ABSTRACT Most colorectal cancers (CRCs) arise from polyps that develop malignant traits over time. As the majority of these are sporadic, environmental determinants including the gut microbiota are increasingly implicated. Dysbiosis is consistently observed in CRC; however, its association with precancerous polyps is less defined. A systematic review of PubMed, Embase and Web of Science from January 2015 to June 2025 was therefore performed, using the following strings: (‘colon’ OR ‘colorectal’) AND (‘adenoma’ OR ‘polyp’ OR ‘neoplasia’) AND (‘microbiota’ OR ‘bacteria’) AND (‘mucosa’ OR ‘tissue’). Human studies comparing microbiota of polyp patients with healthy controls were included. Controls were defined a priori as subjects with a normal colonoscopy. Laboratory methods were extracted and study heterogeneity was addressed through narrative synthesis. The search yielded 722 articles, with 27 studies included, involving 4510 participants. Alpha diversity was unchanged in most studies ( n = 11/14), whereas beta diversity was altered in the majority ( n = 7/13). Escherichia coli , Bacteroides fragilis and Fusobacterium nucleatum were consistently enriched taxa in polyp cohorts ( n = 11/27 studies). Bacterial traits associated with adhesion, invasion, and genotoxicity were enriched in polyp subjects alongside metabolic adaptations for stress. However, overt tissue‐invasive behaviour was not observed. A decrease in the Firmicutes:Bacteroidetes (F:B) ratio is proposed as a potentially relevant biomarker but requires validation. Future translation of this data into clinical settings requires integration of histopathologic and longitudinal analyses.
ABSTRACT Asthma and atopic dermatitis (AD) are common childhood inflammatory diseases linked to type 2 immune responses and early‐life environmental factors. Emerging evidence suggests that nasopharyngeal microbiota and immune‐regulatory cytokines may influence disease development. We investigated the association between plasma IL‐34, IL‐37, and IL‐38 levels at 24 months, nasopharyngeal bacterial colonization, and later asthma and eczema in a Finnish birth cohort ( n = 145). Children with persistent eczema at 13 and 24 months had lower IL‐37 levels than children without eczema ( p = 0.030). No associations were observed between cytokine levels and asthma at 7 years. Among children with nasopharyngeal culture data ( n = 35), those colonized at 24 months with at least one of the following bacterial species: Streptococcus pneumoniae , Moraxella catarrhalis , Staphylococcus aureus , or Haemophilus influenzae , were associated with significantly lower IL‐34 ( p = 0.015) and IL‐37 ( p = 0.006) levels. These findings suggest that IL‐34 and IL‐37 may be involved in immune responses associated with nasopharyngeal bacterial colonization and eczema during early childhood.
ABSTRACT This study evaluated QMAC‐dRAST for rapid antimicrobial susceptibility testing from positive blood cultures in a low‐resistance setting by assessing analytical accuracy, detection of key resistance mechanisms and potential to shorten time to effective therapy. We tested 181 isolates and compared QMAC‐dRAST results with disc diffusion, resolving discrepancies by broth microdilution and calculating categorical agreement (CA) and error rates according to ISO 20776‐1:2019. We analyzed potential clinical impact among 128 patients with bacteremia. Categorical agreement was 92% for Gram‐negative and 91% for Gram‐positive bacteria, with very major errors in 7% and 28% of resistant isolates, respectively. Performance was limited for several key antibiotics: cefotaxime showed high very major error rates, piperacillin–tazobactam resistance was overestimated and meropenem resistance was underestimated. QMAC‐dRAST system correctly detected most critical resistance mechanisms, including all MRSA and VRE isolates and, after user interpretation, 90% of carbapenemase‐producing Enterobacterales. QMAC‐dRAST could have markedly shortened time to effective therapy in 8% of patients, but one false MRSA result risked inappropriate escalation of therapy. In this low‐resistance setting, QMAC‐dRAST offered modest benefit over rapid species identification, while suboptimal performance for key antibiotics, the absence of cefuroxime from the panel, and workflow challenges limited its utility without further optimization.
ABSTRACT Human endogenous retroviruses (HERVs) comprise a substantial portion of the human genome and are increasingly recognized as regulators of developmental and tissue‐specific transcription. While their expression has been widely studied in early embryos and pluripotent stem cells, little is known about their regulation within the ovarian follicular environment. This study aimed to characterize selected HERV families and their main epigenetic repressors in human granulosa cells associated with oocytes at different maturation stages. Expression of HERV‐H, HERV‐K, and HERV‐W families was analyzed, focusing on pol genes, the HERV‐W env gene, and the envelope‐derived proteins Syncytin‐1 and Syncytin‐2. The epigenetic repressors TRIM28 and SETDB1 were also evaluated. Samples were stratified into mature metaphase II (M2) and immature metaphase I–germinal vesicle (M1–GV) groups. All targets were consistently expressed. Quantitative analyses showed comparable transcriptional levels between M2‐ and M1–GV‐associated samples, with no significant differences. In an exploratory analysis restricted to M2 oocytes, lower HERV‐H expression was nominally associated with successful fertilization (unadjusted p = 0.0292), requiring independent confirmation. HERV transcription and its silencing machinery are stably maintained in granulosa cells across oocyte maturation stages, suggesting a tightly regulated transcriptional equilibrium within the follicular microenvironment.
ABSTRACT Pseudomonas aeruginosa represents a critical healthcare challenge, accounting for 7%–10% of hospital‐acquired infections globally, with particularly high prevalence in intensive care, burn, and respiratory units, alongside escalating rates of multidrug‐resistant and extensively drug‐resistant strains. The bacterium evades host immunity through multiple mechanisms, including Type III Secretion System effector translocation and biofilm formation via polysaccharide matrices (alginate, Psl, Pel). Antibiotic‐based therapies are increasingly ineffective, necessitating host‐directed immunotherapeutic strategies. This review synthesizes emerging evidence on monoclonal antibody therapy and immune checkpoint modulation for P. aeruginosa infections. Bispecific antibodies targeting PcrV and Psl enhance opsonophagocytic killing and biofilm disruption through Fc‐mediated mechanisms. Immune checkpoint inhibitors (anti‐PD‐1/PD‐L1) reverse T‐cell exhaustion from chronic antigen exposure and LPS‐driven upregulation of inhibitory receptors, restoring antimicrobial function. Combination approaches integrating mAbs with antibiotics and checkpoint blockade show potential for synergistic bacterial clearance in preclinical pneumonia and burn wound models. Clinical translation remains limited by antigen variability (Psl and PcrV epitope polymorphisms), biofilm heterogeneity, and host immunogenetic diversity (Fc receptor polymorphisms, HLA variants, cytokine profiles). Multi‐omics profiling may enable personalized treatment selection. Safety concerns regarding immune hyperactivation require carefully dosed, biomarker‐guided strategies. Future development demands genomic stratification of responders and optimized therapeutic windows for maximal clinical benefit.
