Document Detail


Interleukin-1beta-induced growth enhancement of Staphylococcus aureus occurs in biofilm but not planktonic cultures.
MedLine Citation:
PMID:  16769197     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Staphylococcus aureus causes recalcitrant infections and forms resistant biofilms. Mechanisms of biofilm resistance to host defenses may include changes in gene expression that confer responsiveness to chemical mediators. In earlier studies fresh clinical isolates responded to inflammatory cytokines, but responsiveness was lost after multiple in vitro passages [Meduri et al. Cytokines IL-1beta, IL-6, and TNF-alpha enhance the In vitro growth of bacteria. Am J Respir Crit Care Med 1999;160:961-7]. Since biofilms more closely resemble in vivo growth and are implicated in recalcitrant infections, we hypothesized that biofilms, but not planktonic cells, would respond to cytokines. Biofilms were induced by ethanol in S. aureus ATCC 12600. Biofilms treated with 2 ng/mL interleukin-1beta (IL-1beta) for 6 h contained 2.5-fold more cells than untreated biofilms, but no growth-enhancement occurred in planktonic cultures. As determined by flow cytometry, IL-beta bound to 63.1% of biofilm cells, but only 11.2% of planktonic cells. Our results provide evidence of a differential response of biofilm and planktonic bacteria to chemical mediators, and suggest that biofilm bacteria may evade host defenses by growing more rapidly in response to the inflammatory mediators released by activated host defense cells.
Authors:
Renee A McLaughlin; Arlene J Hoogewerf
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Microbial pathogenesis     Volume:  41     ISSN:  0882-4010     ISO Abbreviation:  Microb. Pathog.     Publication Date:    2006 Aug-Sep
Date Detail:
Created Date:  2006-09-27     Completed Date:  2006-11-02     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8606191     Medline TA:  Microb Pathog     Country:  England    
Other Details:
Languages:  eng     Pagination:  67-79     Citation Subset:  IM    
Affiliation:
Department of Biology, Calvin College, 1726 Knollcrest Circle SE, Grand Rapids, MI 49546-4403, USA.
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MeSH Terms
Descriptor/Qualifier:
Bacteriological Techniques
Biofilms / drug effects*,  growth & development*
Chemokine CCL4
Dose-Response Relationship, Drug
Flow Cytometry / methods
Interleukin-1 / metabolism,  pharmacology*
Interleukin-6 / pharmacology
Macrophage Inflammatory Proteins / pharmacology
Polysaccharides, Bacterial / biosynthesis,  genetics
Staphylococcus aureus / drug effects*,  metabolism,  physiology*
Tumor Necrosis Factor-alpha / pharmacology
Up-Regulation
Chemical
Reg. No./Substance:
0/Chemokine CCL4; 0/Interleukin-1; 0/Interleukin-6; 0/Macrophage Inflammatory Proteins; 0/Polysaccharides, Bacterial; 0/Tumor Necrosis Factor-alpha; 0/polysaccharide intercellular adhesin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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