Host Defense

Bacteria restricted via C3-mediated autophagy

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Science  01 Jun 2018:
Vol. 360, Issue 6392, pp. 977-978
DOI: 10.1126/science.360.6392.977-d

The complement system has several important host-defense functions. Complement component C3, for example, can enhance phagocytosis, contribute to the bactericidal membrane attack complex, and initiate adaptive immune responses against invading microorganisms. Sorbara et al. uncovered another mechanism by which C3 can control pathogens. They observed interactions between the autophagy protein ATG16L1 and C3. In opsonized intracellular bacteria such as Listeria, this resulted in increased targeting to the autophagy system (xenophagy) and, in turn, greater autophagy-dependent growth restriction. Certain intracellular bacteria, such as Shigella and Salmonella, were able to escape C3-mediated targeting via the omptin proteases IcsP and PgtE, which cleave complement components including C3. Mouse models reveal that C3-mediated autophagy-dependent restriction may be important in protecting host mucosal tissues during the early stages of Listeria infection.

Cell Host Microbe 23, 644 (2018).

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