The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis.

The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis. Research Abstract Details 

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The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis. Abstract Text:

Yankun Li,Ira Tabas,

Two features of advanced atherosclerotic lesions are large numbers of macrophages and a heightened state of inflammation. Some of the macrophages appear to be enriched with free cholesterol (FCMphis), and we have shown that this process induces the synthesis and secretion of inflammatory cytokines, including TNF-alpha and IL-6. However, lesions contain many other macrophages that are not FC-enriched (non-FCMphis). Therefore, we sought to understand how the interaction of these two populations of macrophages would influence the inflammatory response. We show here that non-FCMphis possess a robust ability to deplete TNF-alpha and IL-6 secreted by FCMphis. The mechanism involves enhanced pinocytic uptake and lysosomal degradation of the FCMphi-secreted cytokines by the non-FCMphis. The FCMphis contribute directly to this process by secreting pinocytosis-stimulatory factors that act on non-FCMphis but not on the FCMphis themselves. One of these pinocytosis-stimulatory factors is M-CSF, which is induced by a process involving cholesterol trafficking to the endoplasmic reticulum and signaling through PI-3K and ERK MAPK pathways. However, one or more other FCMphi-secreted factors are also required for stimulating pinocytosis in non-FCMphis. Thus, FCMphis secrete inflammatory cytokines as well as factors that promote the eventual pinocytosis and degradation of these cytokines by neighboring macrophages. This process may normally serve to prevent prolonged or disseminated effects of inflammatory cytokines during inflammation. Moreover, possible perturbation of stimulated pinocytosis during the progression of advanced atherosclerosis may contribute to the heightened inflammatory state of these lesions.

The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis. Publishing Authors By Initials

Y Li,I Tabas,

For similar peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research

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The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of leukocyte biology

VOLUME: 81

Page Numbers: 483-91

Journal Abbreviation: J. Leukoc. Biol.

ISSN: 0741-5400

DAY: 24

MONTH: 10

YEAR: 2006

The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8405628

The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis. Keywords Mesh Terms:

KEYWORDS: Tumor Necrosis Factor-alpha

MESH TERMS: secretion

Chemical & Substance for Abstract: The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis. Information

Substance Name: Macrophage Colony-Stimulating Factor

Registry Number: 81627-83-0

Grant and Affiliation Information for The inflammatory cytokine response of cholesterol-enriched macrophages is dampened by stimulated pinocytosis.

AFFILIATION: Department of Medicine, Columbia University, New York, NY 10032, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL75662

ACRONYM: HL

MEDLINETA: J Leukoc Biol

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