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Eur J Immunol. 2016 Aug;46(8):1926-35. doi: 10.1002/eji.201546118. Epub 2016 Jun 13.

Negative regulation of bacterial killing and inflammation by two novel CD16 ligands.

Author information

Emergency Medicine Department, University of Sao Paulo, Sao Paulo, Brazil.
Inserm Unit 1149 and ERL CNRS 8252, Center for Research on Inflammation, University Paris Diderot, Paris, France.
Vascular Biology Laboratory, Chemistry Institute, University of Sao Paulo, Sao Paulo, Brazil.
Biosciences National Laboratory (LNBio), Campinas, Sao Paulo, Brazil.

Erratum in


Sepsis, a leading cause of death worldwide, involves exacerbated proinflammatory responses and inefficient bacterial clearance. Phagocytic cells play a crucial part in the prevention of sepsis by clearing bacteria through host innate receptors. Here, we used a phage display library to identify two peptides in Escherichia coli that interact with host innate receptors. One of these peptides, encoded by the wzxE gene of E. coli K-12, was involved in the transbilayer movement of a trisaccharide-lipid intermediate in the assembly of enterobacterial common antigen. Peptide-receptor interactions induced CD16-mediated inhibitory immunoreceptor tyrosine-based activating motif signaling, blocking the production of ROS and bacterial killing. This CD16-mediated inhibitory signaling was abrogated in a WzxE(-/-) mutant of E. coli K-12, restoring the production of ROS and bacterial killing. Taken together, the two novel CD16 ligands identified negatively regulate bacterial killing and inflammation. Our findings may contribute toward the development of new immunotherapies for E. coli-mediated infectious diseases and inflammation.


CD16; Escherichia coli; Fc receptors; ITAM; Immunotherapy; Inflammation; Phagocytosis; Sepsis

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