NDLI: Increased saturated fatty acids in obesity alter resolution of inflammation in part by stimulating prostaglandin production.

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Overexpression of CREM in T cells aggravates lipopolysaccharide-induced acute lung injury.

Increased saturated fatty acids in obesity alter resolution of inflammation in part by stimulating prostaglandin production.

Antiviral vaccines license T cell responses by suppressing granzyme B levels in human plasmacytoid dendritic cells.

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Intra-amniotic IL-1ß induces fetal inflammation in rhesus monkeys and alters the regulatory T cell/IL-17 balance.

Macrophage scavenger receptor 1 (Msr1, SR-A) influences B cell autoimmunity by regulating soluble autoantigen concentration.

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The role of JAK-3 in regulating TLR-mediated inflammatory cytokine production in innate immune cells.

Macrophage migration inhibitory factor potentiates autoimmune-mediated neuroinflammation.

Myeloid-derived suppressor cells play crucial roles in the regulation of mouse collagen-induced arthritis.

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Depletion of alveolar macrophages during influenza infection facilitates bacterial superinfections.

Role of IRF4 in IFN-stimulated gene induction and maintenance of Kaposi sarcoma-associated herpesvirus latency in primary effusion lymphoma cells.

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Ficolin-1-PTX3 complex formation promotes clearance of altered self-cells and modulates IL-8 production.

The archaic roles of the amphioxus NF-κB/IκB complex in innate immune responses.

Histamine h2 receptor signaling in the pathogenesis of sepsis: studies in a murine diabetes model.

Cutting edge: the NLRP3 inflammasome links complement-mediated inflammation and IL-1ß release.

Y14 positively regulates TNF- -induced NF-κB transcriptional activity via interacting RIP1 and TRADD beyond an exon junction complex protein.

Regulation of adaptive immunity by the fractalkine receptor during autoimmune inflammation.

Synovial fibroblasts directly induce Th17 pathogenicity via the cyclooxygenase/prostaglandin E2 pathway, independent of IL-23.

Active caspase-3 is stored within secretory compartments of viable mast cells.

Deficiency of phospholipase A2 receptor exacerbates ovalbumin-induced lung inflammation.

Comparison of induced versus natural regulatory T cells of the same TCR specificity for induction of tolerance to an environmental antigen.

A diametric role for OX40 in the response of effector/memory CD4+ T cells and regulatory T cells to alloantigen.

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IL-16 induces intestinal inflammation via PepT1 upregulation in a pufferfish model: new insights into the molecular mechanism of inflammatory bowel disease.

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The encephalitogenic, human myelin oligodendrocyte glycoprotein-induced antibody repertoire is directed toward multiple epitopes in C57BL/6-immunized mice.

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A protective Hsp70-TLR4 pathway in lethal oxidant lung injury.

Dendritic cells regulate high-speed interstitial T cell migration in the lymph node via LFA-1/ICAM-1.

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Adipocytes modulate the phenotype of human macrophages through secreted lipids.

Censoring of self-reactive B cells by follicular dendritic cell-displayed self-antigen.

Common tolerance mechanisms, but distinct cross-reactivities associated with gp41 and lipids, limit production of HIV-1 broad neutralizing antibodies 2F5 and 4E10.

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Butyrophilin 3A1 plays an essential role in prenyl pyrophosphate stimulation of human VÎ³2VÎ´2 T cells.

Tolerance is different in T and B cells.

Antibody polyreactivity in health and disease: statu variabilis.

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Increased saturated fatty acids in obesity alter resolution of inflammation in part by stimulating prostaglandin production.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhang, Michael J. Tang, Yunan Rane, Madhavi Bhatnagar, Aruni Hellmann, Jason Spite, Matthew
Description	Country affiliation: United States Author Affiliation: Hellmann J ( Diabetes and Obesity Center, University of Louisville School of Medicine, Louisville, KY 40202, USA.)
Abstract	Extensive evidence indicates that nutrient excess associated with obesity and type 2 diabetes activates innate immune responses that lead to chronic, sterile low-grade inflammation, and obese and diabetic humans also have deficits in wound healing and increased susceptibility to infections. Nevertheless, the mechanisms that sustain unresolved inflammation during obesity remain unclear. In this study, we report that saturated free fatty acids that are elevated in obesity alter resolution of acute sterile inflammation by promoting neutrophil survival and decreasing macrophage phagocytosis. Using a targeted mass spectrometry-based lipidomics approach, we found that in db/db mice, PGE2/D2 levels were elevated in inflammatory exudates during the development of acute peritonitis. Moreover, in isolated macrophages, palmitic acid stimulated cyclooxygenase-2 induction and prostanoid production. Defects in macrophage phagocytosis induced by palmitic acid were mimicked by PGE2 and PGD2 and were reversed by cyclooxygenase inhibition or prostanoid receptor antagonism. Macrophages isolated from obese-diabetic mice expressed prostanoid receptors, EP2 and DP1, and contained significantly higher levels of downstream effector, cAMP, compared with wild-type mice. Therapeutic administration of EP2/DP1 dual receptor antagonist, AH6809, decreased neutrophil accumulation in the peritoneum of db/db mice, as well as the accumulation of apoptotic cells in the thymus. Taken together, these studies provide new insights into the mechanisms underlying altered innate immune responses in obesity and suggest that targeting specific prostanoid receptors may represent a novel strategy for resolving inflammation and restoring phagocyte defects in obese and diabetic individuals.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1203369
Journal	The Journal of Immunology
Issue Number	3
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Dinoprostone Metabolism Fatty Acids Neutrophils Immunology Prostaglandin D2 Animals Apoptosis Drug Effects Cyclooxygenase 2 Biosynthesis Cyclooxygenase 2 Inhibitors Pharmacology Inflammation Macrophages Mice Mice, Inbred C57bl Mice, Transgenic Obesity Palmitic Acid Peritonitis Phagocytosis Receptors, Prostaglandin Antagonists & Inhibitors Receptors, Prostaglandin E, Ep2 Subtype Xanthones Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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