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exoY increases Pseudomonas aeruginosa virulence
Author(s) -
Prasain Nutan,
Alvarez Diego F.,
Frank Dara W.,
Stevens Troy
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.928.6
Subject(s) - virulence , microbiology and biotechnology , type three secretion system , pseudomonas aeruginosa , biology , bacteria , gene , biochemistry , genetics
Pseudomonas aeruginosa is a principal cause of pneumonia that progresses to sepsis and acute lung injury. Bacterial virulence is due to the type III secretion system (TTSS), which is a functional bacterial needle that introduces exotoxins into host cells. Four known exotoxins are introduced through the TTSS; exoY is a cytosolic adenylyl cyclase that disrupts the endothelial barrier and causes edema. It is not clear whether exoY contributes to P. aeruginosa virulence. Survival analysis was performed in rats exposed to three P. aeruginosa strains, including strains that possess a: (1) functional TTSS, but only inject exoY (exoY + ), (2) functional TTSS, but inject a catalytically inactive exoY (exoY K81M ), and (3) non‐functional TTSS (exoY TM ). Bacteria were introduced by tracheal installation, and survival curves generated over a 7‐day time course. Virulence was greatest in animals treated with exoY + (LD 50 ≈ 10 8 CFU); exoY K81M or exoY TM strains were not virulent (LD 50 > 10 9 CFU). Histological inspection of exoY + ‐treated animals revealed large areas of patchy atelectasis, with significant neutrophil infiltration into alveoli. Alveolar fluid accumulation was prominent, and large peri‐vascular cuffs were observed, consistent with increased endothelial permeability. Thus, introduction of catalytically active exoY by P. aeruginosa is an important determinant of pathogenic virulence. HL‐60024 & HL‐66299