BMC Immunology最新文献

{"title":"Cytokine and chemokine signatures of steady-state sickle cell disease in African children: a cross-sectional study.","authors":"Emmanuel Alote Allotey, David Adedia, Jones Amo Amponsah, Adjoa Agyemang Boakye, Augustina Frimpong, Jones Gyamfi, Elorm Ninsin, Hayford Offei, Henrietta Kwansa-Bentum, Grace Semabia Kpeli, John K A Tetteh, Kokou Hefoume Amegan-Aho, Peter Wisdom Atadja, Lydia Mosi, Kwabena Obeng Duedu","doi":"10.1186/s12865-026-00872-2","DOIUrl":"10.1186/s12865-026-00872-2","url":null,"abstract":"<p><strong>Background: </strong>Sickle cell disease (SCD) is characterized by chronic inflammation, yet the inflammatory landscape defining the clinically defined steady state remains poorly characterized, particularly in African populations where the disease burden is highest. Understanding baseline cytokine and chemokine signatures during the steady state is important for distinguishing physiological disease equilibrium from transitions toward acute complications.</p><p><strong>Methods: </strong>We conducted a cross-sectional study of 129 children aged 2-17 years in Ghana, including 63 children with SCD in steady state and 66 healthy controls. Serum concentrations of 23 cytokines and chemokines were quantified using multiplex immunoassays alongside full blood count parameters. Comparative analyses and cytokine ratio assessments were performed to characterize steady-state SCD inflammatory signatures.</p><p><strong>Results: </strong>Most pro-inflammatory cytokines and chemokines were significantly elevated in children with SCD compared with controls. However, IL-12p70 and IL-23p40 levels were significantly reduced in the SCD cohort, while CCL2 and IL-1β showed no significant differences between groups. Ratio analyses revealed lower IL-12p70/IL-4, IL-23p40/IL-4, and IL-1β/IL-10 ratios, alongside increased IL-1α/IL-4, IL-17A/IL-10, IL-3/IL-10, CCL3/IL-10, and GM-CSF/IL-10 ratios, indicating an imbalanced inflammatory milieu dominated by pro-inflammatory signals. Discriminant analyses using cytokine and hematological parameters further demonstrated clear separation between children with SCD and controls.</p><p><strong>Conclusions: </strong>Steady-state SCD in African children is characterized by a distinct cytokine and chemokine profile marked by persistent pro-inflammatory activation alongside regulatory counterbalances. Reduced ratios of IL-12p70 and IL-23p40 relative to anti-inflammatory cytokines may contribute to maintaining the steady-state inflammatory equilibrium. These findings provide reference signatures that may support future studies investigating inflammatory biomarkers.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13560138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148315668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsa_circ_0077658 serves as a potential diagnostic biomarker for severe pneumonia in children and alleviates lipopolysaccharide-induced damage to bronchial epithelial cells by modulating the miR-15a-5p/NF1 axis.","authors":"Hui Zhang, Chang Liu, Hui Qi, Mei Yang","doi":"10.1186/s12865-026-00867-z","DOIUrl":"10.1186/s12865-026-00867-z","url":null,"abstract":"<p><strong>Background: </strong>Severe pneumonia in children typically presents with the most prominent early lesion being damage to the bronchial mucosa.</p><p><strong>Aim: </strong>To explore the diagnostic value of hsa_circ_0077658 in pediatric severe pneumonia and its possible mechanism of action.</p><p><strong>Materials and methods: </strong>116 children with severe pneumonia, 87 children with pneumonia, and 60 healthy children were included. Lipopolysaccharide (LPS) was used to stimulate BEAS-2B cells to establish a pneumonia cell model. Reverse Transcription quantitative PCR (RT-qPCR) was performed to detect the expression levels of hsa_circ_0077658, miR-15a-5p and Neurofibromatosis type 1(NF1). The Enzyme-Linked Immunosorbent Assay (ELISA) method was performed to detect the levels of oxidative stress markers and inflammatory factors. The Annexin V/PI and Cell Counting Kit-8 (CCK-8) kits were used to assess the apoptosis and proliferation levels of BEAS-2B cells, respectively. Person's correlation analysis, dual luciferase assays and RNA Binding Protein Immunoprecipitation (RIP) experiments were performed to demonstrate the relationship between genes.