Open AccessCpsY Influences Streptococcus iniae Cell Wall Adaptations Important for Neutrophil Intracellular Survival
Author(s) -
Jonathan P. Allen,
Melody N. Neely
Publication year - 2012
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00027-12
Subject(s) - streptococcus iniae , biology , microbiology and biotechnology , peptidoglycan , virulence , innate immune system , pathogen , acquired immune system , phagosome , immunology , phagocytosis , bacteria , immune system , gene , genetics
The ability of a pathogen to evade neutrophil phagocytic killing mechanisms is critically important for dissemination and establishment of a systemic infection. Understanding how pathogens overcome these innate defenses is essential for the development of optimal therapeutic strategies for invasive infections. CpsY is a conserved transcriptional regulator previously identified as an important virulence determinant for systemic infection ofStreptococcus iniae . While orthologs of CpsY have been associated with the regulation of methionine metabolism and uptake pathways, CpsY additionally functions in protection from neutrophil-mediated killing.S. iniae does not alter neutrophil phagosomal maturation but instead is able to adapt to the extreme bactericidal environment of a mature neutrophil phagosome, a property dependent upon CpsY. This CpsY-dependent adaptation appears to involve stabilization of the cell wall through peptidoglycan O-acetylation and repression of cellular autolysins. Furthermore,S. iniae continues to be a powerful model for investigation of bacterial adaptations during systemic streptococcal infection.