INTERACTION OF DEXAMETHASONE AND SALMONELLA-ENTERITIDIS IMMUNE LYMPHOKINES ON SALMONELLA-ENTERITIDIS ORGAN INVASION AND IN-VITRO POLYMORPHONUCLEAR LEUKOCYTE FUNCTION

Citation
Ed. Mcgruder et al., INTERACTION OF DEXAMETHASONE AND SALMONELLA-ENTERITIDIS IMMUNE LYMPHOKINES ON SALMONELLA-ENTERITIDIS ORGAN INVASION AND IN-VITRO POLYMORPHONUCLEAR LEUKOCYTE FUNCTION, FEMS immunology and medical microbiology, 11(1), 1995, pp. 25-34
Citations number
46
Categorie Soggetti
Immunology,Microbiology
ISSN journal
09288244
Volume
11
Issue
1
Year of publication
1995
Pages
25 - 34
Database
ISI
SICI code
0928-8244(1995)11:1<25:IODASI>2.0.ZU;2-T
Abstract
We used an anti-inflammatory dose of dexamethasone (DEX) and Salmonell a enteritidis (SE)-immune lymphokines (ILK) followed by oral SE challe nge to chicks to determine the effects of these treatments on SE organ invasion and in vitro function of PMNs derived from peripheral blood. Endpoints included percent protection against SE organ invasion, numb ers of peripheral blood PMNs, and in vitro PMN adherence, chemotaxis, and SE killing. SE organ invasion was significantly reduced in chicks treated with either ILK alone or DEX + ILK compared to controls. Chick s treated with either DEX alone or DEX + ILK responded with a signific ant increase in numbers of peripheral blood PMNs as compared to contro ls, while numbers of PMNs in the peripheral blood from chicks treated with ILK alone were not significantly increased. PMN adherence and per cent SE killing by PMNs derived from chicks treated with either ILK al one or DEX + ILK were significantly increased compared to controls. Ch emotaxis of PMNs derived from chicks treated with either ILK alone or DEX alone significantly increased 2-fold over control levels. Interest ingly, chemotaxis of PMNs derived from chicks that received DEX + ILK was similar to controls. Generally, ILK abated the anti-inflammatory e ffects of DEX on PMNs in these assays, except for chemotaxis. We inter pret these data to suggest that ILK may confer protection to chicks ag ainst the early phase of SE organ invasion by inducing an inflammatory response predominated by activated PMNs.