Journal ArticleDOI
Lipocalin-2: A Master Mediator of Intestinal and Metabolic Inflammation.
TLDR
While LCN2 in the intestinal tract regulates the composition of the gut microbiota and shows anti-inflammatory activities, it also exhibits proinflammatory activities in other experimental settings.Abstract:
Lipocalin-2 (LCN2), also known as neutrophil gelatinase-associated lipocalin (NGAL), is released by various cell types and is an attractive biomarker of inflammation, ischemia, infection, and kidney damage. Both intestinal and metabolic inflammation, as observed in obesity and related disorders, are associated with increased LCN2 synthesis. While LCN2 in the intestinal tract regulates the composition of the gut microbiota and shows anti-inflammatory activities, it also exhibits proinflammatory activities in other experimental settings. In animal models of metabolic inflammation, type 2 diabetes mellitus (T2DM), or nonalcoholic steatohepatitis (NASH), increased LCN2 expression favors inflammation via the recruitment of inflammatory cells, such as neutrophils, and the induction of proinflammatory cytokines. A better understanding of this crucial marker of innate immunity might pave the way for targeting this pathway in future therapies.read more
Citations
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Journal ArticleDOI
The Intestinal Barrier and Current Techniques for the Assessment of Gut Permeability
Ida Schoultz,Åsa V. Keita +1 more
TL;DR: In vivo, in vitro and ex vivo techniques and how these methods can be utilized for thorough investigation of the intestinal barrier are outlined and discussed.
Journal ArticleDOI
Obesity, Bioactive Lipids, and Adipose Tissue Inflammation in Insulin Resistance
TL;DR: Recent studies indicate that the accumulation of biologically active lipids in adipose tissue may regulate the synthesis/secretion of adipokines and proinflammatory cytokines, which may lead to insulin resistance and type 2 diabetes.
Journal ArticleDOI
The Regulation of Inflammation by Innate and Adaptive Lymphocytes
TL;DR: This work has shown that a memory-conditioned inflammatory response, in conjunction with other secondary effector T cell functions, results in better control and more rapid resolution of both infection and the associated tissue pathology.
Journal ArticleDOI
Adipokines and inflammation: is it a question of weight?
Vera Francisco,Jesús Pino,Miguel A. González-Gay,Antonio Mera,Francisca Lago,Rodolfo Gómez,Ali Mobasheri,Oreste Gualillo +7 more
TL;DR: The most recent findings concerning the involvement of adipokines in inflammation and immune responses, in particular in rheumatic, inflammatory and degenerative diseases are explored.
Journal ArticleDOI
Disruption of maternal gut microbiota during gestation alters offspring microbiota and immunity
Donald D. Nyangahu,Donald D. Nyangahu,Katie Lennard,Bryan P. Brown,Bryan P. Brown,Matthew Darby,Jerome M. Wendoh,Enock Havyarimana,Pete Smith,James Butcher,Alain Stintzi,Nicola Mulder,William G. C. Horsnell,William G. C. Horsnell,William G. C. Horsnell,Heather B. Jaspan,Heather B. Jaspan +16 more
TL;DR: P perturbations to maternal gut microbiota dictate neonatal adaptive immunity, and changes in the microbiota of stomach contents (as a proxy for breastmilk) and pup gut signify an indirect mechanism through which maternal intestinal microbiota influences extra-intestinal and neonatal commensal colonization.
References
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Lipocalin 2 mediates an innate immune response to bacterial infection by sequestrating iron.
Trude Helen Flo,Kelly D. Smith,Kelly D. Smith,Shintaro Sato,David J. Rodriguez,Margaret A. Holmes,Roland K. Strong,Shizuo Akira,Alan Aderem +8 more
TL;DR: This finding represents a new component of the innate immune system and the acute phase response to infection and limits bacterial growth by sequestrating the iron-laden siderophore.
Journal ArticleDOI
A Cell-Surface Receptor for Lipocalin 24p3 Selectively Mediates Apoptosis and Iron Uptake
TL;DR: Cl cloning of the 24p3 cell-surface receptor reveals an unanticipated role for intracellular iron regulation in an apoptotic pathway relevant to BCR-ABL-induced myeloproliferative disease and its treatment.