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The Effects of Fatty Acids on Inflammation

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Lipids".

Deadline for manuscript submissions: closed (1 December 2023) | Viewed by 8950

Special Issue Editor

School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW 2308, Australia
Interests: diet; fat; fiber; obesity; asthma; lung disease; exercise; inflammation; hormones

Special Issue Information

Dear Colleagues,

Inflammation is a normal process that is part of host defence and tissue healing. However, unresolved or excessive inflammation can contribute to the development or progression of many chronic diseases, including asthma, inflammatory bowel disease, cardiovascular disease and type 2 diabetes. Dietary fatty acids modulate inflammatory responses, with the direction of the effect being dependent on the type of fatty acid being examined. For example, saturated fatty acids promote inflammation, via the NLRP3 (nucleotide oligomerization domain-like receptor protein 3) inflammasome. Conversely, omega-3 polyunsaturated fatty acids exert anti-inflammatory effects through a variety of mechanisms, including decreased production of eicosanoids and reduced expression of NF-κB. However, the efficacy of fish oil supplementation in reducing inflammation in specific chronic diseases, such as asthma and inflammatory bowel disease, is unclear. Omega-6-derived lipid mediators appear to enhance inflammation, but this is dependent on the ratio of omega-6/omega-3. Further research is needed to clarify the roles of fatty acids in modulating inflammation, including the impact this has on chronic disease risk and outcomes.

In this Special Issue, we welcome state-of-the-art research, including original and review contributions, examining the impact of fatty acids on inflammation. Contributions examining the impact of fatty acids on chronic disease are also encouraged.

Dr. Hayley A. Scott
Guest Editor

Manuscript Submission Information

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Keywords

  • fatty acids
  • dietary fat
  • inflammation
  • saturated fatty acids
  • omega-3 PUFA
  • omega-6 PUFA
  • inflammatory disease
  • cytokine
  • MUFA
  • arachidonic acid

Published Papers (3 papers)

