1997Allergology InternationalOpen access

Cytoplasmic lipid bodies in eosinophils: Central roles in eicosanoid generation

Peter F. Weller, Patrı́cia T. Bozza, Wengui Yu, Ann M. Dvořàk

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Abstract

Lipid bodies are non-membrane bound, lipid-rich cytoplasmic inclusions that form in diverse cell types. Characteristically, lipid body numbers increase when eosinophils and other leukocytes are participating in inflammatory processes. Moreover, lipid bodies are numerous in other sites active in eicosanoid formation, such as the amnion epithelium at parturition. Our interests in lipid bodies relate to the roles that these structures play in arachidonate metabolism by eosinophils and other leukocytes involved in inflammation. Findings indicate that lipid bodies in these leukocytes can function as intracellular domains that are both depots of esterified arachidonate and sites at which regulated enzymatic events relevant to arachidonate metabolism can occur. Lipid bodies are discrete intracellular structures whose formation is specifically inducible early, whose increased numbers correlate with the 'priming' responses of leukocytes to form enhanced amounts of both cyclooxygenase- and lipoxygenase-derived eicosanoids and whose inhibition of formation correlates with reduced synthesis of these eicosanoids. Inhibition of lipid body formation represents a novel pharmacologic target to block the formation of eicosanoid mediators of inflammation.

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Lipid bodies are non-membrane bound, lipid-rich cytoplasmic inclusions that form in diverse cell types. Characteristically, lipid body numbers increase when eosinophils and other leukocytes are participating in inflammatory processes. Moreover, lipid bodies are numerous in other sites active in eicosanoid formation, such as the amnion epithelium at parturition. Our interests in lipid bodies relate to the roles that these structures play in arachidonate metabolism by eosinophils and other leukocytes involved in inflammation. Findings indicate that lipid bodies in these leukocytes can function as intracellular domains that are both depots of esterified arachidonate and sites at which regulated enzymatic events relevant to arachidonate metabolism can occur. Lipid bodies are discrete intracellular structures whose formation is specifically inducible early, whose increased numbers correlate with the 'priming' responses of leukocytes to form enhanced amounts of both cyclooxygenase- and lipoxygenase-derived eicosanoids and whose inhibition of formation correlates with reduced synthesis of these eicosanoids. Inhibition of lipid body formation represents a novel pharmacologic target to block the formation of eicosanoid mediators of inflammation.

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Available abstract

Lipid bodies are non-membrane bound, lipid-rich cytoplasmic inclusions that form in diverse cell types. Characteristically, lipid body numbers increase when eosinophils and other leukocytes are participating in inflammatory processes. Moreover, lipid bodies are numerous in other sites active in eicosanoid formation, such as the amnion epithelium at parturition. Our interests in lipid bodies relate to the roles that these structures play in arachidonate metabolism by eosinophils and other leukocytes involved in inflammation. Findings indicate that lipid bodies in these leukocytes can function as intracellular domains that are both depots of esterified arachidonate and sites at which regulated enzymatic events relevant to arachidonate metabolism can occur. Lipid bodies are discrete intracellular structures whose formation is specifically inducible early, whose increased numbers correlate with the 'priming' responses of leukocytes to form enhanced amounts of both cyclooxygenase- and lipoxygenase-derived eicosanoids and whose inhibition of formation correlates with reduced synthesis of these eicosanoids. Inhibition of lipid body formation represents a novel pharmacologic target to block the formation of eicosanoid mediators of inflammation.

Key concepts: Lipid droplet, Eicosanoid, Eicosanoid metabolism, Lipid metabolism, Lipid signaling, Cytoplasm, Intracellular, Inflammation

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