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Paper of the Month

Chlamydia trachomatis paralyzes neutrophils to evade the host innate immune response

Autoren: Karthika Rajeeve, Sudip Das, Bhupesh K. Prusty und Thomas Rudel

Vollständiger Artikel: https://www.ncbi.nlm.nih.gov/pubmed/?term=29946164externer Link

Rajeeve

Foto: Erstautorin Karthika Rajeeve

Kommentar: Wir konnten zeigen, dass obligat human-pathogene Chlamydien (C. trachomatis) das Immunsystem des infizierten Wirts schwächen, indem sie die Aktivierung von polymorph-nuklearen Leukozyten (PMNs) verhindern. Hierbei konnten von uns das erste Mal Details des entsprechenden Mechanismus beschrieben werden, auf welche Weise C. trachomatis aktiv die Aktivierung von PMNs unterbindet und somit einer Immunantwort des Wirts entgeht.  

Abstract: Chlamydia trachomatis, an obligate intracellular human pathogen, is a major cause of sexually transmitted diseases. Infections often occur without symptoms, a feature that has been attributed to the ability of the pathogen to evade the host immune response. We show here that C. trachomatis paralyzes the host immune system by preventing the activation of polymorphic nuclear leukocytes (PMNs). PMNs infected with Chlamydia fail to produce neutrophil extracellular traps (NETs) and the bacteria are able to survive in PMNs for extended periods of time. We have identified the secreted chlamydial protease like activating factor (CPAF) as an effector mediating the evasion of the innate immune response since CPAF-deficient Chlamydia activate PMNs and are subsequently efficiently killed. CPAF suppresses the oxidative burst and interferes with chemical-mediated activation of neutrophils. We identified formyl peptide receptor 2 (FPR2) as a target of CPAF, which is inactivated by cleavage and released from the surface of PMNs. In contrast to previously described subversion mechanisms that mainly act on already activated PMNs, we describe here the first details of how Chlamydia actively paralyzes PMNs, including the formation of NETs, to evade the host’s innate immune response.

Letztauthor/Corresponding author:

Prof. Dr. Thomas Rudel
Lehrstuhl für Mikrobiologie
Biozentrum der Universität Würzburg
Am Hubland
97074 Würzburg
Tel.: 0931 31 84401
thomas.rudel@biozentrum.uni-wuerzburg.de