</p><p><strong>Results: </strong>Hsa_circ_0077658 and NF1 were downregulated in patients with pneumonia and in LPS-induced BEAS-2B cells, while miR-15a-5p was upregulated. Hsa_circ_0077658 showed excellent diagnostic performance, with an AUC of 0.820 (95% CI: 0.749-0.890) in healthy vs. pneumonia children comparison and 0.931 (95% CI: 0.894-0.966) for distinguishing pneumonia children from severe pneumonia children. Following exposure to LPS, BEAS-2B cells exhibited heightened oxidative stress, apoptosis, and inflammatory responses, while cellular proliferation was suppressed. Hsa_circ_0077658 targets miR-15a-5p, and NF1 is the downstream effect target of miR-15a-5p. Overexpression of hsa_circ_0077658 can alleviate the oxidative stress, apoptosis and inflammatory response in LPS-BEAS-2B cells, thereby promoting proliferation. This effect was reversed by overexpression of miR-15a-5p. Furthermore, overexpression of NF1 can reverse the exacerbating effect of miR-15a-5p overexpression on the damage caused by LPS to BEAS-2B cells.</p><p><strong>Conclusion: </strong>Hsa_circ_0077658 may be a biomarker for pediatric severe pneumonia, potentially influencing disease progression via the miR-15a-5p/NF1 axis.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13560433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148315762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and immunological factors associated with gastrointestinal involvement in common variable immunodeficiency: a real-world study.","authors":"Emrah Harman, Fatih Çölkesen, Mehmet Emin Gerek, Ferhat Sağun, Seçim Kolak, Şükran Aslan Savaş, İsmail Yiğitdöl, Ümmügülsüm Yılmaz Ergün, Şevket Arslan","doi":"10.1186/s12865-026-00870-4","DOIUrl":"10.1186/s12865-026-00870-4","url":null,"abstract":"<p><strong>Background: </strong>Gastrointestinal (GI) involvement is a common and clinically significant manifestation of common variable immunodeficiency (CVID); however, its relationship with immunological parameters remains incompletely understood.</p><p><strong>Objective: </strong>This study aimed to evaluate the association between GI involvement and immunological markers, particularly serum immunoglobulin levels and B-cell subsets, and to assess their discriminative performance.</p><p><strong>Methods: </strong>In this single-center retrospective study, 109 adult patients with CVID were included and categorized based on GI involvement. Clinical, endoscopic, histopathological, and immunological data were analyzed. Multivariable logistic regression analysis was performed to identify factors independently associated with GI involvement. Receiver operating characteristic (ROC) curve analysis was conducted to evaluate discriminative performance.</p><p><strong>Results: </strong>GI involvement was present in 58.7% of patients. Patients with GI involvement had significantly lower serum IgA and IgM levels, as well as reduced percentages of CD19⁺CD27⁺IgD⁻ switched memory B cells. In multivariable analysis, low IgM levels (OR = 0.161, 95% CI: 0.041-0.633, p = 0.009) and decreased switched memory B-cell percentage (OR = 0.918, 95% CI: 0.855-0.986, p = 0.019) were independently associated with GI involvement. ROC analysis demonstrated good discriminative ability for serum IgM (AUC = 0.799, 95% CI: 0.708-0.889) and moderate discriminative performance for switched memory B cells (AUC = 0.695, 95% CI: 0.589-0.802). Endoscopic abnormalities were detected in 87.7% of evaluated patients, with inflammatory bowel disease-like patterns being the most common histopathological finding.</p><p><strong>Conclusion: </strong>GI involvement is common in CVID and is independently associated with reduced IgM levels and decreased switched memory B cells, suggesting a potential role of impaired B-cell maturation in its pathophysiology. These findings may help identify patients at higher risk and support the clinical utility of immunophenotyping. Prospective multicenter studies are needed to validate these findings and to establish clinically relevant cutoff values.