Urinary tract infection: recent insight into the evolutionary arms race between uropathogenic Escherichia coli and our immune system.
Urinary tract infections (UTIs) are among the most common bacterial infections worldwide. Humans evolved various immune-dependent and independent defense mechanisms, while pathogens evolved multiple virulence factors to fight back. This article summarizes recent findings regarding the arms race between hosts and pathogens in UTIs. It was recently reported that macrophage subsets regulate neutrophil-mediated defense in primary UTIs but seem to subvert adaptive immunity upon re-infection. Moreover, some bacterial strains can survive inside macrophages, leading to recurrent infections. Inflammasome activation results in infected host cell death and pathogen release, facilitating the removal of intracellular bacteria. As a counteraction, some bacteria evolved mechanisms to disrupt inflammasome activation. Mucosal-associated invariant T cells are further effectors that can lyse infected epithelial cells and release intracellular bacteria. Once released, the bacteria are phagocytosed by neutrophils. However, some bacteria can inhibit neutrophil migration and deprive neutrophils of nutrients. Furthermore, the complement system, considered generally bactericidal, is exploited by the bacteria for cellular invasion. Another weapon against UTI is antimicrobial peptides, e.g. ribonuclease 7, but its production is inhibited by certain bacterial strains. Thus the arms race in UTI is ongoing, and knowing the enemy's methods can help in developing new drugs to win the race.
Institute of Molecular Medicine and Experimental Immunology, Friedrich-Wilhelms University, Bonn, Germany.|Medical Clinic I, Rheinische Friedrich-Wilhelms University, Bonn, Germany.
Sebastian
S
Schwab
Institute of Molecular Medicine and Experimental Immunology, Friedrich-Wilhelms University, Bonn, Germany.
Katarzyna
K
Jobin
Institute of Molecular Medicine and Experimental Immunology, Friedrich-Wilhelms University, Bonn, Germany.
Christian
C
Kurts
D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D024901:Drug Resistance, Multiple, Bacterial / Q000187:drug effects / Q000276:immunology*; D004927:Escherichia coli Infections / Q000188:drug therapy / Q000276:immunology* / Q000382:microbiology; D006801:Humans; D007107:Immune System / Q000187:drug effects*; D014552:Urinary Tract Infections / Q000188:drug therapy / Q000276:immunology* / Q000382:microbiology; D056689:Uropathogenic Escherichia coli / Q000187:drug effects / Q000276:immunology* / Q000472:pathogenicity
D000900:Anti-Bacterial Agents
chronic inflammation; complement; immunology; macrophage; urinary tract infection