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|Title:||Essential Fatty Acid Deficiency: Effects on Prostaglandin Synthesis and Immune Response|
|Author(s):||Boissonneault, Gilbert Andre|
|Department / Program:||Food Science|
|Degree Granting Institution:||University of Illinois at Urbana-Champaign|
|Subject(s):||Health Sciences, Nutrition|
|Abstract:||Essential fatty acid (EFA) deficiency is known to alter prostaglandin (PG) synthesis and immune response in several species. These experiments were designed to investigate PG production and the immune response of EFA-deficient Lewis rats and A/J mice.
Splenic PGF and PGE levels which were stimulated by an i.v. injection of sheep erythrocytes (sRBC) were lower in EFA-deficient rats at several time points post-injection. The primary plaque forming cell (PFC) response was higher in EFA-deficient rats than in EFA-adequate controls. Injecting EFA-adequate rats with indomethacin, an inhibitor of PG synthesis, resulted in increase in the PFC response. This indicated that the alteration of the PFC response of EFA-deficient rats was probably a result of altered PG production. A/J mice fed an EFA-deficient diet also responded to a sRBC injection with an increase in primary PFC. When an i.p. route of antigen administration was used, no difference between diets was seen in the primary PFC response. Splenic PGF production in response to sRBC injection was lower in EFA-deficient A/J mice than in EFA-adequate mice. Both rats and mice responded in the same manner, supporting the contention that these two species respond similarly to an immune challenge. Cellular immunity was also altered in EFA-deficient rats as shown by a decrease in inflammatory swelling in the delayed-type hypersensitivity response. Reactivity of peritoneal macrophages from EFA-deficient rats to migration inhibition factor was increased, resulting in greater inhibition of random migration than that exhibited by EFA-adequate macrophages.
Liver homogenates from EFA-deficient rats produced less PGF upon incubation at 37(DEGREES)C for 15 minutes than EFA-adequate homogenates. No correlation was seen between the ratio of 20:3(omega)9 to 20:4(omega)6 in liver lipids and PGF production by liver homogenates. Exogenous arachidonate (AA) added to homogenates resulted in the negation of differences in PGF levels produced between dietary treatments, indicating that release of 20:3(omega)9 was responsible for decreased PGF production in EFA-deficient homogenates. Addition of quinacrine suppressed the stimulation in PGF synthesis seen with supplemental AA.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1982.
|Date Available in IDEALS:||2015-05-13|
This item appears in the following Collection(s)
Dissertations and Theses - Food Science and Human Nutrition
Graduate Dissertations and Theses at Illinois
Graduate Theses and Dissertations at Illinois