n-3 polyunsaturated fatty acids prevent disruption of epithelial barrier function induced by proinflammatory cytokines

Li, Qiurong; Zhang, Qiang; Wang, Meng; Zhao, Sumin; Xu, Guowang; Li, Jieshou

doi:10.1016/j.molimm.2007.09.003

Cited by 88 publications

(65 citation statements)

References 36 publications

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“…Dietary modifications that alter TJs have already been described (40), and it is intriguing to speculate that modifications that modulate membrane lipid content could regulate the onset or severity of inflammation via this mechanism. Polyunsaturated fatty acids (n-3 PUFA) enhance intestinal epithelial barrier function (57) and reportedly relocalize occludin and ZO-1 to lipid raft fractions (23). In vivo, n-3 PUFA supplementation has been shown to attenuate inflammation or promote remission in both murine (8,32) and human (55) IBD.…”

Section: Discussionmentioning

confidence: 99%

Lipid rafts are disrupted in mildly inflamed intestinal microenvironments without overt disruption of the epithelial barrier

Bowie

Donatello

Lyes

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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Section: Discussionmentioning

confidence: 99%

Lipid rafts are disrupted in mildly inflamed intestinal microenvironments without overt disruption of the epithelial barrier

Bowie

Donatello

Lyes

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Pigs challenged with endotoxin showed altered intestinal TER eompared with their eontrols, indicating that changes have occurred in intestinal integrity and junction organization (Albin et al, 2007). Furthermore, treatment with the n-3 fatty acids, eicosapentanoic acid and docosahexaenoic acid, has effectively been shown to prevent reduced TER induced by the proinflammatory eytokines, interferon-y, and TNF-a and prevent the redistribution of occludin and ZO-1 (Li et al, 2008). Also, doeosahexaenoic acid treatment of Caco-2 monolayers has been shown to increase paracellular permeability via the intracellular redistribution of the tight junction proteins (Roig-Pérez et al, 2004).…”

Section: Endotoxin Signaling and Transportmentioning

confidence: 99%

GROWTH AND DEVELOPMENT SYMPOSIUM: Endotoxin, inflammation, and intestinal function in livestock1,2

Mani

Weber

Baumgard

et al. 2012

Journal of Animal Science

155

131

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Endotoxin, also referred to as lipopolysaccharide (LPS), can stimulate localized or systemic inflammation via the activation of pattern recognition receptors. Additionally, endotoxin and inflammation can regulate intestinal epithelial function by altering integrity, nutrient transport, and utilization. The gastrointestinal tract is a large reservoir of both gram-positive and gram-negative bacteria, of which the gram-negative bacteria serve as a source of endotoxin. Luminal endotoxin can enter circulation via two routes: 1) nonspecific paracellular transport through epithelial cell tight junctions, and 2) transcellular transport through lipid raft membrane domains involving receptor-mediated endocytosis. Paracellular transport of endotoxin occurs through dissociation of tight junction protein complexes resulting in reduced intestinal barrier integrity, which can be a result of enteric disease, inflammation, or environmental and metabolic stress. Transcellular transport, via specialized membrane regions rich in glycolipids, sphingolipids, cholesterol, and saturated fatty acids, is a result of raft recruitment of endotoxin-related signaling proteins leading to endotoxin signaling and endocytosis. Both transport routes and sensitivity to endotoxin may be altered by diet and environmental and metabolic stresses. Intestinal-derived endotoxin and inflammation result in suppressed appetite, activation of the immune system, and partitioning of energy and nutrients away from growth toward supporting the immune system requirements. In livestock, this leads to the suppression of growth, particularly suppression of lean tissue accretion. In this paper, we summarize the evidence that intestinal transport of endotoxin and the subsequent inflammation leads to decrease in the production performance of agricultural animals and we present an overview of endotoxin detoxification mechanisms in livestock.

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“…91 In contrast, n-3 PUFA prevent this disruption of barrier function. 92 Bacterial compounds are recognized by a variety of receptors, including TLRs and nucleotide-binding oligomerization domain (NOD, a family of intracellular bacterial sensors) and are potent stimuli of innate immune responses. In vitro evidence suggests that types of fatty acids modulate NOD-or TLRmediated inflammation: activation by saturated fatty acids and inhibition by DHA in several cell types (IEC, 93 macrophages, 94 and dendritic cells 95 ).…”

Section: Intestinal Barrier Function and Gut Microbiotamentioning

confidence: 99%

Polyunsaturated Fatty Acids in Inflammatory Bowel Diseases

Marion‐Letellier

Savoye

Beck

et al. 2013

Inflammatory Bowel Diseases

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Recent epidemiological studies highlight the key role of the type of consumed unsaturated fatty acid and the development of ulcerative colitis (UC). We aimed to review the potential mechanisms behind the antiinflammatory effects of unsaturated fatty acids on intestinal inflammation, to discuss their potential limitations, and to propose a new reappraisal of polyunsaturated fatty acids (PUFAs) in the pathophysiology of inflammatory bowel disease (IBD). A literature search using PubMed was carried out to identify relevant studies (basic science, epidemiological studies, or clinical trials) with unsaturated fatty acids and IBD. Only articles published in English were included. IBD patients exhibit an altered lipid metabolism. While in vitro and in vivo studies have demonstrated the antiinflammatory properties of n-3 polyunsaturated fatty acids in experimental models IBD, results of clinical trials have been disappointing. In addition, the impact of fatty acid on innate immunity as an alternative therapeutic approach is explored. This may offer insight into therapeutic avenues for designing n-3 PUFA diet therapy for IBD.

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n-3 polyunsaturated fatty acids prevent disruption of epithelial barrier function induced by proinflammatory cytokines

Cited by 88 publications

References 36 publications

Lipid rafts are disrupted in mildly inflamed intestinal microenvironments without overt disruption of the epithelial barrier

Lipid rafts are disrupted in mildly inflamed intestinal microenvironments without overt disruption of the epithelial barrier

GROWTH AND DEVELOPMENT SYMPOSIUM: Endotoxin, inflammation, and intestinal function in livestock1,2

Polyunsaturated Fatty Acids in Inflammatory Bowel Diseases

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