and act in lung disease, focusing on their release of proteases, production of reactive oxygen species, and formation of extracellular traps. We also describe repair-promoting neutrophil types and treatments that aim to reduce damage while keeping normal neutrophil defense intact.</p><p><strong>Key messages: </strong>Learning how neutrophils change within the lung microenvironment will help create better and more precise treatments for lung inflammation and tissue damage.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"16-34"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12757115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145648091","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":"Inhibition of <italic>Pseudomonas aeruginosa</italic> Biofilm Formation by Peptidyl-Arginine Deiminases 2 and 4.","authors":"Rory Baird, Debananda Gogoi, Luke Forde, Sara Waqas Ahmed, Mengxin Niu, Brenton Cavanagh, Fidelma Fitzpatrick, Emer P Reeves","doi":"10.1159/000550256","DOIUrl":"10.1159/000550256","url":null,"abstract":"<p><strong>Introduction: </strong>Pseudomonas aeruginosa is a significant pathogen associated with acute and chronic infections, particularly in immunocompromised individuals. Its capacity for biofilm formation, combined with antibiotic resistance, plays a critical role in the persistence of these infections. Peptidyl-arginine deiminases (PADs), including PAD2 and PAD4 isoforms, are involved in neutrophil phagocytic killing of P. aeruginosa. This study aimed to investigate the impact of PAD enzymes on biofilm development and virulence factor production in P. aeruginosa, with focus on the multidrug resistant strain, PGO2330.</p><p><strong>Methods: </strong>Biofilm formation was assessed using crystal violet assays and confocal scanning laser microscopy. Quorum sensing (QS) gene expression and QS-related virulence factor production were quantified using qPCR and virulence factor assays.</p><p><strong>Results: </strong>Exposure to 20 n<sc>m</sc> of PAD2 or PAD4 reduced PGO2330 surface attachment (p < 0.0001) and biofilm formation to 67.9 ± 5.6% (p < 0.0001) and 68.2 ± 4.2% (p = 0.0004), respectively. Moreover, rPAD2 and rPAD4 citrullinated multiple protein substrates of P. aeruginosa, yet citrullination activity was not required by rPADs to reduce P. aeruginosa biofilm formation. PGO2330 exposed to PAD2 and PAD4 showed reduced lasR, lasI, rhlR, rhlI, and mvfR gene expression and reduced levels of extracellular DNA, rhamnolipids, pyocyanin, and protease activity.</p><p><strong>Conclusion: </strong>These results demonstrate that PADs inhibit P. aeruginosa biofilm formation and decrease the production of QS-related virulence factors, highlighting their potential as novel antimicrobials and supporting further research into the development of PAD-based therapeutics.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"104-119"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12948390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146018735","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":"Pharmacological Stimulator of Interferon Genes Activation Enhances Autophagy-Mediated Clearance of <italic>Mycobacterium tuberculosis</italic> in Human Macrophages.","authors":"Fei Niu, Ronghao Zhong, Feifei Pu, Xiyong Dai, Junwen Wang, Jing Feng, Ping Xia","doi":"10.1159/000550530","DOIUrl":"10.1159/000550530","url":null,"abstract":"<p><strong>Introduction: </strong>The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is a critical sensor in the innate immune response to intracellular pathogens, yet its therapeutic potential for augmenting macrophage-mediated control of Mycobacterium tuberculosis (Mtb) remains incompletely understood. This study investigated whether pharmacological activation of the STING pathway could enhance autophagy to promote Mtb clearance in human macrophages.</p><p><strong>Methods: </strong>Human THP-1 monocytes were differentiated into macrophages and infected with Mtb. The effects of the STING agonist MIW815 (ADU-S100) on Mtb phagocytosis, intracellular bacterial survival, and autophagic flux were assessed using a combination of molecular and cellular techniques, including quantitative real-time polymerase chain reaction, Western blotting, colony-forming unit (CFU) assays, and confocal immunofluorescence microscopy. The dependency on the cGAS-STING pathway was confirmed using small interfering RNA-mediated gene silencing.</p><p><strong>Results: </strong>Pharmacological activation of STING with ADU-S100 significantly enhanced Mtb phagocytosis and subsequent intracellular clearance. This enhanced bactericidal activity was mechanistically linked to an increase in autophagic flux, as evidenced by elevated LC3-II protein levels and significantly increased colocalization of Mtb with lysosomal compartments. Importantly, treatment with the autophagy inhibitor hydroxychloroquine or silencing of cGAS significantly reversed these phenotypes, confirming the pivotal role of the STING-autophagy axis.