Open AccessListeria monocytogenes infection in the face of innate immunity
Author(s) -
Corr Sinead C.,
O'Neill Luke A. J.
Publication year - 2009
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2009.01294.x
Subject(s) - biology , innate immune system , inflammasome , nod1 , immune system , immunity , listeria monocytogenes , pyroptosis , nod2 , acquired immune system , effector , pattern recognition receptor , microbiology and biotechnology , immunology , inflammation , genetics , bacteria
Summary Pathogen recognition and induction of immune responses are important for efficient elimination of infection. However, pathogens such as Listeria monocytogenes employ strategies to evade or modulate these defences, thus creating a more favourable environment that ensures their survival and pathogenesis. New insights into these strategies, particularly those targeting innate immunity, have recently emerged. L. monocytogenes is initially detected at the cell surface or in phagosomes by toll‐like receptor 2 and in the cytosol by nuclear oligodimerization domain (NOD)‐like receptors (NOD1, NOD2) and NALP3 and Ipaf. It carries out N‐deacetylation of peptidoglycan to avoid this detection by toll‐like receptor 2 and NOD‐like receptors. L. monocytogenes modulates transcription of host immunity genes through modification of histones and chromatin remodelling. Furthermore, L. monocytogenes has recently been shown to avoid autophagy and induce apoptosis in immune effector cells. In this review we discuss some of these strategies, which have provided new insights into the interaction between L. monocytogenes and the immune response at a crucial stage of infection.