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13551818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148300818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-18a-3p as a biomarker for neonatal respiratory distress syndrome and its effects in alveolar epithelial type II cells.","authors":"Yujie Shi, Ye Jin, Hui Yu","doi":"10.1186/s12865-026-00864-2","DOIUrl":"10.1186/s12865-026-00864-2","url":null,"abstract":"<p><strong>Background: </strong>Neonatal respiratory distress syndrome (NRDS) is a major cause of significant morbidity and mortality among neonates, particularly in preterm infants. Existing studies have highlighted various microRNAs (miRNAs) implicated in NRDS, yet the precise molecular mechanisms, particularly regarding miR-18a-3p, remain incompletely understood. This research aimed to elucidate the role of miR-18a-3p as a potential biomarker for NRDS and to explore its functional mechanisms in alveolar type II epithelial cells.</p><p><strong>Method: </strong>A total of 35 NRDS patients and 35 healthy controls were enrolled, with samples of amniotic fluid and neonatal blood collected for expression analysis of miR-18a-3p. Utilizing cell culture, transfection, qRT-PCR techniques, CCK-8 assay, and ELISA assay, the function of miR-18a-3p in alveolar epithelial type II cells (an immortalized cell line, IHPEC-II, and AEC2-like cells derived from human pluripotent stem cells) was investigated. The binding relationship between miR-18a-3p and surfactant pulmonary-associated protein C (SFTPC) was predicted and validated using a dual-luciferase reporter assay.</p><p><strong>Results: </strong>Elevated levels of miR-18a-3p levels were observed in the serum of NRDS cases, with an area under the ROC curve (AUC) of 0.86 for distinguishing NRDS from healthy controls. Increased miR-18a-3p levels were also detected in amniotic fluid from these NRDS cases, yielding an ROC AUC of 0.82 for discriminating between NRDS cases and healthy controls. A positive correlation between serum miR-18a-3p levels and those in amniotic fluid was observed. Functional assays demonstrated that inhibition of miR-18a-3p significantly enhanced cell viability and increased SPC secretion in alveolar epithelial type II cells following surfactant stimulation. Dual-luciferase reporter assays confirmed that miR-18a-3p modulated SFTPC expression.</p><p><strong>Conclusion: </strong>MiR-18a-3p was increased in NRDS cases. MiR-18a-3p can inhibit alveolar epithelial type II cell function, suggesting its potential role in fetal lung development.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13523267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148275933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potential role of the gut microbiota in the development of autoantibodies associated with Spondyloarthritis: a narrative review.","authors":"Alaa Elsaghir, Al-Hassan Soliman Wadan, Torsten Witte","doi":"10.1186/s12865-026-00855-3","DOIUrl":"10.1186/s12865-026-00855-3","url":null,"abstract":"<p><p>Spondyloarthritis (SpA) is a set of immune-inflammatory conditions characterized by musculoskeletal and extra-articular manifestations. Increasing evidence indicates that alterations in the gut microbiota (dysbiosis) may influence both mucosal and systemic immune responses, potentially contributing to the loss of tolerance and the development of autoantibodies in SpA.This narrative review examines the current evidence linking gut dysbiosis to autoantibody development in SpA, with particular focus on ankylosing spondylitis (AS) and psoriatic arthritis (PsA).We summarized key mechanistic pathways, including Th17 axis activation, molecular mimicry, increased intestinal permeability (\"leaky gut\"), and altered microbial metabolite signaling. We discussed the potential relevance of these mechanisms to SpA-associated autoantibodies such as anti-CD74, anti-HSP65, and anti-Kaiso. Where direct evidence in SpA is limited, findings from other autoimmune diseases are considered as mechanistic analogies rather than definitive parallels.We further review microbiome-targeted therapeutic strategies, including probiotics, prebiotics, and bacterially based therapies, and highlight differences between preclinical findings and available clinical data. Although biologically plausible mechanisms, direct causal evidence linking gut dysbiosis to autoantibody production in SpA remains limited, and clear methodological heterogeneity persists across microbiome studies.Overall, while modulation of the gut-immune axis represents a promising research direction in SpA, further mechanistic and longitudinal human studies are required before microbiota-targeted interventions can be considered applicable for autoantibody modulation.