Characterization of the pattern of inflammatory cell influx in chicks following the intraperitoneal administration of live Salmonella enteritidis and Salmonella enteritidis-immune lymphokines

We characterized the inflammatory cell influx in day-old chicks induced by the i.p. administration of live Salmonella enteritidis (SE) and lymphokines from concanavalin A-stimulated SE-immune T lymphocytes (ILK). An i.p. injection of ILK along with 5 X 10(3) cfu SE increased the survival rate of chi...

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Veröffentlicht in:Poultry science 1995-01, Vol.74 (1), p.8-17
Hauptverfasser: Kogut, M.H. (USDA, ARS, Food Animal Protection Research Laboratory, College Station, TX), McGruder, E.D, Hargis, B.M, Corrier, D.E, DeLoach, J.R
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container_end_page 17
container_issue 1
container_start_page 8
container_title Poultry science
container_volume 74
creator Kogut, M.H. (USDA, ARS, Food Animal Protection Research Laboratory, College Station, TX)
McGruder, E.D
Hargis, B.M
Corrier, D.E
DeLoach, J.R
description We characterized the inflammatory cell influx in day-old chicks induced by the i.p. administration of live Salmonella enteritidis (SE) and lymphokines from concanavalin A-stimulated SE-immune T lymphocytes (ILK). An i.p. injection of ILK along with 5 X 10(3) cfu SE increased the survival rate of chicks 48 h later from 70% (ILK-treated controls) compared with 25% (saline-treated). The injection of both the ILK and live SE (but not formalinkilled SE) resulted in an increased influx of inflammatory heterophils into the peritoneum that peaked at 4 h after the injections with no increase in peritoneal macrophages. The heterophil accumulation was not influenced by polymyxin B, but was sensitive to heat treatment (100 C for 1 h) of the ILK, suggesting that lipopolysaccharide (LPS) did not contribute to the induced accumulation of heterophils. Treatment of the chicks with nordihydroguaiaretic acid or indomethacin did not abrogate the induced heterophil accumulation, suggesting that arachidonic acid metabolites were not involved in the SE/ILK-induced accumulation of peritoneal heterophils. The results from the current studies indicate that 1) ILK-mediated resistance to SE-induced mortality is mediated by a rapid influx of inflammatory heterophils to the site of infection; 2) live SE, during invasion, are vital for the site-directed migration of the heterophils; and 3) the mechanisms of induced heterophil accumulation are unknown but involve neither LPS nor arachidonic acid metabolites
doi_str_mv 10.3382/ps.0740008
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(USDA, ARS, Food Animal Protection Research Laboratory, College Station, TX) ; McGruder, E.D ; Hargis, B.M ; Corrier, D.E ; DeLoach, J.R</creator><creatorcontrib>Kogut, M.H. (USDA, ARS, Food Animal Protection Research Laboratory, College Station, TX) ; McGruder, E.D ; Hargis, B.M ; Corrier, D.E ; DeLoach, J.R</creatorcontrib><description>We characterized the inflammatory cell influx in day-old chicks induced by the i.p. administration of live Salmonella enteritidis (SE) and lymphokines from concanavalin A-stimulated SE-immune T lymphocytes (ILK). An i.p. injection of ILK along with 5 X 10(3) cfu SE increased the survival rate of chicks 48 h later from 70% (ILK-treated controls) compared with 25% (saline-treated). The injection of both the ILK and live SE (but not formalinkilled SE) resulted in an increased influx of inflammatory heterophils into the peritoneum that peaked at 4 h after the injections with no increase in peritoneal macrophages. The heterophil accumulation was not influenced by polymyxin B, but was sensitive to heat treatment (100 C for 1 h) of the ILK, suggesting that lipopolysaccharide (LPS) did not contribute to the induced accumulation of heterophils. Treatment of the chicks with nordihydroguaiaretic acid or indomethacin did not abrogate the induced heterophil accumulation, suggesting that arachidonic acid metabolites were not involved in the SE/ILK-induced accumulation of peritoneal heterophils. 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(USDA, ARS, Food Animal Protection Research Laboratory, College Station, TX)</creatorcontrib><creatorcontrib>McGruder, E.D</creatorcontrib><creatorcontrib>Hargis, B.M</creatorcontrib><creatorcontrib>Corrier, D.E</creatorcontrib><creatorcontrib>DeLoach, J.R</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Poultry science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kogut, M.H. 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An i.p. injection of ILK along with 5 X 10(3) cfu SE increased the survival rate of chicks 48 h later from 70% (ILK-treated controls) compared with 25% (saline-treated). The injection of both the ILK and live SE (but not formalinkilled SE) resulted in an increased influx of inflammatory heterophils into the peritoneum that peaked at 4 h after the injections with no increase in peritoneal macrophages. The heterophil accumulation was not influenced by polymyxin B, but was sensitive to heat treatment (100 C for 1 h) of the ILK, suggesting that lipopolysaccharide (LPS) did not contribute to the induced accumulation of heterophils. Treatment of the chicks with nordihydroguaiaretic acid or indomethacin did not abrogate the induced heterophil accumulation, suggesting that arachidonic acid metabolites were not involved in the SE/ILK-induced accumulation of peritoneal heterophils. The results from the current studies indicate that 1) ILK-mediated resistance to SE-induced mortality is mediated by a rapid influx of inflammatory heterophils to the site of infection; 2) live SE, during invasion, are vital for the site-directed migration of the heterophils; and 3) the mechanisms of induced heterophil accumulation are unknown but involve neither LPS nor arachidonic acid metabolites</abstract><cop>England</cop><pmid>7899216</pmid><doi>10.3382/ps.0740008</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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subjects ACIDE ARACHIDONIQUE
ACIDO ARAQUIDONICO
Animals
Arachidonic Acid - metabolism
Cell Movement - immunology
Chickens - immunology
Chickens - microbiology
FACTEUR IMMUNOLOGIQUE
FACTORES INMUNOLOGICOS
Female
IMMUNITE CELLULAIRE
INFLAMACION
INFLAMMATION
Inflammation - immunology
Inflammation - veterinary
INMUNIDAD CELULAR
LEUCOCITOS
LEUCOCYTE
LINFOCITOS
LIPOPOLISACARIDOS
LIPOPOLYSACCHARIDE
Lipopolysaccharides - pharmacology
LYMPHOCYTE
Lymphokines - immunology
MACROFAGOS
MACROPHAGE
PERITOINE
Peritoneal Cavity - cytology
PERITONEO
Phagocytes - physiology
POLLITO
Poultry Diseases - immunology
POUSSIN
SALMONELLA ENTERITIDIS
Salmonella enteritidis - immunology
Salmonella Infections, Animal - immunology
title Characterization of the pattern of inflammatory cell influx in chicks following the intraperitoneal administration of live Salmonella enteritidis and Salmonella enteritidis-immune lymphokines
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