File:Influenza-reduces-immune-response-to-secondary-bacterial-infection.jpg

Summary
Wack, A. Stop the executioners. Nature Immunology 16, 6–8 (2015).

(a) Infection with S. pneumoniae (1) leads to the recognition of bacterial ligands by pattern-recognition receptors (PRRs) (2), which triggers activation of NF-κB and its translocation to the nucleus (3). NF-κB-mediated induction of Cxcl1 (4) leads to the production and secretion of CXCL1 and to the recruitment of neutrophils (5), which control bacterial spread and eliminate bacteria (6). (b) During coinfection, infection with influenza virus (1) leads to the production of type I interferons (INF-α and IFN-β) by infected airway epithelial cells (2) and other cells, which induces Setdb2 production in lung macrophages (3) and other cells. Recognition of the secondary infection with S. pneumoniae (4) activates the NF-κB pathway, but NF-κB-mediated induction of Cxcl1 is reduced by the repressive histone mark H3K9me3 established by Setdb2 at the Cxcl1 promoter (5). Reduced production of CXCL1 leads to reduced recruitment of neutrophils (6) and bacterial outgrowth due insufficient bacterial control (7). IFN-α/βR, receptor for IFN-α and IFN-β.