Polyunsaturated Fatty Acids in Inflammatory Bowel Diseases

Marion‐Letellier, Rachel; Savoye, Guillaume; Beck, Paul L.; Panaccione, Remo; Ghosh, Subrata

doi:10.1097/mib.0b013e3182810122

Cited by 96 publications

(46 citation statements)

References 130 publications

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“…A potential mechanism to explain the inverse association between fish and CD is through marine ω3 PUFA content in fish 15, 47–50 . Dietary ω3 PUFA may inhibit, through competitive mechanisms, formation of pro-inflammatory leukotrienes and prostaglandins through the arachidonic pathway and also inhibit adaptive immune responses through the peroxisome proliferator-activated receptor pathway 50 .…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Dietary ω3 PUFA may inhibit, through competitive mechanisms, formation of pro-inflammatory leukotrienes and prostaglandins through the arachidonic pathway and also inhibit adaptive immune responses through the peroxisome proliferator-activated receptor pathway 50 . Additionally, ω3 PUFA may inhibit vascular adhesion, migration and angiogenesis 50 . In contrast to a few prior studies suggesting an inverse association between ω3 PUFA intake and risk of UC 12, 15 , in the present study, we did not identify any association between high school fish intake or total PUFA intake and risk of UC.…”

Section: Discussionmentioning

confidence: 99%

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High School Diet and Risk of Crohnʼs Disease and Ulcerative Colitis

Ananthakrishnan

Khalili

Song

et al. 2015

Inflammatory Bowel Diseases

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Introduction Diet may play an important role in the pathogenesis of Crohn’s disease (CD) and ulcerative colitis (UC), yet there are few prospective studies of dietary factors. None have examined the association between adolescent diet and risk of inflammatory bowel diseases (IBD; CD and UC). Methods This study included women enrolled in Nurses’ Health Study II who completed a validated high school dietary questionnaire in 1998. We examined the effect of dietary patterns (prudent or western diet) and individual components of each patterns. We documented incident cases of CD and UC through 2011 based on physician review of medical records and used Cox proportional hazards models adjusting for confounders to estimate hazard ratios (HR) and confidence intervals (CI) for CD and UC. Results Over 763,229 person-years of follow-up, we identified 70 incident cases of CD and 103 cases of UC. Compared to women in the lowest quartile of a prudent diet score (characterized by greater intake of fruits, vegetables, and fish), women in the highest quartile had a 53% lower risk of CD (Hazard ratio (HR) 0.47, 95% confidence interval (CI) 0.23 – 0.98; Ptrend=0.04). Specifically, greater intake of fish (Ptrend=0.01) and fiber (Ptrend=0.06) were associated with lower risk of CD. In contrast, Western diet score was not associated with risk of CD. Neither dietary patterns nor individual food or nutrient groups was associated with UC. Conclusion Adolescent diet is associated with risk of CD, but not UC, offering insights into disease pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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High School Diet and Risk of Crohnʼs Disease and Ulcerative Colitis

Ananthakrishnan

Khalili

Song

et al. 2015

Inflammatory Bowel Diseases

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“…Arachidonic acid (AA), an n-6 PUFA is a precursor to generation of pro-inflammatory eicosanoids such as leukotriene B4 (LTB4), this conversion occurring through a series of enzymatic steps 16, 18 . On the other hand, n-3 polyunsaturated fatty acids like docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have anti-inflammatory effects through generation of resolvins, protectins, and other endogenous factors that down regulate inflammation 16, 18 . Genome-wide association studies (GWAS) have identified that genetic variation can influence plasma and tissue n-3 and n-6 PUFA concentrations and their biological pathways 19-21 .…”

Section: Introductionmentioning

confidence: 99%

Genetic Polymorphisms in Fatty Acid Metabolism Modify the Association Between Dietary n3

