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Nutrients
Special Issues
Inflammation and Nutritional Therapy
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Inflammation and Nutritional Therapy

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

Deadline for manuscript submissions: 15 June 2024 | Viewed by 3222

Special Issue Editors

Prof. Dr. Noriyuki Inaki

E-Mail Website
Guest Editor
Department of Gastrointestinal Surgery/Breast Surgery, Graduate School of Medical Science, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Ishikawa, Japan
Interests: esophageal cancer; gastric cancer; minimally invasive surgery; laparoscopic surgery; postoperative complications; upper gastrointestinal surgery; nutrition
Dr. Ryota Matsui

E-Mail Website
Co-Guest Editor
Department of Gastroenterological Surgery, Cancer Institute Ariake Hospital, 3-8-31 Ariake, Koto-ku, Tokyo 135-8550, Japan
Interests: gastric cancer; malnutrition; nutrition; postoperative complication; prognosis; sarcopenia; visceral fat

Special Issue Information

Dear Colleagues,

Nutrition guidelines have recommended that patients diagnosed with malnutrition be asked to determine whether their malnutrition is due to inflammation or not. The Global Leadership Initiative on malnutrition (GLIM) criteria, published in 2019, incorporate the presence of inflammation into the diagnosis of malnutrition. However, not many reports of malnutrition focus on inflammation.

It has been reported that the intensity of inflammation makes a difference in the effectiveness of nutritional therapy. In cancer patients, we should distinguish between acute inflammation, such as pneumonia, and chronic inflammation, such as cachexia. In addition, cut-off values for the intensity of inflammation have rarely been investigated.

Immunonutrition is an option for nutritional therapy in the presence of inflammation. Immunonutrition contains nutrients to optimize inflammation. However, this may lead to different outcomes in patients undergoing elective surgery as opposed to patients with sepsis. Therefore, further studies with defined patient backgrounds are needed.

This Special Issue on inflammation and nutritional therapy aims to clarify whether nutritional therapy for inflammation improves outcomes. We welcome studies focused on changing the daily clinical practice of the readers of this Special Issue.

Prof. Dr. Noriyuki Inaki
Dr. Ryota Matsui
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cachexia
  • immunonutrition
  • inflammation
  • nutritional therapy
  • sepsis
  • surgery

Published Papers (3 papers)