</p><p><strong>Conclusion: </strong>Activating the STING pathway with ADU-S100 is a potent host-directed strategy to bolster macrophage autophagy and enhance the elimination of intracellular Mtb. This provides a strong rationale for exploring STING agonists as a novel therapeutic intervention for tuberculosis, addressing a significant and clinically relevant challenge in infectious disease.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"126-136"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13046366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146093216","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":"Neutrophil Heterogeneity after Myocardial Infarction.","authors":"Marie Piollet, Jana Grune, Clément Cochain","doi":"10.1159/000551240","DOIUrl":"10.1159/000551240","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular diseases (CVDs), including myocardial infarction (MI), are the leading cause of death worldwide. Neutrophils have emerged as actors in noninfectious pathologies and play major roles in CVDs: after MI, neutrophils are the first cell recruited to the ischemic heart and display multifaceted roles in orchestrating post-MI tissue healing and repair. Interestingly, recent studies described a high heterogeneity in neutrophils during this process.</p><p><strong>Summary: </strong>At steady state, neutrophils present diversity during their development in hematopoietic organs and in the circulation after reaching maturity. Inflammatory environments elicit neutrophil reprogramming and further complexify neutrophil heterogeneity, especially leading to the emergence of tissue-specific populations including SiglecF+ neutrophils. Neutrophils play beneficial and deleterious roles after MI: they originate from diverse sources including the bone marrow, the spleen, and from the marginated neutrophil pool and display a time-dependent appearance of heterogeneous profile within the cardiac tissue.</p><p><strong>Key messages: </strong>Neutrophil heterogeneity in the cardiac tissue could explain the contrasting roles ascribed to neutrophils after MI. Increased knowledge in neutrophil diversity will enable the identification of specific targets to improve cardiac healing processes.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"139-155"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13095199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147317378","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":"Editors' Choice 2025 <italic>Journal of Innate Immunity</italic>: From Receptor Proximal Training to Metabolic and Fibrotic Control.","authors":"Catherine M Greene, Emer P Reeves","doi":"10.1159/000550988","DOIUrl":"10.1159/000550988","url":null,"abstract":"","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"137-138"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13048727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146197821","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":"Characterization of the Cellular Immune Response to Group B Streptococcal Vaginal Colonization.","authors":"Brady L Spencer, Dustin T Nguyen, Stephanie M Marroquin, Laurent Gapin, Rebecca L O'Brien, Kelly S Doran","doi":"10.1159/000548044","DOIUrl":"10.1159/000548044","url":null,"abstract":"<p><strong>Introduction: </strong>Group B Streptococcus (GBS) asymptomatic colonizes the female genital tract (FGT) but can contribute to adverse pregnancy outcomes including pre-term birth, chorioamnionitis, and neonatal infection. We previously observed that GBS elicits FGT cytokine responses, including IL-17, during murine vaginal colonization; yet the anti-GBS cellular immune response during colonization remained unknown. We hypothesized that GBS may induce cellular immunity, resulting in FGT clearance.</p><p><strong>Methods: </strong>Herein, we utilize depleting antibodies and knockout mice and performed flow cytometry to investigate cellular immunes responses during GBS colonization.</p><p><strong>Results: </strong>We found that neutrophils (effectors of the IL-17 response) are important for GBS mucosal control as neutrophil depletion promoted increased GBS burdens in FGT tissues. Flow cytometric analysis of immune populations in the vagina, cervix, and uterus revealed, however, that GBS colonization did not induce a marked increase in FGT CD45+ immune cells. We also found that that Vγ6+ γδ T cells comprise a primary source of FGT IL-17. Finally, using knockout mice, we observed that IL-17-producing γδ T cells are important for the control of GBS in the FGT during murine colonization.</p><p><strong>Conclusions: </strong>Taken together, this work characterizes FGT cellular immunity and suggests that GBS colonization does not elicit a significant immune response, which may be a bacterial directed adaptive outcome. However, certain FGT immune cells, such as neutrophils and ɣδ T cells, contribute to host defense and control of GBS colonization.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"1-22"},"PeriodicalIF":3.0,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12659609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145232680","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}