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The Role of Dietary Management in Chronic Inflammation

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

Deadline for manuscript submissions: 25 May 2026 | Viewed by 385

Special Issue Editors


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Guest Editor
Cell Transplant Center, Diabetes Research Institute (DRI), University of Miami Miller School of Medicine, 1450 NW 10th Ave, Miami, FL 33136, USA
Interests: diabetes mellitus; stem cell differentiation; regenerative medicine; stem cells; diabetes; cell culture; surgery; autoimmunity; T lymphocytes; stem cell biology
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Inflammation Research Foundation, Peabody, MA, USA
Interests: diet; hormonal response; genetic expression; inflammation

Special Issue Information

Dear Colleagues,

Chronic low-level inflammation is a primary driver of many chronic diseases that are significant causes of mortality and morbidity worldwide.  It is a major underlying factor in the development of type 2 diabetes, heart disease, stroke, neurological conditions, and aging, leading to a significant decrease in healthspan.

Much of this inflammation is ultimately caused by dietary factors, thus offering the potential to address the root cause of many chronic diseases by dietary intervention as opposed to merely treating their symptoms with pharmacology.

Chronic low-level inflammation is often below the perception of pain. However, it can be measured by various blood markers, changes in the expression of inflammatory mediators, and changes in inflammatory gene expression. Although dietary interventions can attenuate many of these inflammatory markers, they are only one of the pillars of the healthspan ecosystem that is important to adhere to for the prevention and treatment of chronic disease. Nevertheless, they are critically important components of any realistic healthspan extension strategy.

This Special Issue aims to identify and assess dietary interventions as well as specific nutrients that can decrease the levels of chronic low-level inflammation. Furthermore, addressing the molecular mechanisms of their interventions at the level of metabolic control points at the cellular level, activation or inhibition of gene transcription factors, and epigenetic changes that the diet can induce is another goal of this Special Issue.

We wish to encourage all investigators who work in this field to contribute with original research or reviews on the molecular basis of anti-inflammatory dietary interventions to submit their work to this Special Issue to widen our knowledge and open new research pathways for using dietary interventions to treat the underlying cause of conditions associated with chronic low-level inflammation.

Prof. Dr. Camillo Ricordi
Dr. Barry Sears
Guest Editors

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Keywords

  • dietary intervention
  • omega-3 fatty acids
  • polyphenols
  • fermentable fiber
  • gut barrier
  • immune responses
  • inflammation
  • healthspan
  • epigenetic changes
  • gene transcription factors

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Published Papers (1 paper)

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Research

18 pages, 6469 KB  
Article
A Short-Term High-Sugar Diet Induces Glucose Intolerance, Visceral Adipose Tissue Inflammation, and Exacerbates Experimental Allergic Asthma
by Mateus C. Casaro, Vanessa de Souza, Eduardo Mendes, Juliana Carvalho Pereira, Fernando A. Oliveira and Caroline M. Ferreira
Nutrients 2026, 18(9), 1475; https://doi.org/10.3390/nu18091475 - 6 May 2026
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Abstract
Background: Diets composed of various components have been shown to influence inflammatory diseases such as asthma. While most studies have focused on fiber-rich diets to investigate their effects on the immune system and, consequently, on asthma, little is known about the impact of [...] Read more.
Background: Diets composed of various components have been shown to influence inflammatory diseases such as asthma. While most studies have focused on fiber-rich diets to investigate their effects on the immune system and, consequently, on asthma, little is known about the impact of sugar-rich diets, particularly when such diets are consumed over short periods of time. Methods: To investigate the short-term effects of a sugar-rich diet on allergic airway inflammation, A/J mice were fed either a standard diet or a sugar-enriched diet and subsequently sensitized and challenged with ovalbumin or PBS. Airway inflammation was assessed by bronchoalveolar lavage (BAL) cell analysis, including eosinophil counts and cytokine levels (IL-4, TNF-α, IL-33), and by lung histology (H&E for inflammatory infiltrate and PAS for mucus). Serum IgE levels were also measured. In addition, glucose tolerance, visceral and subcutaneous adipose tissue mass, and inflammatory markers in visceral adipose tissue were evaluated. Results: Short-term consumption of a sugar-rich diet induced glucose intolerance and expansion of adipose tissue, particularly visceral fat, independent of ovalbumin sensitization. Gonadal adipose tissue analysis revealed a shift toward M1 macrophage polarization, characterized by elevated TNF-α, IL-6, and IL-1β, increased leptin levels, and reduced adiponectin. In OVA-sensitized mice, the sugar-rich diet significantly exacerbated eosinophil infiltration in BAL, increased IL-4, TNF-α, and IL-33, and enhanced PAS-positive mucus accumulation and inflammatory infiltrates in the lung. Moreover, total serum IgE was significantly higher in allergic mice fed the sugar-rich diet compared with allergic mice on the standard diet. Importantly, in non-sensitized mice fed the sugar-rich diet, no pulmonary inflammation was detected by BAL, demonstrating that HSD alone does not induce asthma but amplifies allergic responses when sensitization is present. Conclusions: Our findings demonstrate that short-term consumption of a sugar-rich diet is sufficient to exacerbate, but not initiate, allergic pulmonary inflammation. From a translational perspective, reducing dietary sugar intake may represent a valuable adjuvant strategy in the management of allergic asthma. Full article
(This article belongs to the Special Issue The Role of Dietary Management in Chronic Inflammation)
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