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13281335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The clinical significance of serum complement fibroblast growth factor 21 in patients with rheumatoid arthritis.","authors":"Meiling Chen, Yu Fu, Xiaoli Li, Tingting Zhou, Lingling Liu, Jin Gu, Hongyuan Li, Beibei Zu","doi":"10.1186/s12865-026-00868-y","DOIUrl":"10.1186/s12865-026-00868-y","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to assess serum fibroblast growth factor 21 (FGF-21) levels and explore their clinical significance in patients with rheumatoid arthritis (RA).</p><p><strong>Methods: </strong>A total of 187 patients with RA, who were treated at Xuzhou Central Hospital between January 2023 and December 2024, were enrolled in this study. Based on carotid intima-media thickness (cIMT) measurements, they were categorized into a plaque group (n = 118) and a plaque-free group (n = 69). Additionally, 139 healthy individuals undergoing routine physical examinations were recruited as healthy controls (HC). Clinical data were collected from all participants, including lipid profiles, HOMA-IR, ESR, CRP, RF, anti-CCP antibody levels, and serum FGF-21 concentrations. We analyzed the associations between serum FGF-21 levels and both disease activity and atherosclerotic status in RA patients. Statistical analyses, including the chi-square test, Student's t-test, Pearson correlation analysis, and logistic regression, were performed to evaluate these relationships.</p><p><strong>Results: </strong>Serum levels of FGF-21 were significantly elevated in patients with RA compared with healthy controls (805.7 ± 188.68 vs. 203.8 ± 50.7 pg/mL, p < 0.001). Among RA patients, those with carotid plaques exhibited higher FGF-21 levels than those without plaques (840.7 ± 203.6 vs. 745.6 ± 142.2 pg/mL, p < 0.001). Correlation analyses revealed that serum FGF-21 levels were positively associated with LDL-C (r = 0.544), HOMA-IR (r = 0.625), anti-CCP antibodies (r = 0.617), rheumatoid factor (r = 0.366), DAS28 (r = 0.309), and cIMT (r = 0.604) (all p < 0.001). Conversely, FGF-21 levels were negatively correlated with the use of disease-modifying antirheumatic drugs (DMARDs) (r = - 0.569, p < 0.001) and flow-mediated dilation (FMD) (r = - 0.294, p < 0.001). Multivariate logistic regression analysis identified the serum FGF-21 level as an independent factor associated with increased cIMT (odds ratio [OR] = 1.003, 95% confidence interval [CI]: 1.001-1.006, p = 0.006).</p><p><strong>Conclusions: </strong>Our findings suggest a potential correlation between elevated FGF-21 levels and RA disease activity as well as certain metabolic parameters. Further replication studies are needed to clarify whether FGF-21 might serve as a research biomarker in the context of cardiovascular comorbidity in RA.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13449313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of characteristic genes of pressure ulcers based on angiogenesis-related genes and construction of miRNA, transcription factor, and molecular drug regulatory networks.","authors":"Na Wang, Haijing Xiao, Liping Wu, Dongmei Bao, Yawen Ma, Qianqian Wang, Qing Xu, Xiaoli Xu, Xi Zhang","doi":"10.1186/s12865-026-00866-0","DOIUrl":"10.1186/s12865-026-00866-0","url":null,"abstract":"<p><p>This study aimed to analyze transcriptomic changes in pressure ulcer (PU) samples, identify angiogenesis-related differentially expressed genes (AR-DEGs), and explore their potential as diagnostic and therapeutic targets for PU, with a particular focus on the role of CDKN1A. Transcriptomic data from dataset GSE137897, which included 381 PU samples and 391 healthy controls, were utilized to investigate these changes. Differential expression analysis was performed to identify AR-DEGs, which were subsequently analyzed for enrichment in regulatory and signaling pathways. Protein-protein interaction (PPI) network analysis was carried out to highlight key hub AR-DEGs. In addition, correlation analysis was performed to examine the relationships between these genes. Regulatory networks involving microRNAs (miRNAs), transcription factors (TFs), and targeted drugs were constructed using miRNet and DGIdb. A rat PU model was established to validate the expression of CDKN1A in vivo and to investigate the effects of CDKN1A knockout on PU healing. Through differential expression analysis, 128 AR-DEGs were identified and found to be enriched in various regulatory and signaling pathways. PPI network