title: Suppression of innate immunity by a nasal carriage strain of Staphylococcus aureus increases its colonization on nasal epithelium.
abstract: Nasal carriage of Staphylococcus aureus is an important source of nosocomial infection and community-acquired methicillin-resistant S. aureus (MRSA). Previous studies by our laboratory revealed that nasal carriage of S. aureus is accompanied by subclinical inflammation, which is insufficient to prevent colonization, and that carriage might also be a result of adaptation and selection of certain S. aureus strains to the host's nasal environment. In the present study we observed that a carrier strain of S. aureus preferentially colonizes and attaches to nasal epithelial cells (NEC) compared to a non-carrier S. aureus strain. Conversely, when naive NEC were pretreated with interleukin-1beta for 24 hr, the growth and attachment of the carrier strain of S. aureus were significantly reduced in comparison to the non-carrier strain, emphasizing the pivotal role played by host innate immunity in the initial events of nasal carriage. While both strains up-regulated the expression of the pattern recognition receptor, Toll-like receptor 2 (TLR2), NEC exposed to the nasal carrier strain had a 4-hr delay in TLR2 expression compared with NEC exposed to non-carrier S. aureus. Moreover, even after 20 hr of colonization the expression of two principal epithelial antimicrobial peptides, human beta-defensin-2 and human beta-defensin-3, was negligibly induced in NEC exposed to the nasal carrier strain of S. aureus in comparison to the non-carrier strain. These results suggest that carrier strains of S. aureus retain a competitive advantage over non-carrier strains by delaying the host's innate response to epithelial colonization and infection.
authors.affiliation: Laboratory of Innate Host Defense, Department of Molecular Biology and Microbiology, Burnett College of Biomedical Sciences, University of Central Florida, Orlando, FL 32816, USA.
authors.forename: Gerry A
authors.initials: GA
authors.lastname: Quinn
authors.forename: Alexander M
authors.initials: AM
authors.lastname: Cole
mesh_terms: D001422:Bacterial Adhesion; D002353:Carrier State / Q000276:immunology* / Q000382:microbiology; D002478:Cells, Cultured; D015536:Down-Regulation / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D004847:Epithelial Cells / Q000382:microbiology; D006801:Humans; D053583:Interleukin-1beta / Q000276:immunology; D009296:Nasal Cavity / Q000276:immunology* / Q000382:microbiology; D009297:Nasal Mucosa / Q000276:immunology / Q000382:microbiology; D016133:Polymerase Chain Reaction / Q000379:methods; D013203:Staphylococcal Infections / Q000276:immunology* / Q000382:microbiology; D013211:Staphylococcus aureus / Q000145:classification / Q000276:immunology / Q000472:pathogenicity* / Q000502:physiology; D051195:Toll-Like Receptor 2 / Q000378:metabolism; D015854:Up-Regulation / Q000276:immunology; D023083:beta-Defensins / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; C495342:TLR2 protein, human; D051195:Toll-Like Receptor 2; D023083:beta-Defensins