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© Institut Pasteur et Institut Imagine
Scanning electron micrograph of segmented filamentous bacterium (SFB). Segmented filamentous bacteria (SFB) are bacteria from the Clostridiaceae family that colonize the intestines of many species, likely including humans, without causing disease; they live in symbiosis with epithelial cells and are involved in the maturation of intestinal immunity.
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Nature microbiology - 21 Dec 2020

Connor MG, Camarasa TMN, Patey E, Rasid O, Barrio L, Weight CM, Miller DP, Heyderman RS, Lamont RJ, Enninga J, Hamon MA,

Link to Pubmed [PMID] – 33349663

Link to DOI – 10.1038/s41564-020-00805-8

Nat Microbiol 2020 Dec; ():

Streptococcus pneumoniae is a natural colonizer of the human respiratory tract and an opportunistic pathogen. Although epithelial cells are among the first to encounter pneumococci, the cellular processes and contribution of epithelial cells to the host response are poorly understood. Here, we show that a S. pneumoniae serotype 6B ST90 strain, which does not cause disease in a murine infection model, induces a unique NF-κB signature response distinct from an invasive-disease-causing isolate of serotype 4 (TIGR4). This signature is characterized by activation of p65 and requires a histone demethylase KDM6B. We show, molecularly, that the interaction of the 6B strain with epithelial cells leads to chromatin remodelling within the IL-11 promoter in a KDM6B-dependent manner, where KDM6B specifically demethylates histone H3 lysine 27 dimethyl. Remodelling of the IL-11 locus facilitates p65 access to three NF-κB sites that are otherwise inaccessible when stimulated by IL-1β or TIGR4. Finally, we demonstrate through chemical inhibition of KDM6B with GSK-J4 inhibitor and through exogenous addition of IL-11 that the host responses to the 6B ST90 and TIGR4 strains can be interchanged both in vitro and in a murine model of infection in vivo. Our studies therefore reveal how a chromatin modifier governs cellular responses during infection.

https://pubmed.ncbi.nlm.nih.gov/33349663