Molecular Determinants in Phagocyte-Bacteria Interactions

Phagocytes are crucial for host defense against bacterial pathogens. As first demonstrated by Metchnikoff, neutrophils and mononuclear phagocytes share the capacity to engulf, kill, and digest microbial invaders. Generally, neutrophils focus on extracellular, and mononuclear phagocytes on intracellu...

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Veröffentlicht in:Immunity (Cambridge, Mass.) Mass.), 2016-03, Vol.44 (3), p.476-491
Hauptverfasser: Kaufmann, Stefan H.E., Dorhoi, Anca
Format: Artikel
Sprache:eng
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Zusammenfassung:Phagocytes are crucial for host defense against bacterial pathogens. As first demonstrated by Metchnikoff, neutrophils and mononuclear phagocytes share the capacity to engulf, kill, and digest microbial invaders. Generally, neutrophils focus on extracellular, and mononuclear phagocytes on intracellular, pathogens. Reciprocally, extracellular pathogens often capitalize on hindering phagocytosis and killing of phagocytes, whereas intracellular bacteria frequently allow their engulfment and then block intracellular killing. As foreseen by Metchnikoff, phagocytes become highly versatile by acquiring diverse phenotypes, but still retaining some plasticity. Further, phagocytes engage in active crosstalk with parenchymal and immune cells to promote adjunctive reactions, including inflammation, tissue healing, and remodeling. This dynamic network allows the host to cope with different types of microbial invaders. Here we present an update of molecular and cellular mechanisms underlying phagocyte functions in antibacterial defense. We focus on four exemplary bacteria ranging from an opportunistic extracellular to a persistent intracellular pathogen. Progress in the field of phagocyte biology reveals that macrophages and neutrophils are multitaskers that interact flexibly with bacterial pathogens. Kaufmann and Dorhoi review these advances and provide insights into molecular interactions between phagocytes and extra- and intracellular bacteria, emphasizing microbial strategies that have evolved to counteract phagocyte killing.
ISSN:1074-7613
1097-4180
DOI:10.1016/j.immuni.2016.02.014