Abstract:
:Clinical isolates of Pseudomonas aeruginosa are either invasive or cytotoxic towards mammalian epithelial cells, endothelial cells, and macrophages. Invasion requires host cell actin cytoskeleton function, and ExsA-regulated proteins of P. aeruginosa that inhibit invasion (ExoS and ExoT) can disrupt the cytoskeleton. Another ExsA regulated protein, ExoU, is involved in the cytotoxic activity of cytotoxic strains. Src-family kinases are thought to participate in the regulation of cytoskeleton function. Recent studies have suggested that Src-family tyrosine kinases, p60-Src and p59-Fyn, are activated during P. aeruginosa invasion. Using fibroblasts homozygous for mutation of csk (-/-), we tested the hypothesis that mutation of csk, encoding a negative regulator of Src-family tyrosine kinases, would be important in P. aeruginosa invasion and cytotoxicity. Mutation of csk was found to reduce invasion by approximately 8-fold, without reducing bacterial adherence to cells (P=0.0001). Conversely, csk (-/-) cells were approximately 5-fold more susceptible to ExoU-dependent cytotoxicity (P=0.024), which was accompanied by a small increase in ExsA-regulated adherence. ExoT-dependent invasion inhibitory activity of cytotoxic P. aeruginosa was attenuated in csk (-/-) cells as compared to normal fibroblasts. These data show that fibroblasts, like epithelial cells, are susceptible to P. aeruginosa invasion and cytotoxicity. They also show a role for Csk in P. aeruginosa invasion, while providing further evidence that actin cytoskeleton disruption contributes to ExsA-regulated P. aeruginosa cytotoxicity and invasion inhibition.
journal_name
Microb Pathogjournal_title
Microbial pathogenesisauthors
Evans DJ,Kuo TC,Kwong M,Van R,Fleiszig SMdoi
10.1006/mpat.2002.0521subject
Has Abstractpub_date
2002-09-01 00:00:00pages
135-43issue
3eissn
0882-4010issn
1096-1208pii
S0882401002905218journal_volume
33pub_type
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