Ananthakrishnan

Khalili

Song

et al. 2017

Inflammatory Bowel Diseases

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Introduction High intake of dietary n-3 polyunsaturated fatty acids (PUFA) is associated with a decreased risk of ulcerative colitis (UC) and Crohn's disease (CD). However, results have been heterogeneous suggesting that genetic variations in PUFA metabolism may modify this risk. Methods We conducted a case-control study nested within two prospective cohorts, the Nurses' Health Study (NHS) and NHS II. Among women providing blood (n=62,437) or buccal cells (n=59,543) for genotyping, we confirmed new diagnoses of CD or UC. Dietary intake was assessed 4 years prior to diagnosis. Confirmed cases were matched 1:2 to controls. Subjects were genotyped for SNPs at CYP4F3, FADS1, and FADS2 loci. Conditional logistic regression models examined the interaction between genotype, n3:n6 PUFA intake and risk of CD and UC. Results Our study included 101 CD and 139 UC patients matched to 495 controls. On multivariable analysis, high intake of n3:n6 PUFA (above median) demonstrated a trend towards reduced risk of UC (Odds ratio (OR) 0.71, 95% confidence interval (CI) 0.47 – 1.09, p=0.11). High n3:n6 PUFA intake was associated with a reduced risk of UC in individuals with the GG/AG genotype at a SNP in CYP4F3 (OR 0.57, 95% CI 0.32 – 0.99) but not those with the AA genotype (OR 0.95, 95% CI 0.47 – 1.93) (p-interaction = 0.049). No gene-diet interactions were noted for CD. Conclusion The association between dietary n3:n6 PUFA intake and risk of UC may be modified variants at CYP4F3. Further gene-environment studies of the association between diet and IBD risk are warranted.

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“…Omega-3 polyunsaturated fatty acids such as docosahexanoic acid (DHA) and eicosapentaenoic acid (EPA) are potent anti-inflammatory and immunoregulatory agents in a wide variety of diseases associated with chronic inflammation, including metabolic syndrome [22], neurodegeneration [23], inflammatory bowel diseases [24], cardiovascular disease [25], and cancer [26]. DHA- and EPA-induced anti-inflammatory responses are mediated by their respective bioactive mediators such as resolvins and protectins, which act as inhibitors of leukocyte infiltration and signaling activity of inflammatory cytokines, particularly TNF-α [27,28].…”

Section: Introductionmentioning

confidence: 99%

Docosahexanoic acid antagonizes TNF-α-induced necroptosis by attenuating oxidative stress, ceramide production, lysosomal dysfunction, and autophagic features

et al. 2014

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Objective It was previously reported that docosahexanoic acid (DHA) reduces TNF-α-induced necrosis in L929 cells. However, the mechanisms underlying this reduction have not been investigated. The present study was designed to investigate cellular and biochemical mechanisms underlying the attenuation of TNF-α-induced necroptosis by DHA in L929 cells. Methods L929 cells were pre-treated with DHA prior to exposure to TNF-α, zVAD, or Necrostatin-1 (Nec-1). Cell death and survival were assessed by MTT and caspase activity assays, and microscopic visualization. Reactive oxygen species (ROS) were measured by flow cytometry. C16- and C18-ceramide were measured by mass spectrometry. Lysosomal membrane permeabilization (LMP) was evaluated by fluorescence microscopy and flow cytometry using Acridine Orange. Cathepsin L activation was evaluated by immunoblotting and fluorescence microscopy. Autophagy was assessed by immunoblotting of LC3-II and Beclin. Results Exposure of L929 cells to TNF-α alone for 24 h induced necroptosis, as evidenced by inhibition of cell death by Nec-1, absence of caspase-3 activity and lamin B cleavage, and morphological analysis. DHA attenuated multiple biochemical events associated with TNF-α-induced necroptosis, including ROS generation, ceramide production, lysosomal dysfunction, cathepsin L activation, and autophagic features. DHA also attenuated zVAD-induced necroptosis but did not attenuate the enhanced apoptosis and necrosis induced by combination of TNF-α with Actinomycin D or zVAD, respectively, suggesting that its protective effects might be limited by the strength of the cell death insult induced by TNF-α. Conclusions DHA effectively attenuates TNF-α-induced necroptosis and autophagy, most likely via its ability to inhibit TNF-α-induced sphingolipid metabolism and oxidative stress. These results highlight the role of this Omega-3 fatty acid in antagonizing inflammatory cell death.

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Polyunsaturated Fatty Acids in Inflammatory Bowel Diseases

Cited by 96 publications

References 130 publications

High School Diet and Risk of Crohnʼs Disease and Ulcerative Colitis

High School Diet and Risk of Crohnʼs Disease and Ulcerative Colitis

Genetic Polymorphisms in Fatty Acid Metabolism Modify the Association Between Dietary n3

Docosahexanoic acid antagonizes TNF-α-induced necroptosis by attenuating oxidative stress, ceramide production, lysosomal dysfunction, and autophagic features

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