Journal
JOURNAL OF BACTERIOLOGY
Volume 189, Issue 6, Pages 2203-2209Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.01839-06
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Funding
- NHLBI NIH HHS [HL69809, PH50HL74005, R01 HL069809, P50 HL074005] Funding Source: Medline
- NIGMS NIH HHS [5 R25 GM48972-06, R25 GM048972] Funding Source: Medline
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Pseudomonas aeruginosa is one of the major causative agents of mortality and morbidity in hospitalized patients due to a multiplicity of virulence factors associated with both chronic and acute infections. Acute P. aeruginosa infection is primarily mediated by planktonic bacteria expressing the type III secretion system (TTSS), a surface-attached needle-like complex that injects cytotoxins directly into eukaryotic cells, causing cellular damage. Lipopolysaccharide (LPS) is the principal surface-associated virulence factor of P. aeruginosa. This molecule is known to undergo structural modification (primarily alterations in the A- and B-band O antigen) in response to changes in the mode of life (e.g., from biofilm to planktonic). Given that LPS exhibits structural plasticity, we hypothesized that the presence of LPS lacking O antigen would facilitate eukaryotic intoxication and that a correlation between the LPS O-antigen serotype and TTSS-mediated cytotoxicity would exist. Therefore, strain PAO1 (A(+) B+ O-antigen serotype) and isogenic mutants with specific O-antigen defects (A(+) B-, A(-) B+, and A(-) B-) were examined for TTSS expression and cytotoxicity. A strong association existed in vitro between the absence of the large, structured B-band 0 antigen and increased cytotoxicity of these strains. In vivo, all three LPS mutant strains demonstrated significantly increased lung injury compared to PAOI. Clinical strains lacking the B-band O antigen also demonstrated increased TTSS secretion. These results suggest the existence of a cooperative association between LPS O-antigen structure and the TTSS in both laboratory and clinical isolates of P. aeruginosa.
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