analysis identified seven hub AR-DEGs (JUN, HIF1A, CCND1, FOS, HDAC1, CDKN1A, CCL2), which exhibited strong diagnostic potential for PU. Correlation analysis revealed that CDKN1A was negatively correlated with CCND1, CCL2, and FOS, while HIF1A was positively correlated with CDKN1A and HDAC1. Validation experiments in a rat PU model confirmed that CDKN1A was significantly upregulated at both the mRNA and protein levels in wound tissues. Furthermore, silencing CDKN1A in dermal fibroblasts enhanced cell viability, migration (wound healing), and collagen secretion in vitro. In vivo, CDKN1A knockout significantly accelerated wound healing in PU rats, as evidenced by improved wound closure, reduced inflammation, and increased collagen deposition. This study demonstrates that CDKN1A plays a pivotal role in modulating inflammation and collagen synthesis in PUs. The findings suggest that CDKN1A holds promise as a therapeutic target for PU treatment, providing novel insights into the management of this condition.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13520517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148238948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-6 (-174 G/C) and IL-10 (-1082 G/A) polymorphisms and serum levels in Sudanese patients with end-stage renal disease and overt hepatitis B infection: a pilot comparative study.","authors":"Omer Boshra Mohamedsalih Shmed, Waleed Abdelateif Hussein","doi":"10.1186/s12865-026-00854-4","DOIUrl":"10.1186/s12865-026-00854-4","url":null,"abstract":"<p><strong>Background: </strong>Patients with end-stage renal disease (ESRD) undergoing maintenance hemodialysis are at increased risk for persistent hepatitis B virus (HBV) infection. Host immunogenetic variations, particularly in cytokines regulating pro- and anti-inflammatory responses, may influence viral chronicity. This study evaluated the association of IL-6 - 174G/C and IL-10 - 1082G/A polymorphisms and their corresponding serum levels in Sudanese patients with overt HBV and ESRD-HBV.</p><p><strong>Methods: </strong>A case-control study was conducted among 68 HBV-infected individuals (31 ESRD-HBV and 37 overt HBV). Genotyping was performed using sequence-specific primer PCR (SSP-PCR), and serum cytokine concentrations were measured by ELISA. Statistical analyses were conducted using R software, applying non-parametric Wilcoxon rank-sum and Kruskal-Wallis tests.</p><p><strong>Results: </strong>No significant differences were observed between groups in IL-6 serum levels (p = 0.29) or genotype frequencies (p = 0.738), nor in IL-10 genotype distribution (p = 0.194). In contrast, IL-10 serum levels were significantly higher in the ESRD-HBV group compared to the overt HBV group (p = 0.00024). A significant genotype-phenotype association for IL-10 was identified within the ESRD-HBV cohort (p = 0.018), where carriers of the GA genotype exhibited higher serum IL-10 levels compared to AA and GG genotypes. This association was not observed in the overt HBV group (p = 0.33).</p><p><strong>Conclusion: </strong>No significant variation in IL-6 or IL-10 genotype frequencies was detected between the groups. Nevertheless, the IL-10 (- 1082G/A) polymorphism was related to differences in serum IL-10 concentrations among patients with concurrent HBV infection and ESRD. However, given the limited sample size and absence of key clinical confounders, these findings should be interpreted as exploratory and require validation in larger, well-characterized cohorts.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13523524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148223101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lower respiratory microbiota as modulators of tumor immunity in lung adenocarcinoma.","authors":"Yingchun Chen, Minliang Kuang, Qingqi Li, Zhongan Chen, Hongyan Zhou","doi":"10.1186/s12865-026-00852-6","DOIUrl":"10.1186/s12865-026-00852-6","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma is common type of cancer with high morbidity and mortality. Emerging evidence suggests that microbial colonization in the lower respiratory airways may modulate immune activation and response to immunotherapy. However, the immunologic relevance of microbiome diversity in lung cancer remains unclear.