GSE141931 Mycobacterium tuberculosis is protected from NADPH oxidase and LC3-associated phagocytosis by the LCP protein CpsA

Contributors : Stefan K öster ; Sandeep Upadhyay ; Pallavi Chandra ; Kadamba Papavinasasundaram ; Guozhe Yang ; Amir Hassan ; Steven J Grigsby ; Ekansh Mittal ; Heidi S Park ; Victoria Jones ; Fong-Fu Hsu ; Mary Jackson ; Christopher M Sassetti ; Jennifer A PhilipsSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusMycobacterium tuberculosis ’success as a pathogen comes from itsability to evade degradation by macrophages. Normally macro-phages clear microorganisms that activate pathogen-recognitionreceptors (PRRs) through a lysosomal-trafficking pathway called“LC3-associated phagocytosis”(LAP). AlthoughM.tuberculosisac-tivates num erous PRRs, for reasons that are poorly understoodLAP does not substantially contribute toM.tuberculosiscontrol.LAP depends upon reactive oxygen species (ROS) generated byNADPH oxidase, butM.tuberculosisfails to generate a robustoxidative response. Here, we show that CpsA, a LytR-CpsA-Psr(LCP) domai n-containing protein, is required forM.tuberculosisto evade killing by NADPH oxidase and LAP. Unlike phagosomescontaining wild-type bacilli, phagosomes containing theΔcpsAmutant recruited NADPH oxidase, produced ROS, associated withLC3, and matured into antibacterial lysosomes. Moreover, CpsAwas su fficient to impair NADPH oxidase recruitment to fungal par-ticles that are normally cleared by LAP. Intracellular survival of theΔcpsAmutant was largely restored in macrophages missing LAPcomponents (Nox2,R...

Source: GEO: Gene Expression Omnibus - December 13, 2019 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Mus musculus Source Type: research