ijms-logo

Journal Browser

Journal Browser

Immuno-Metabolism of Sepsis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1531

Special Issue Editors


E-Mail Website
Guest Editor
Faculty of Medicine, Universidade de São Paulo, Sao Paulo, Brazil
Interests: sepsis; inflammation

E-Mail Website
Guest Editor
Faculty of Medicine, Universidade de São Paulo, Sao Paulo, Brazil
Interests: inflammation; lipid metabolism; HDL

Special Issue Information

Dear Colleagues, 

Background: Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. The release of immune chemicals by innate immune cells plays a major role in mediating septic death. For example, HMGB1 can bind to multiple cell surface receptors, including RAGE and TLR4, to produce proinflammatory cytokines, chemokines, and adhesion molecules in various immune cells. Moreover, extracellular HMGB1 is capable of binding to various immune stimuli, such as lipopolysaccharide (LPS), DNA, and IgG, to produce synergistic effects on the inflammatory response. There are 31.5 million cases of sepsis globally, with an estimated death of 5.3 million people annually. The mortality rate of sepsis and septic shock varies from 25 to 30% and 40 to 50%.

Goal: Immunometabolism is an interdisciplinary field derived from classical immunology and metabolism with two main focuses: (1) the study of changes in cell immune metabolism that determine their fate, and (2) the effect of immune cells on tissue and systemic metabolism supporting the adaptation of individual changes. Metabolomics is a new area yet to be explored in sepsis.

Areas to be covered in this Special Issue may include, but are not limited to:

  • Immune cell function and metabolism during sepsis;
  • Lipidic metabolism in sepsis: free fat acids, cholesterol, triglycerides;
  • Reactive oxygen species and nitrogen reactive species;
  • Oxidative phosphorylation (OXPHOS) as a major metabolic pathway, uncoupled respiration;
  • Electron transport chain (ETC) in mitochondria;
  • Krebs or tricarboxylic acid (TCA) cycle and glycolysis;
  • The role of NADH and PARP;
  • Persistent inflammatory, immunosuppressed, catabolic syndrome;
  • Metabolic reprogramming.

Prof. Dr. Francisco Garcia Soriano
Prof. Dr. Marisa Passarelli
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • sepsis
  • inflammation
  • immune metabolism
  • Krebs cycle
  • lipid
  • cholesterol
  • late sequels
  • PICS
  • chronicle critical disease
  • genetic reprogramming
  • epigenetic

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

26 pages, 5380 KiB  
Article
LncRNA 220: A Novel Long Non-Coding RNA Regulates Autophagy and Apoptosis in Kupffer Cells via the miR-5101/PI3K/AKT/mTOR Axis in LPS-Induced Endotoxemic Liver Injury in Mice
by Ying Yang, Tian Tian, Shan Li, Nanhong Li, Haihua Luo and Yong Jiang
Int. J. Mol. Sci. 2023, 24(13), 11210; https://doi.org/10.3390/ijms241311210 - 07 Jul 2023
Cited by 1 | Viewed by 1277
Abstract
Sepsis is a severe medical condition distinguished by immune systematic dysfunction and multiple organic injury, or even failure, resulting from an acute systemic inflammatory response. Acute liver injury (ALI) could be considered as a notable inflammatory outcome of sepsis. Studies have demonstrated the [...] Read more.
Sepsis is a severe medical condition distinguished by immune systematic dysfunction and multiple organic injury, or even failure, resulting from an acute systemic inflammatory response. Acute liver injury (ALI) could be considered as a notable inflammatory outcome of sepsis. Studies have demonstrated the essential roles played by long non-coding RNAs (lncRNAs) in mediating the processes of various diseases, including their ability to engage in interactions with microRNAs (miRNAs) as complexes of competing endogenous RNA (ceRNA) to modulate signaling pathways. In this study, a newly discovered lncRNA, named 220, was identified to function in regulating autophagy and apoptosis in Kupffer cells treated with lipopolysaccharide (LPS). This was achieved through sponging miR-5101 as a ceRNA complex, as identified via high-throughput sequencing. The expression of 220 was found to be significantly different in the hepatic tissues of endotoxemic mice that were treated with LPS for 8 h, ultimately modulating the ALI process. Our studies have collectively demonstrated that 220 is a novel regulator that acts on LPS-induced autophagy and apoptosis in Kupffer cells, thereby mediating the ALI process induced by LPS. Furthermore, the validation of our findings using clinical databases suggests that 220 could potentially serve as a molecular target of clinical, diagnostic, and therapeutic significance in septic liver injury. Full article
(This article belongs to the Special Issue Immuno-Metabolism of Sepsis)
Show Figures

Figure 1

Back to TopTop