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Research

19 pages, 3962 KiB  
Article
Probiotic Limosilactobacillus reuteri DSM 17938 Changes Foxp3 Deficiency-Induced Dyslipidemia and Chronic Hepatitis in Mice
Nutrients 2024, 16(4), 511; https://doi.org/10.3390/nu16040511 - 12 Feb 2024
Viewed by 692
Abstract
The probiotic Limosilactobacillus reuteri DSM 17938 produces anti-inflammatory effects in scurfy (SF) mice, a model characterized by immune dysregulation, polyendocrinopathy, enteropathy, and X-linked inheritance (called IPEX syndrome in humans), caused by regulatory T cell (Treg) deficiency and is due to a Foxp3 gene [...] Read more.
The probiotic Limosilactobacillus reuteri DSM 17938 produces anti-inflammatory effects in scurfy (SF) mice, a model characterized by immune dysregulation, polyendocrinopathy, enteropathy, and X-linked inheritance (called IPEX syndrome in humans), caused by regulatory T cell (Treg) deficiency and is due to a Foxp3 gene mutation. Considering the pivotal role of lipids in autoimmune inflammatory processes, we investigated alterations in the relative abundance of lipid profiles in SF mice (± treatment with DSM 17938) compared to normal WT mice. We also examined the correlation between plasma lipids and gut microbiota and circulating inflammatory markers. We noted a significant upregulation of plasma lipids associated with autoimmune disease in SF mice, many of which were downregulated by DSM 17938. The upregulated lipids in SF mice demonstrated a significant correlation with gut bacteria known to be implicated in the pathogenesis of various autoimmune diseases. Chronic hepatitis in SF livers responded to DSM 17938 treatment with a reduction in hepatic inflammation. Altered gene expression associated with lipid metabolism and the positive correlation between lipids and inflammatory cytokines together suggest that autoimmunity leads to dyslipidemia with impaired fatty acid oxidation in SF mice. Probiotics are presumed to contribute to the reduction of lipids by reducing inflammatory pathways. Full article
(This article belongs to the Special Issue The Effects of Fatty Acids on Inflammation)
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11 pages, 735 KiB  
Article
Red Blood Cell Membrane Fatty Acid Composition, Dietary Fatty Acid Intake and Diet Quality as Predictors of Inflammation in a Group of Australian Adults
Nutrients 2023, 15(10), 2405; https://doi.org/10.3390/nu15102405 - 21 May 2023
Cited by 1 | Viewed by 2105
Abstract
Evidence suggests that diet can play a role in modulating systemic inflammation. This study aims to examine the relationship between fatty acids (FAs) (self-reported dietary intake and red blood cell (RBC) membrane fatty acid concentrations), three diet quality scores, and the plasma concentrations [...] Read more.
Evidence suggests that diet can play a role in modulating systemic inflammation. This study aims to examine the relationship between fatty acids (FAs) (self-reported dietary intake and red blood cell (RBC) membrane fatty acid concentrations), three diet quality scores, and the plasma concentrations of inflammatory markers (interleukin-6, IL-6; tumour necrosis factor alpha, TNF-α; and C-reactive protein, CRP) in a group of Australian adults (n = 92). Data were collected on their demographic characteristics, health status, supplement intake, dietary intake, RBC-FAs and plasma inflammatory markers over a nine-month period. Mixed-effects models were used to determine the relationship between RBC-FAs, dietary intake of FAs, diet quality scores and inflammatory markers to determine which variable most strongly predicted systemic inflammation. A significant association was identified between dietary saturated fat intake and TNF-α (β = 0.01, p < 0.05). An association was also identified between RBC membrane saturated fatty acids (SFA) and CRP (β = 0.55, p < 0.05). Inverse associations were identified between RBC membrane monounsaturated fatty acids (MUFAs) (β = −0.88, p < 0.01), dietary polyunsaturated fatty acids (PUFAs) (β = −0.21, p < 0.05) and CRP, and the Australian Eating Survey Modified Mediterranean Diet (AES-MED) score and IL-6 (β = −0.21, p < 0.05). In summary, using both objective and subjective measures of fat intake and diet quality, our study has confirmed a positive association between saturated fat and inflammation, while inverse associations were observed between MUFAs, PUFAs, the Mediterranean diet, and inflammation. Our results provide further evidence that manipulating diet quality, in particular fatty acid intake, may be useful for reducing chronic systemic inflammation. Full article
(This article belongs to the Special Issue The Effects of Fatty Acids on Inflammation)
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17 pages, 3512 KiB  
Article
Zinc Laurate Protects against Intestinal Barrier Dysfunction and Inflammation Induced by ETEC in a Mice Model
Nutrients 2023, 15(1), 54; https://doi.org/10.3390/nu15010054 - 22 Dec 2022
Cited by 2 | Viewed by 2001
Abstract
Enterotoxigenic Escherichia coli (ETEC) infection is one of the most common bacterial causes of diarrhea in children and young farm animals. Medium-chain fatty acids (MCFAs) have been widely used for their antibacterial and immune functions. However, there is limited information regarding the role [...] Read more.
Enterotoxigenic Escherichia coli (ETEC) infection is one of the most common bacterial causes of diarrhea in children and young farm animals. Medium-chain fatty acids (MCFAs) have been widely used for their antibacterial and immune functions. However, there is limited information regarding the role of MCFAs chelated with Zn in diarrhea induced by ETEC infection. Here, zinc laurate (ZnLa) was used to evaluate its protective effect in a mice diarrhea model induced by ETEC. A total of 45 ICR-weaned female mice were randomly assigned to marginal zinc deficiency (dZn), dZn, and ETEC infection groups (dZn+ETEC); ETEC infection was co-treated with a low, middle, or high dose of ZnLa (ZnLa LOW+ETEC, ZnLa MID+ETEC, and ZnLa HIGH+ETEC), respectively, to explore the effect and its mechanism of ZnLa on diarrhea and intestinal health of mice challenged with ETEC. To further compare the antibacterial efficiency of ZnLa and ZnSO4 in mice with ETEC infection, a total of 36 ICR-weaned female mice were randomly divided into ZnLa, ZnLa+ETEC, ZnSO4, and ZnSO4 and ETEC infection groups (ZnSO4+ETEC); moreover, the growth curve of ETEC also compared ZnLa and ZnSO4 in vitro. Mice pretreated with ZnLa were effectively guarded against body weight losses and increases in diarrhea scores induced by ETEC. ZnLa pretreatment also prevented intestinal barrier damage and ion transport in mice challenged with ETEC, as evidenced by the fact that the intestinal villus height and the ratio of villus height and crypt depth, tight junction protein, and Na+ absorption were higher, whereas intestinal permeability and anion secretion were lower in mice pretreated with ZnLa. In addition, ZnLa conferred effective protection against ETEC-induced intestinal inflammatory responses, as the increases in protein and mRNAs of proinflammatory cytokines were prevented in serum and jejunum, which was likely associated with the TLR4/MYD88/NF-κB signaling pathway. The increase in ETEC shedding and virulence-related gene expression was prevented in mice with ZnLa pretreatment. Finally, the growth of ETEC and virulence-related gene expression were lower in the ZnLa group than in ZnSO4 with an equal concentration of zinc. These findings suggest that ZnLa is a promising prevention strategy to remedy ETEC infection. Full article
(This article belongs to the Special Issue The Effects of Fatty Acids on Inflammation)
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