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and 
1
,
Departments of
* Microbiology and Immunology,
Pediatrics, and
Pathology, Dalhousie University, Halifax, Nova Scotia, Canada
The mechanisms of neutrophil (PMN) recruitment to
Pseudomonas aeruginosa infection remain incompletely
defined. Mast cells (MC) involvement in this process has not been
studied previously. In this study, we demonstrate that human cord
blood-derived MC phagocytose P. aeruginosa and release
mediators that activate HUVEC monolayers for supporting PMN
transmigration. Pretreatment of supernatants from P.
aeruginosa-MC cocultures with neutralizing anti-IL-1
plus anti-IL-1
Abs, or IL-1R antagonist before addition to HUVEC
for stimulation completely abrogated MC-induced PMN transmigration,
while anti-TNF- treatment had no effect. The expression of
E-selectin and ICAM-1 on HUVEC, the latter a ligand for PMN CD11/CD18,
was significantly up-regulated by P. aeruginosa-induced
MC mediators. Pretreatment of human PMN with anti-CD18 mAb or
pretreatment of HUVEC with a combination of three mAbs (against ICAM-1,
ICAM-2, and E-selectin) inhibited by 85% the MC-dependent PMN
transmigration. Moreover, P. aeruginosa-induced
production of IL-1 and IL-1 was down-regulated by IL-10 and
dexamethasone. This study demonstrates for the first time that MC may
mediate P. aeruginosa-induced PMN recruitment via
production of IL-1 and . These findings have important
implications for diseases involving P. aeruginosa
infection and suggest novel targets for modulating P.
aeruginosa-induced inflammation.
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