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Your search keyword '"epi-lipoxins"' showing total 2 results
Start Over Descriptor "epi-lipoxins" Topic inflammation
2 results on '"epi-lipoxins"'

1. Lipoxins: nature's way to resolve inflammation.

Author

Jayashree A., Chandrasekharan, and Sharma-Walia, Neelam

Subjects
INFLAMMATION treatment, LIPOXINS, ANTI-inflammatory agents, PATHOGENIC microorganisms, HOSTS (Biology), HOMEOSTASIS
Abstract

An effective host defense mechanism involves inflammation to eliminate pathogens from the site of infection, followed by the resolution of inflammation and the restoration of tissue homeostasis. Lipoxins are endogenous anti-inflammatory, pro-resolving molecules that play a vital role in reducing excessive tissue injury and chronic inflammation. In this review, the mechanisms of action of lipoxins at the site of inflammation and their interaction with other cellular signaling molecules and transcription factors are discussed. Emphasis has also been placed on immune modulatory role(s) of lipoxins. Lipoxins regulate components of both the innate and adaptive immune systems including neutrophils, macrophages, T-, and B-cells. Lipoxins also modulate levels of various transcription factors such as nuclear factor B, activator protein-1, nerve growth factor-regulated factor 1A binding protein 1, and peroxisome proliferator activated receptor and control the expression of many inflammatory genes. Since lipoxins and aspirin-triggered lipoxins have clinical relevance, we discuss their important role in clinical research to treat a wide range of diseases like inflammatory disorders, renal fibrosis, cerebral ischemia, and cancer. A brief overview of lipoxins in viral malignancies and viral pathogenesis especially the unexplored role of lipoxins in Kaposi's sarcoma-associated herpes virus biology is also presented. [ABSTRACT FROM AUTHOR]

Published
2015
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2. 15-epi-lipoxin A4–mediated Induction of Nitric Oxide Explains How Aspirin Inhibits Acute Inflammation

Author

Dianne Cooper, Niloufar Moradi-Bidhendi, Mark J. Paul-Clark, Derek W. Gilroy, and Thong van Cao

Subjects
Male, NF-KAPPA-B, nonsteroidal antiinflammatory drugs, Nitric Oxide Synthase Type II, CARRAGEENAN-INDUCED PLEURISY, Pharmacology, Research & Experimental Medicine, DEFICIENT MICE, chemistry.chemical_compound, Mice, Enos, Mechanism of action of aspirin, Leukocytes, Immunology and Allergy, ENDOTHELIAL CELL-ADHESION, Mice, Knockout, Aspirin, biology, LIPOXIN A(4), Anti-Inflammatory Agents, Non-Steroidal, Nitric Oxide Synthase Type III, 11 Medical And Health Sciences, Nitric oxide synthase, Lipoxins, STABLE ANALOGS, Medicine, Research & Experimental, medicine.symptom, Life Sciences & Biomedicine, Intravital microscopy, medicine.drug, Immunology, LEUKOCYTE ADHESION, Inflammation, Peritonitis, Nitric Oxide, Article, Nitric oxide, NO-RELEASING ASPIRIN, medicine, Animals, Endothelium, Rats, Wistar, Nitrites, leukocyte trafficking, Science & Technology, Dose-Response Relationship, Drug, business.industry, Microcirculation, resolution, biology.organism_classification, Rats, Mice, Inbred C57BL, chemistry, epi-lipoxins, biology.protein, microvascular endothelium, Nitric Oxide Synthase, business, PROSTAGLANDIN-H SYNTHASE, Interleukin-1
Abstract

The established model for the mechanism of action of aspirin is the inhibition of prostaglandin synthesis. However, this has never fully explained aspirin's repertoire of antiinflammatory properties. We found in acute pleuritis that aspirin, but not salicylate, indomethacin, or piroxicam, increased plasma nitric oxide (NO), which correlated with a reduction in inflammation. Inhibiting aspirin-elicited NO pharmacologically in this model nullified the antiinflammatory effects of aspirin. Moreover, aspirin was not antiinflammatory in either constitutive (eNOS) or inducible NO synthase (iNOS) knockout mice with IL-1β–induced peritonitis. It transpires that aspirin generates NO through its unique ability to trigger the synthesis of 15-epi-lipoxin A4. Aspirin and 15-epi-lipoxin A4 were shown to inhibit leukocyte trafficking in an NO-dependent manner using intravital microscopy on IL-1β–stimulated mouse mesentery. Not only did aspirin inhibit leukocyte–endothelial interaction in a manner similar to NO in wild-type mice but both aspirin and 15-epi-lipoxin A4 had markedly reduced effects on leukocyte–endothelial cell adherence in eNOS- and iNOS-deficient mice compared with wild type. Collectively, these data suggest that aspirin triggers the synthesis of 15-epi-lipoxin A4, which increases NO synthesis through eNOS and iNOS. This aspirin-elicited NO exerts antiinflammatory effects in the microcirculation by inhibiting leukocyte–endothelium interactions.

Published
2004

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