ArcA-regulated glycosyltransferase lic2B promotes complement evasion and pathogenesis of nontypeable Haemophilus influenzae
UMass Chan Affiliations
Department of Medicine, Division of Infectious Diseases and ImmunologyDepartment of Microbiology and Physiological Systems
Document Type
Journal ArticlePublication Date
2011-05-02Keywords
AnimalsBacterial Proteins
Blotting, Western
Cell Separation
Complement System Proteins
Flow Cytometry
Gene Expression
Gene Expression Profiling
Gene Expression Regulation, Bacterial
Haemophilus Infections
Haemophilus influenzae
Humans
Immune Evasion
Lipopolysaccharides
Mice
Oxidation-Reduction
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction
Immunology and Infectious Disease
Microbiology
Physiology
Metadata
Show full item recordAbstract
Signaling mechanisms used by Haemophilus influenzae to adapt to conditions it encounters during stages of infection and pathogenesis are not well understood. The ArcAB two-component signal transduction system controls gene expression in response to respiratory conditions of growth and contributes to resistance to bactericidal effects of serum and to bloodstream infection by H. influenzae. We show that ArcA of nontypeable H. influenzae (NTHI) activates expression of a glycosyltransferase gene, lic2B. Structural comparison of the lipooligosaccharide (LOS) of a lic2B mutant to that of the wild-type strain NT127 revealed that lic2B is required for addition of a galactose residue to the LOS outer core. The lic2B gene was crucial for optimal survival of NTHI in a mouse model of bacteremia and for evasion of serum complement. The results demonstrate that ArcA, which controls cellular metabolism in response to environmental reduction and oxidation (redox) conditions, also coordinately controls genes that are critical for immune evasion, providing evidence that NTHI integrates redox signals to regulate specific countermeasures against host defense.Source
Infect Immun. 2011 May;79(5):1971-83. Epub 2011 Feb 28. Link to article on publisher's siteDOI
10.1128/IAI.01269-10Permanent Link to this Item
http://hdl.handle.net/20.500.14038/36445PubMed ID
21357723Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1128/IAI.01269-10