Influenza is an acute respiratory illness, caused by influenza A, B, and C viruses,that occurs in local outbreaks or seasonal epidemics. Clinical illness follows a shortincubation period and presentation ranges from asymptomatic to fulminant, dependingon the characteristics of both the virus and the individual host. Influenza A virusescan also cause sporadic infections or spread worldwide in a pandemic when novel strainsemerge in the human population from an animal host. New approaches to influenza preventionand treatment for management of both seasonal influenza epidemics and pandemics aredesirable.
Source: Influenza – The Lancet
Images in Clinical Medicine from The New England Journal of Medicine — Severe Plantar Warts in an Immunocompromised Patient
Severe pneumonia predisposes to recurrent infection by functionally impairing antigen presenting cells.
Normally, the lumen of the colon lacks oxygen. Fastidiously anaerobic butyrate-producing bacteria thrive in the colon; by ablating these organisms, antibiotic treatment removes butyrate. Byndloss et al. discovered that loss of butyrate deranges metabolic signaling in gut cells (see the Perspective by Cani). This induces nitric oxidase to generate nitrate in the lumen and disables β-oxidation in epithelial cells that would otherwise mop up stray oxygen before it enters the colon. Simultaneously, regulatory T cells retreat, and inflammation is unchecked, which contributes yet more oxygen species to the colon. Then, facultative aerobic pathogens, such as Escherichia coli and Salmonella enterica , can take advantage of the altered environment and outgrow any antibiotic-crippled and benign anaerobes.Science , this issue p. ; see also p.  : /lookup/doi/10.1126/science.aam9949 : /lookup/doi/10.1126/science.aao2202
Gut microbes are key partners in host defense against potential pathogens ( 1 ). This might be achieved through cross-talk between gut bacteria, epithelial cells lining the gut (colonocytes), and immune cells ( 2 ). Part of this cross-talk involves metabolites derived from the bacteria, such as the short-chain fatty acid butyrate. This can bind to specific G protein-coupled receptors in colonocytes and immune cells, leading to antimicrobial immune responses ( 3 ). However, what if this cross-talk were not the full story? On page 570 of this issue, Byndloss et al. ( 4 ) show that butyrate instructs colonocytes to consume oxygen through the β-oxidation metabolic pathway and consequently protects the host against the expansion of potentially pathogenic bacteria that can lead to inflammatory bowel diseases.