DYNAMICS OF AVIAN INFLAMMATORY RESPONSE TO SALMONELLA-IMMUNE LYMPHOKINES - CHANGES IN AVIAN BLOOD LEUKOCYTE POPULATIONS

Citation
Mh. Kogut et al., DYNAMICS OF AVIAN INFLAMMATORY RESPONSE TO SALMONELLA-IMMUNE LYMPHOKINES - CHANGES IN AVIAN BLOOD LEUKOCYTE POPULATIONS, Inflammation, 18(4), 1994, pp. 373-388
Citations number
58
Categorie Soggetti
Cytology & Histology
Journal title
ISSN journal
03603997
Volume
18
Issue
4
Year of publication
1994
Pages
373 - 388
Database
ISI
SICI code
0360-3997(1994)18:4<373:DOAIRT>2.0.ZU;2-E
Abstract
Investigations in our laboratories have indicated that an increased re sistance to SE organ infectivity in chicks was conferred by the immuno prophylactic administration of SE-immune lymphokines (SE-ILK). This re sistance was associated with an increase in the lamina propria thickne ss due to a marked infiltration of inflammatory polymorphonuclear cell s (PMNs). In the present study, we determined whether the hematologica l profile of SE-ILK-treated chicks might reflect changes that are asso ciated with the protection against organ invasion by SE, As protection has been observed in previous studies within 24 h of SE-ILK administr ation, we evaluated alterations in the circulating leukocyte profile i n 1-day-old Leghorn chicks during this time period. We also determined whether the alterations in the peripheral blood leukocytes correlated with the increased protection against SE organ invasion induced by th e SE-ILK. Within 4 h after an intraperitoneal injection of SE-ILK and challenge with SE, the number of circulating leukocytes increased sign ificantly (P < 0.05) from all of the other treatment groups. The numbe r of circulating PMNs was found to account for more than 80% of the in crease in the number of circulating leukocytes. Using correlation anal ysis, we found a strong association between the number of circulating PMNs and the protection induced by SE-ILK against SE organ invasion. T hese studies associate the expansion of the available pool of circulat ing PMNs and the expression of innate resistance to organ invasion by SE.