Open AccessEspJ of enteropathogenic and enterohaemorrhagic Escherichia coli inhibits opsono‐phagocytosis
Author(s) -
Marchès Oliver,
Covarelli Valentina,
Dahan Sivan,
Cougoule Céline,
Bhatta Pallavi,
Frankel Gad,
Caron Emmanuelle
Publication year - 2008
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.1462-5822.2007.01112.x
Subject(s) - biology , internalization , phagocytosis , enteropathogenic escherichia coli , microbiology and biotechnology , opsonin , effector , secretion , macrophage , receptor , escherichia coli , in vitro , gene , biochemistry
Summary A key strategy in microbial pathogenesis is the subversion of the first line of cellular immune defences presented by professional phagocytes. Enteropathogenic and enterohaemorrhagic Escherichia coli (EPEC and EHEC respectively) remain extracellular while colonizing the gut mucosa by attaching and effacing mechanism. EPEC use the type three secretion system effector protein EspF to prevent their own uptake into macrophages. EPEC can also block in trans the internalization of IgG‐opsonized particles. In this study, we show that EspJ is the type three secretion system effector protein responsible for trans ‐inhibition of macrophage opsono‐phagocytosis by both EPEC and EHEC. While EspF plays no role in trans ‐inhibition of opsono‐phagocytosis, espJ mutants of EPEC or EHEC are unable to block uptake of opsonized sheep red blood cells (RBC), a phenotype that is rescued upon complementation with the espJ gene. Importantly, ectopic expression of EspJ EHEC in phagocytes is sufficient to inhibit internalization of both IgG‐ and C3bi‐opsonized RBC. These results suggest that EspJ targets a basic mechanism common to these two unrelated phagocytic receptors. Moreover, EspF and EspJ target independent aspects of the phagocytic function of mammalian macrophages in vitro .