Too much of a good thing: How modulating LTB actions restore host defense in homeostasis or disease.

Brandt SL, Serezani CH
Semin Immunol. 2017 33: 37-43

PMID: 29042027 · PMCID: PMC5679129 · DOI:10.1016/j.smim.2017.08.006

The ability to regulate inflammatory pathways and host defense mechanisms is critical for maintaining homeostasis and responding to infections and tissue injury. While unbalanced inflammation is detrimental to the host; inadequate inflammation might not provide effective signals required to eliminate pathogens. On the other hand, aberrant inflammation could result in organ damage and impair host defense. The lipid mediator leukotriene B (LTB) is a potent neutrophil chemoattractant and recently, its role as a dominant molecule that amplifies many arms of phagocyte antimicrobial effector function has been unveiled. However, excessive LTB production contributes to disease severity in chronic inflammatory diseases such as diabetes and arthritis, which could potentially be involved in poor host defense in these groups of patients. In this review we discuss the cellular and molecular programs elicited during LTB production and actions on innate immunity host defense mechanisms as well as potential therapeutic strategies to improve host defense.

Copyright © 2017 Elsevier Ltd. All rights reserved.

MeSH Terms (10)

Animals Cell Movement Homeostasis Humans Immunity, Innate Immunomodulation Inflammation Leukotriene B4 Neutrophils Phagocytosis

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