Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8743722 | Seminars in Immunology | 2017 | 7 Pages |
Abstract
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 B4 (LTB4) 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 LTB4 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 LTB4 production and actions on innate immunity host defense mechanisms as well as potential therapeutic strategies to improve host defense.
Keywords
PRRPI3KPAMPCysLTERKAP1BLTcPLA2cAMPNFκBCyclic adenosine monophosphateArachidonic acidinflammationInnate immunityFlapHost defensenuclear factor kappa Bcytosolic phospholipase A2phosphoinositide 3-kinaseMicrobicidal activityLeukotriene B4LeukotrienelipoxygenaseImmune regulationpathogen associated molecular patterns5-Lipoxygenase-activating proteinactivator protein 1Protein kinase Cextracellular signal-related kinasepattern recognition receptor
Related Topics
Life Sciences
Immunology and Microbiology
Immunology
Authors
Stephanie L. Brandt, C. Henrique Serezani,