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Research

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14 pages, 3644 KiB  
Article
Mycobacterium avium paratuberculosis Infection Suppresses Vitamin D Activation and Cathelicidin Production in Macrophages through Modulation of the TLR2-Dependent p38/MAPK-CYP27B1-VDR-CAMP Axis
by Muna M. Talafha, Ahmad Qasem and Saleh A. Naser
Nutrients 2024, 16(9), 1358; https://doi.org/10.3390/nu16091358 - 30 Apr 2024
Viewed by 540
Abstract
Background: Vitamin D plays a vital role in modulating both innate and adaptive immune systems. Therefore, vitamin D deficiency has been associated with higher levels of autoimmune response and increased susceptibility to infections. CYP27B1 encodes a member of the cytochrome P450 superfamily of [...] Read more.
Background: Vitamin D plays a vital role in modulating both innate and adaptive immune systems. Therefore, vitamin D deficiency has been associated with higher levels of autoimmune response and increased susceptibility to infections. CYP27B1 encodes a member of the cytochrome P450 superfamily of enzymes. It is instrumental in the conversion of circulating vitamin D (calcifediol) to active vitamin D (calcitriol). This is a crucial step for macrophages to express Cathelicidin Anti-microbial Peptide (CAMP), an anti-bacterial factor released during the immune response. Our recent study indicated that a Crohn’s disease (CD)-associated pathogen known as Mycobacterium avium paratuberculosis (MAP) decreases vitamin D activation in macrophages, thereby impeding cathelicidin production and MAP infection clearance. The mechanism by which MAP infection exerts these effects on the vitamin D metabolic axis remains elusive. Methods: We used two cell culture models of THP-1 macrophages and Caco-2 monolayers to establish the effects of MAP infection on the vitamin D metabolic axis. We also tested the effects of Calcifediol, Calcitriol, and SB203580 treatments on the relative expression of the vitamin D metabolic genes, oxidative stress biomarkers, and inflammatory cytokines profile. Results: In this study, we found that MAP infection interferes with vitamin D activation inside THP-1 macrophages by reducing levels of CYP27B1 and vitamin D receptor (VDR) gene expression via interaction with the TLR2-dependent p38/MAPK pathway. MAP infection exerts its effects in a time-dependent manner, with the maximal inhibition observed at 24 h post-infection. We also demonstrated the necessity to have toll-like receptor 2 (TLR2) for MAP infection to influence CYP27B1 and CAMP expression, as TLR2 gene knockdown resulted in an average increase of 7.78 ± 0.88 and 13.90 ± 3.5 folds in their expression, respectively. MAP infection also clearly decreased the levels of p38 phosphorylation and showed dependency on the p38/MAPK pathway to influence the expression of CYP27B1, VDR, and CAMP which was evident by the average fold increase of 1.93 ± 0.28, 1.86 ± 0.27, and 6.34 ± 0.51 in their expression, respectively, following p38 antagonism. Finally, we showed that calcitriol treatment and p38/MAPK blockade reduce cellular oxidative stress and inflammatory markers in Caco-2 monolayers following macrophage-mediated MAP infection. Conclusions: This study characterized the primary mechanism by which MAP infection leads to diminished levels of active vitamin D and cathelicidin in CD patients, which may explain the exacerbated vitamin D deficiency state in these cases. Full article
(This article belongs to the Special Issue Inflammation and Nutritional Therapy)
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17 pages, 4319 KiB  
Article
Ser9p-GSK3β Modulation Contributes to the Protective Effects of Vitamin C in Neuroinflammation
by Melania Ruggiero, Antonia Cianciulli, Rosa Calvello, Chiara Porro, Francesco De Nuccio, Marianna Kashyrina, Alessandro Miraglia, Dario Domenico Lofrumento and Maria Antonietta Panaro
Nutrients 2024, 16(8), 1121; https://doi.org/10.3390/nu16081121 - 10 Apr 2024
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Abstract
Background. The prolonged activation of microglia and excessive production of pro-inflammatory cytokines can lead to chronic neuroinflammation, which is an important pathological feature of Parkinson’s disease (PD). We have previously reported the protective effect of Vitamin C (Vit C) on a mouse model [...] Read more.
Background. The prolonged activation of microglia and excessive production of pro-inflammatory cytokines can lead to chronic neuroinflammation, which is an important pathological feature of Parkinson’s disease (PD). We have previously reported the protective effect of Vitamin C (Vit C) on a mouse model of PD. However, its effect on microglial functions in neuroinflammation remains to be clarified. Glycogen synthase kinase 3β (GSK3β) is a serine/threonine kinase having a role in driving inflammatory responses, making GSK3β inhibitors a promising target for anti-inflammatory research. Methods. In this study, we investigated the possible involvement of GSK3β in Vit C neuroprotective effects by using a well-known 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced animal model of PD and a cellular model of neuroinflammation, represented by Lipopolysaccharide (LPS)-activated BV-2 microglial cells. Results. We demonstrated the ability of Vit C to decrease the expression of different mediators involved in the inflammatory responses, such as TLR4, p-IKBα, and the phosphorylated forms of p38 and AKT. In addition, we demonstrated for the first time that Vit C promotes the GSK3β inhibition by stimulating its phosphorylation at Ser9. Conclusion. This study evidenced that Vit C exerts an anti-inflammatory function in microglia, promoting the upregulation of the M2 phenotype through the activation of the Wnt/β-catenin signaling pathway. Full article
(This article belongs to the Special Issue Inflammation and Nutritional Therapy)
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Review

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14 pages, 933 KiB  
Review
Measures for Identifying Malnutrition in Geriatric Rehabilitation: A Scoping Review
by Shinta Nishioka, Yoji Kokura, Ryo Momosaki and Yutaka Taketani
Nutrients 2024, 16(2), 223; https://doi.org/10.3390/nu16020223 - 10 Jan 2024
Viewed by 1693
Abstract
Malnutrition is a common condition in geriatric rehabilitation settings; however, the accuracy and predictive validity of the measures to identify malnutrition have not been established. The current scoping review followed the Joanna Briggs Institute’s evidence synthesis manual and the Preferred Reporting Items for [...] Read more.
Malnutrition is a common condition in geriatric rehabilitation settings; however, the accuracy and predictive validity of the measures to identify malnutrition have not been established. The current scoping review followed the Joanna Briggs Institute’s evidence synthesis manual and the Preferred Reporting Items for Systematic Reviews and Meta-Analysis Extension for Scoping Reviews checklist. Literature published through September 2023 was searched using MEDLINE and CINAHL. The inclusion criteria selected studies reporting malnutrition measures, which include static body weight and weight loss. Identified tools were classified as nutritional screening tools, nutritional assessment tools, or diagnostic criteria. The domains of each tool/criterion and their accuracy and predictive validity were extracted. Fifty-six articles fulfilled the inclusion criteria, and six nutritional screening tools, three nutritional assessment tools, and three diagnostic criteria for malnutrition were identified. These measures consisted of various phenotypes, e.g., weight loss, causes such as inflammation/disease, and risk factors of malnutrition, e.g., functional impairment. The predictive validity of nutritional screening tools (n = 6) and malnutrition diagnostic criteria (n = 5) were inconsistently reported, whereas those for nutritional assessment tools were scarce (n = 1). These findings highlight the need to distinguish the functional impairment of nutritional origin from that of non-nutritional origin in nutritional assessment procedures, and the need to study the accuracy and the predictive validity of these measures in geriatric rehabilitation patients. Full article
(This article belongs to the Special Issue Inflammation and Nutritional Therapy)
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