</p><p><strong>Methods: </strong>We analyzed bronchoalveolar lavage fluid (BALF), serum cytokines, immune cell subsets, and checkpoint molecule expression from 350 patients with lung adenocarcinoma. Microbiome diversity was quantified by phylum- and genus-level richness derived from binary detection of specific bacterial groups. Associations between microbial diversity, immune parameters, and clinical prognosis were evaluated using correlation and comparative statistical analyses.</p><p><strong>Results: </strong>Among 350 samples, there was no major compositional difference between patients who died and those who recovered. Microbial diversity showed no significant associations with systemic cytokines, including IL-6, IL-1β, TNF-α, IL-10, and IFN-γ. Genus richness showed positive correlation with PD-1 expression, while phylum richness correlated inversely with PD-L1. Specific taxa demonstrated distinct immune associations: TM7 correlated with increased regulatory T cells, Actinobacteria and Veillonella correlated with lower IL-1β, while Neisseria correlated with CTLA-4 expression.</p><p><strong>Conclusion: </strong>Lower airway microbiota in lung adenocarcinoma display moderate diversity and meaningful immunologic associations, particularly with PD-1/PD-L1 pathways, Tregs, and IL-1β regulation. Although diversity alone is not prognostic, specific microbial taxa may shape immune landscapes relevant to immunotherapy response and represent potential targets for future microbiome-based interventions.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13459375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early diagnostic value of serum procalcitonin, C-reactive protein, white blood cell count and the neutrophil percentage in bacterial and fungal bloodstream infections.","authors":"Shihui Zhai, Chunhua Luo","doi":"10.1186/s12865-026-00856-2","DOIUrl":"10.1186/s12865-026-00856-2","url":null,"abstract":"<p><strong>Background: </strong>Bloodstream infections (BSIs) are severe systemic disorders caused by pathogenic microorganisms, including bacteria and fungi, invading the bloodstream. Associated with high morbidity and mortality, BSIs represent one of the leading causes of death globally. There is an urgent demand for simple, rapid, and accurate laboratory biomarkers to facilitate the diagnosis and differential diagnosis of patients with suspected BSIs, thereby guiding timely and targeted antimicrobial therapy.</p><p><strong>Objective: </strong>To evaluate the value of serum procalcitonin (PCT), C-reactive protein (CRP), white blood cell count (WBC), and neutrophil percentage (NEUT%) for early and differential diagnosis of bacterial vs. fungal bloodstream infections (BSIs), a cross-sectional study was conducted.</p><p><strong>Methods: </strong>A total of 1649 patients with suspected BSI were included in this retrospective study. Of these, 1357 patients with positive blood cultures were classified as the BSI group (experimental group), and 292 patients with negative blood cultures were assigned to the non-BSI group (control group). Serum PCT, CRP, WBC/NEUT% were measured using a bioMerieux VIDAS 30 analyzer, SIEMENS ADVIA 2400 and by Sysmex XN-9000, respectively. Microbial identification was based on bioMerieux VITEK 2 systems. The diagnostic performance of these biomarkers in the discrimination in bacterial and fungal bloodstream infections were compared using receiver operating characteristic (ROC) curves.</p><p><strong>Results: </strong>For BSI discrimination, a PCT level > 0.687 ng/mL could demonstrate the optimal performance (AUC = 0.788, sensitivity 61.7%, specificity 80.1%). The PCT level < 0.5 ng/mL for 3 consecutive days could effectively rule out BSI (sensitivity 98.1%, specificity 79.5%). Elevated PCT (> 1.78 ng/mL) and CRP (> 79.76 mg/L) levels were associated with bacterial BSIs (AUC = 0.686 for the combined markers). A PCT level > 1.98 ng/mL suggested Gram-negative BSI (sensitivity 68.4%). The positive diagnostic rates of the PCT + CRP+NEUT% combined test for G- bacterial and G+ bacterial BSIs reached 96.17% and 92.86% respectively, which significantly improved the diagnostic positive rate compared with single diagnosis.</p><p><strong>Conclusions: </strong>PCT could reliably excludes BSI (3-day < 0.5 ng/mL rule) and aids differentiation (bacterial/fungal: PCT + CRP; G-/G+: PCT+NEUT%). Multi-parameter approaches optimize diagnostic accuracy for timely intervention.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13455401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}