Advances in Pathogenesis and Treatment of Infectious Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Microbiology in Human Health and Disease".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 1428

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Guest Editor
Instituto de Investigación Sanitaria Hospital “Ramón y Cajal” (IRYCIS), 28034 Madrid, Spain
Interests: HIV; infectious disease epidemiology; tuberculosis; infectious disease control and prevention; tropical diseases

Special Issue Information

Dear Colleagues,

Infectious diseases remain a significant global health challenge, exacerbated by increasing antimicrobial resistance, biofilm-associated infections, and emerging pathogens. Recent advances in molecular diagnostics, phage therapy, and recombinant antibody technologies offer promising new strategies for targeted interventions. However, substantial gaps persist in translating these innovations into clinical practice, particularly regarding polymicrobial infections, the optimization of host-directed tolerance mechanisms, and the reduction of diagnostic delays.

This Special Issue invites submissions that address the pathogenesis of bacterial, viral, and fungal infections, as well as novel therapeutic approaches and innovative diagnostic tools. Contributions focused on antimicrobial stewardship, microbiome engineering, and interdisciplinary strategies to overcome resistance and enhance patient outcomes are especially encouraged. Original research articles, comprehensive reviews, and clinical trials advancing our understanding of infection dynamics and therapeutic frontiers are all welcome.

Join us in shaping the future of infectious disease management by contributing to this critical scientific discourse.

Dr. Francesca Gioia
Guest Editor

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Keywords

  • antimicrobial resistance
  • phage therapy
  • host–pathogen interactions
  • molecular diagnostics
  • immunotherapy

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Published Papers (1 paper)

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Research

22 pages, 13539 KB  
Article
Trained Immunity in Bladder ILC3s Enhances Mucosal Defense Against Recurrent Urinary Tract Infections
by Qiaoqiao Pei, Jiaqi Liu, Ziwen Tang, Jiaqing Tan, Xu Han, Xinrong Hu, Zhou Liang, Feng Li, Changjian Zhu, Ruoni Lin, Ruilin Zheng, Jiani Shen, Qinghua Liu, Haiping Mao, Kefei Wu, Wei Chen and Yi Zhou
Biomedicines 2026, 14(1), 78; https://doi.org/10.3390/biomedicines14010078 - 30 Dec 2025
Cited by 1 | Viewed by 1101
Abstract
Background: Urinary tract infections (UTIs) rank among the most prevalent infectious diseases globally, with recurrent UTIs (rUTIs) posing substantial therapeutic challenges due to the lack of durable protective immunity. While trained immunity augments innate immune responses, its induction and functional significance in [...] Read more.
Background: Urinary tract infections (UTIs) rank among the most prevalent infectious diseases globally, with recurrent UTIs (rUTIs) posing substantial therapeutic challenges due to the lack of durable protective immunity. While trained immunity augments innate immune responses, its induction and functional significance in bladder-resident group 3 innate lymphoid cells (ILC3s) remain unknown. This study investigates whether ILC3s develop trained immunity following uropathogenic Escherichia coli (UPEC) exposure and how they contribute to mucosal defense against rUTIs. Methods: The ILC3 counts were detected in bladder sections from UTI patients and health controls (HC). A recurrent UTI mouse model was established through primary and secondary urethral UPEC inoculation. Bacterial loads in tissues were assessed, and single-cell suspensions were analyzed via flow cytometry. Bladder naïve- and UPEC-trained ILC3s were adoptively transferred, with evaluations of histopathology, epithelial barrier function, inflammation, and antimicrobial peptides. The in vitro ILC3 cell line MNK-3 was detected for IL-17A and IL-22 production following primary and secondary UPEC lysate stimulation. Results: We demonstrate that primary UPEC infection triggers ILC3 expansion in both human and murine bladders. Upon secondary challenge, these ILC3s develop trained immunity, characterized by enhanced proliferation, amplified IL-17A and IL-22 production, and improved pathogen clearance. Mechanistically, trained ILC3s reinforce urothelial barrier integrity through upregulation of antimicrobial peptides (Reg3b/Reg3g) and attenuate inflammatory pathology by suppressing pro-inflammatory cytokines (IL-6, TNF-α). Conclusions: We uncover an endogenous defense mechanism wherein UPEC primes bladder ILC3s via trained immunity, enabling amplified IL-17A- and IL-22-mediated protection against recurrent infections. These findings establish ILC3-trained immunity as a novel conceptual foundation, providing a basis for developing immunotherapies against rUTIs. Full article
(This article belongs to the Special Issue Advances in Pathogenesis and Treatment of Infectious Diseases)
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