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Enhancement of chicken lymphocyte activation and lymphokine release by avian influenza virus

Identifieur interne : 000409 ( Istex/Curation ); précédent : 000408; suivant : 000410

Enhancement of chicken lymphocyte activation and lymphokine release by avian influenza virus

Auteurs : Peter S. Holt [Grèce]

Source :

RBID : ISTEX:FD92777172466EF77F45437717BE0821675CCAE4

English descriptors

Abstract

Abstract: We had previously found that inactivated avian influenza virus (AIV) could enhance the response of chicken lymphocytes to mitogen or antigen activation. An investigation into the possible mechanisms of this enhancement was undertaken. Peripheral blood lymphocytes (PBL) were incubated with AIV expressing different hemagglutinin (HA) types (H1–H13) along with doses of concanavalin A (Con A) which induce maximum (0.5 μg) or submaximum (0.125 μg) PBL activation. The lymphocyte activation was measured 72 h later. All of the HA types except H13 enhanced the Con A response. Diminished but significant enhancement could be observed when AIV administration was delayed by as much as 48 h of the 72-h incubation time. The AIV A/ck/Ala/75 (H4N8) was also examined for its effect on interleukin 2 (IL 2) synthesis by Con A-activated PBL and was found to modestly increase the synthesis of this lymphokine. All of the AIV hemagglutinin types agglutinated the PBL with titers slightly lower than that observed for the chicken erythrocyte agglutination. These results indicate that the AIV-induced enhancement of Con A responsiveness by chicken PBL is due, at least partly, to increased synthesis of IL 2 and that the effect may be due to some viral component other than the agglutinin.

Url:
DOI: 10.1016/0145-305X(90)90037-F

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ISTEX:FD92777172466EF77F45437717BE0821675CCAE4

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<term>Activation</term>
<term>Allantoic fluids</term>
<term>Assay</term>
<term>Avian</term>
<term>Avian influenza</term>
<term>Avian influenza virus</term>
<term>Blood cells</term>
<term>Chicken erythrocytes</term>
<term>Chicken lymphocyte activation</term>
<term>Chicken lymphocytes</term>
<term>Enhancement</term>
<term>Hazleton research products</term>
<term>Holt</term>
<term>Immune system</term>
<term>Incubation time</term>
<term>Indicator cells</term>
<term>Influenza</term>
<term>Influenza virus</term>
<term>Influenza viruses</term>
<term>Interleukin</term>
<term>Lymphocyte</term>
<term>Lymphocyte agglutination</term>
<term>Pelleted cells</term>
<term>Possible mechanisms</term>
<term>Poultry research laboratory</term>
<term>Proliferative response</term>
<term>Room temperature</term>
<term>Same superscript letter</term>
<term>Serial dilutions</term>
<term>Similar effects</term>
<term>Stimulatory effect</term>
<term>Supernatant cells</term>
<term>Various doses</term>
<term>Viral</term>
<term>Viral component</term>
<term>Virus</term>
<term>World health organ</term>
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<div type="abstract" xml:lang="en">Abstract: We had previously found that inactivated avian influenza virus (AIV) could enhance the response of chicken lymphocytes to mitogen or antigen activation. An investigation into the possible mechanisms of this enhancement was undertaken. Peripheral blood lymphocytes (PBL) were incubated with AIV expressing different hemagglutinin (HA) types (H1–H13) along with doses of concanavalin A (Con A) which induce maximum (0.5 μg) or submaximum (0.125 μg) PBL activation. The lymphocyte activation was measured 72 h later. All of the HA types except H13 enhanced the Con A response. Diminished but significant enhancement could be observed when AIV administration was delayed by as much as 48 h of the 72-h incubation time. The AIV A/ck/Ala/75 (H4N8) was also examined for its effect on interleukin 2 (IL 2) synthesis by Con A-activated PBL and was found to modestly increase the synthesis of this lymphokine. All of the AIV hemagglutinin types agglutinated the PBL with titers slightly lower than that observed for the chicken erythrocyte agglutination. These results indicate that the AIV-induced enhancement of Con A responsiveness by chicken PBL is due, at least partly, to increased synthesis of IL 2 and that the effect may be due to some viral component other than the agglutinin.</div>
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