Urinary Tract Infection Molecular Mechanisms and Clinical Translation

被引:17
作者
Godaly, Gabriela [1 ]
Ambite, Ines [1 ]
Puthia, Manoj [1 ]
Nadeem, Aftab [1 ]
Ho, James [1 ]
Nagy, Karoly [1 ]
Huang, Yujing [1 ]
Rydstrom, Gustav [1 ]
Svanborg, Catharina [1 ]
机构
[1] Lund Univ, Dept Microbiol Immunol & Glycobiol MIG, Inst Lab Med, S-22100 Lund, Sweden
基金
英国医学研究理事会;
关键词
innate immunity; immunomodulation; urinary tract infection; susceptibility; genetics; TOLL-LIKE RECEPTOR-4; ESCHERICHIA-COLI; GENETIC DIVERSITY; INNATE IMMUNITY; SUSCEPTIBILITY; FIMBRIAE; INTERLEUKIN-8; ACTIVATION; MICE; LPS;
D O I
10.3390/pathogens5010024
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Rapid developments in infection biology create new and exciting options for individualized diagnostics and therapy. Such new practices are needed to improve patient survival and reduce morbidity. Molecular determinants of host resistance to infection are being characterized, making it possible to identify susceptible individuals and to predict their risk for future morbidity. Immunotherapy is emerging as a new strategy to treat infections worldwide and controlled boosting of the host immune defense represents an important therapeutic alternative to antibiotics. In proof of concept studies, we have demonstrated that this approach is feasible. The long-term goal is not just to remove the pathogens but to also develop technologies that restore resistance to infection in disease-prone patients and devise personalized therapeutic interventions. Here, we discuss some approaches to reaching these goals, in patients with urinary tract infection (UTI). We describe critical host signaling pathways that define symptoms and pathology and the genetic control of innate immune responses that balance protection against tissue damage. For some of these genes, human relevance has been documented in clinical studies, identifying them as potential targets for immune-modulatory therapies, as a complement to antibiotics.
引用
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页数:9
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