Lipopolysaccharide-induced leukocyte lipid body formation in vivo: innate immunity elicited intracellular Loci involved in XXXX metabolism.

@entity1 @entity25084 @entity558 @entity295 @entity8285 @entity1996 @entity19 @entity9610 @entity1421 @entity12213 @entity5751 @entity3804 @entity1990 @entity637
Lipid bodies are rapidly inducible, specialized cytoplasmic domains for @entity9610 -forming enzyme localization, which we hypothesize to have specific roles in enhanced inflammatory mediator production during pathological conditions, including @entity295 . However, little is known about the origins, composition, or functions of lipid bodies in vivo. We show that lipid body numbers were increased in leukocytes from septic @entity1 in comparison with healthy subjects. Analogously, the intrathoracic administration of @entity558 into @entity19 induced a dose- and time-dependent increase in lipid body numbers. Pretreatment with anti- @entity5751 or anti- @entity3804 / @entity12213 mAb drastically inhibited @entity558 -induced lipid body formation. Moreover, @entity558 failed to form lipid bodies in C3H/HeJ ( @entity1990 mutated) @entity19 , demonstrating a requisite role for @entity558 receptors in lipid body formation. @entity558 -induced lipid body formation was also inhibited by the platelet-activating factor-receptor antagonists, suggesting a role for endogenous platelet-activating factor. The @entity9610 -forming enzymes, @entity25084 and @entity1996 , were immunolocalized within experimentally induced ( @entity558 in @entity19 ) or naturally occurring (septic @entity1 ) lipid bodies. The proinflammatory cytokine involved in the pathogenesis of @entity295 , @entity637 , was also shown to colocalize within lipid bodies. Prior stimulation of leukocytes to form lipid bodies enhanced the capacity of leukocytes to produce @entity8285 and @entity1421 . In conclusion, our studies indicate that lipid bodies formed after @entity558 stimulation and @entity295 are sites for @entity9610 -forming enzymes and cytokine localization and may develop and function as structurally distinct, intracellular sites for paracrine @entity9610 synthesis during inflammatory conditions.
