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ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #135067
Title: FUNCTIONAL COMPARISON OF HETEROPHILS ISOLATED FROM COMMERCIAL BROILER CHICKENS

Author
item Swaggerty, Christina - Christi
item LOWRY, VIRGINIA - TX A&M UNIVERSITY
item FARNELL, MORGAN - TX A&M UNIVERSITY
item Kogut, Michael - Mike

Submitted to: Research Workers in Animal Diseases Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 11/11/2002
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Heterophils from two pure lines (A and B) of commercial broiler chickens were isolated on days 1, 4, and 7 post hatch to evaluated their ability to: (1) phagocytize Salmonella enteritidis (2) degranulate when exposed to immune-IgG opsonized SE, and (3) produce an oxidative burst. On days 1 and 4, heterophils from line A were functionally more efficient compared to heterophils from line B. By 7 days post hatch, heterophil functions for both lines were comparable. To determine if heterophil functional efficiency is heritable, heterophils from F1 crosses of the immunological efficient (A) and non-efficient (B) lines were evaluated for functional activity (line C = male B x female A; line D = male A x female B) and compared to parent lines. Heterophils from D had a more efficient heterophil function when compared to heterophils from C. Based on these results, heterophil function and efficiency can be genetically transferred to progeny. More specifically, the data suggests heterophil function is sex-associated and genetically controlled by the rooster since progeny of line A males maintained immuno-dominant characteristics whereas heterophils from the progeny of line B roosters remained immunologically inefficient. To our knowledge, this is the first report to describe a functional relationship between pure and F1 crosses of broiler chickens with regard to heterophils and the innate immune response.