title: Lymphokine-augmented activation of avian heterophils.
abstract: Heterophils are important mediators of innate resistance in poultry, especially in young birds that have not yet developed an acquired immune response. Invasion of the intestinal mucosa by Salmonella spp. initiates the recruitment of large numbers of heterophils to the lamina propria. Thus, the heterophilic response can control, but not eliminate, bacterial numbers in the bird until development of acquired immunity. Unfortunately, chicks and turkey poults are highly susceptible to Salmonella infections during the first 4 d posthatch due to the functional immaturity of both the innate and acquired immune systems. We have previously shown that the administration of Salmonella enteritidis (SE)-immune lymphokines (ILK) into either 18-d-old developing embryos or day-of-hatch chicks and poults conferred increased resistance to SE organ invasion. In this review, we present evidence that the protection induced by ILK is mediated by vigorous recruitment and activation of heterophils. These activated heterophils migrate rapidly to the site of bacterial invasion where they phagocytize and kill the SE. Specifically, in vitro studies demonstrate an enhancement of functional activities of the heterophils including chemotaxis, adherence, phagocytosis, and bacterial killing. In addition, during the activation process, membrane expression of adhesion molecules rapidly changes from L-selectins to beta2 integrins (CB11b/CD18) on the cells that become activated. These results further demonstrate the validity of preventive activation in poultry to induce the migration of large numbers of activated phagocytic cells to the site of infection by a pathogenic organism. Importantly, this immunopotentiation of the inflammatory response by ILK, as described here, induces the functional maturation of heterophils during the first 4 d posthatch.
authors.affiliation: USDA-ARS, Food Animal Protection Research Laboratory, College Station, Texas 77845, USA. KOGUT@USDA.TAMU.EDU
authors.forename: M H
authors.initials: MH
authors.lastname: Kogut
authors.forename: V K
authors.initials: VK
authors.lastname: Lowry
authors.forename: R B
authors.initials: RB
authors.lastname: Moyes
authors.forename: L L
authors.initials: LL
authors.lastname: Bowden
authors.forename: R
authors.initials: R
authors.lastname: Bowden
authors.forename: K
authors.initials: K
authors.lastname: Genovese
authors.forename: J R
authors.initials: JR
authors.lastname: Deloach
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D015815:Cell Adhesion Molecules / Q000032:analysis; D007113:Immunity, Innate; D008222:Lymphokines / Q000494:pharmacology*; D018375:Neutrophil Activation; D009504:Neutrophils / Q000166:cytology / Q000502:physiology*; D011200:Poultry / Q000276:immunology*; D018123:Receptors, Interleukin / Q000032:analysis; D023062:Receptors, Interleukin-8A
chemical_list: D015703:Antigens, CD; D015815:Cell Adhesion Molecules; D008222:Lymphokines; D018123:Receptors, Interleukin; D023062:Receptors, Interleukin-8A