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Life
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New Insights into the Role of Mitochondria in Inflammation
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New Insights into the Role of Mitochondria in Inflammation

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 3152

Special Issue Editor

Dr. Mariasole Perrone

E-Mail Website
Guest Editor
Department of Medical Sciences, Section of Pathology, Oncology and Experimental Biology, University of Ferrara, Ferrara, Italy
Interests: mitochondria; inflammation; NLRP3 inflammasome; cancer; autophagy

Special Issue Information

Dear Colleagues,

In addition to their ancestral role as cellular powerhouses, mitochondria are multifaceted organelles that execute a wide array of functions, including orchestration of apoptosis, regulation of calcium (Ca2+) homeostasis and differentiation. Mitochondria are the primary source of cellular reactive oxygen species (ROS) and are therefore highly involved in oxidative stress. Under physiological conditions, ROS act as mitogen signals that provide many cellular functions; on the other hand, ROS overproduction leads to uncontrolled reactions with proteins, mtDNA and lipids, resulting in cell dysfunction and/or death. Mitochondria contain their own DNA genome (mtDNA) and they change their shape and number in response to physiological or metabolic conditions and guard against deleterious stresses that preserve cellular homeostasis. In addition to their dynamic behavior in programmed cell death and metabolism, mitochondria are now considered central platforms in the control of innate immunity and inflammatory responses. These organelles have emerged as being necessary for both the establishment and maintenance of innate and adaptive immune cell responses. In this Special Issue, we aim to discuss the new insights into the role of mitochondria in coordinating proinflammatory signaling, starting from their key function in modulating the innate immunity response and further investigating mitochondrial dysfunction in different diseases known to be supported and promoted by inflammation. Moreover, we will discuss the therapies that target the mitochondria-driven inflammatory response.

Dr. Mariasole Perrone
Guest Editor

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. Life is an international peer-reviewed open access monthly 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 2600 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

  • inflammation
  • mitochondria
  • inflammasomes
  • immunity
  • mtDNA and mitochondrial reactive oxygen species

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Published Papers (1 paper)

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Research

17 pages, 1753 KiB  
Article
Butyrate Supplementation Exacerbates Myocardial and Immune Cell Mitochondrial Dysfunction in a Rat Model of Faecal Peritonitis
by Vera B. M. Peters, Nishkantha Arulkumaran, Miranda J. Melis, Charlotte Gaupp, Thierry Roger, Manu Shankar-Hari and Mervyn Singer
Life 2022, 12(12), 2034; https://doi.org/10.3390/life12122034 - 6 Dec 2022
Cited by 4 | Viewed by 2653
Abstract
Mitochondrial dysfunction and immune cell dysfunction are commonplace in sepsis and are associated with increased mortality risk. The short chain fatty acid, butyrate, is known to have anti-inflammatory effects and promote mitochondrial biogenesis. We therefore explored the immunometabolic effects of butyrate in an [...] Read more.
Mitochondrial dysfunction and immune cell dysfunction are commonplace in sepsis and are associated with increased mortality risk. The short chain fatty acid, butyrate, is known to have anti-inflammatory effects and promote mitochondrial biogenesis. We therefore explored the immunometabolic effects of butyrate in an animal model of sepsis. Isolated healthy human volunteer peripheral mononuclear cells were stimulated with LPS in the presence of absence of butyrate, and released cytokines measured. Male Wistar rats housed in metabolic cages received either intravenous butyrate infusion or placebo commencing 6 h following faecal peritonitis induction. At 24 h, splenocytes were isolated for high-resolution respirometry, and measurement of mitochondrial membrane potential (MMP), reactive oxygen species (mtROS), and intracellular cytokines (TNF alpha, IL-10) using flow cytometry. Isolated splenocytes from septic and septic butyrate treated rats were stimulated with LPS for 18 h and the effects of butyrate on cytokine release assessed. Ex vivo, butyrate (1.8 mM) reduced LPS-induced TNF alpha (p = 0.019) and IL-10 (p = 0.001) release by human PBMCs. In septic animals butyrate infusion reduced the respiratory exchange ratio (p < 0.001), consistent with increased fat metabolism. This was associated with a reduction in cardiac output (p = 0.001), and increased lactate (p = 0.031) compared to placebo-treated septic animals (p < 0.05). Butyrate treatment was associated with a reduction in splenocyte basal respiration (p = 0.077), proton leak (p = 0.022), and non-mitochondrial respiration (p = 0.055), and an increase in MMP (p = 0.007) and mtROS (p = 0.027) compared to untreated septic animals. Splenocyte intracellular cytokines were unaffected by butyrate, although LPS-induced IL-10 release was impaired (p = 0.039). In summary, butyrate supplementation exacerbates myocardial and immune cell mitochondrial dysfunction in a rat model of faecal peritonitis. Full article
(This article belongs to the Special Issue New Insights into the Role of Mitochondria in Inflammation)
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