Journal
VIRULENCE
Volume 5, Issue 8, Pages 835-851Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/21505594.2014.965580
Keywords
antimicrobial peptide; bacterial pathogens; cell envelope; gene regulation; peptidoglycan; phospholipid; stress response; teichoic acid; virulence gene; BFP; bundle-forming pilus; CAMP; cationic antimicrobial peptide; ESR; envelope stress response; CF; cystic fibrosis; ECF; extracytoplasmic function; EPEC; enteropathogenic E; coli; HMV; hypermucoviscosity; IM; inner membrane; LPS; lipopolysaccharide; LTA; lipoteichoic acids; OM; outer membrane; OMP; outer membrane protein; PG; phosphatidylglycerol; T(2; 3; 4)SS; type II; III; IV secretion system; UPEC; uropathogenic E; coli; WTA; wall teichoic acids
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Funding
- National Institute of Allergy and Infectious Diseases of the National Institutes of Health [R01AI052148]
- Burroughs Wellcome Fund
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The bacterial cytoplasm lies within a multilayered envelope that must be protected from internal and external hazards. This protection is provided by cell envelope stress responses (ESRs), which detect threats and reprogram gene expression to ensure survival. Pathogens frequently need these ESRs to survive inside the host, where their envelopes face dangerous environmental changes and attack from antimicrobial molecules. In addition, some virulence genes have become integrated into ESR regulons. This might be because these genes can protect the cell envelope from damage by host molecules, or it might help ESRs to reduce stress by moderating the assembly of virulence factors within the envelope. Alternatively, it could simply be a mechanism to coordinate the induction of virulence gene expression with entry into the host. Here, we briefly describe some of the bacterial ESRs, followed by examples where they control virulence gene expression in both Gram-negative and Gram-positive pathogens.
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