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Advanced Research in Gut Inflammation and Gut-Mediated Disorders
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Advanced Research in Gut Inflammation and Gut-Mediated Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 August 2024) | Viewed by 6429

Special Issue Editor

Dr. Soonjae Hwang

E-Mail Website
Guest Editor
1. Department of Biomedical Laboratory Science, College of Software and Digital Healthcare Convergence, Yonsei University MIRAE Campus, Wonju 26493, Republic of Korea
2. Department of Biochemistry, Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, 155 Gaetbeol-ro, Yeonsu-gu, Inchon 21999, Republic of Korea
Interests: gut inflammation; colitis; colitis-associated cancer; gut microbiota; bacterial infection; inflammatory bowel diseases; colorectal cancer; gut–organ axis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Gut inflammation is a normal physiological process for host defense, but chronic intestinal inflammation can promote conditions such as inflammatory bowel diseases and colorectal cancer. In addition to this, gut inflammation also mediates many diseases and exacerbates inflammatory disease in other organs, such as the liver, lung, skin, and brain. Gut inflammation is modulated by gut microbiota. Gut microbiota may trigger inflammation in the intestinal tissue through cross-talk with hosts via microbial metabolites/toxins and the intestinal immune microenvironment. Therefore, we encourage researchers who are studying basic research and treatment mechanisms to submit research and review papers to this Special Issue.

This Special Issue encourages the submission of not only basic and therapeutic mechanism research on the gut, but also disease phenotype and mechanism research in other organs with inflammatory disorders that can be mediated by gut inflammation. Papers published in the IJMS (International Journal of Molecular Sciences) are encouraged to include results at the molecular level.

Dr. Soonjae Hwang
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. 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

  • gut inflammation
  • colitis
  • bacterial infection
  • gut microbiota
  • microbial metabolites
  • inflammatory bowel diseases
  • colorectal cancer
  • gut–organ axis

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Published Papers (3 papers)

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24 pages, 4575 KiB  
Article
The Role of Propionate-Induced Rearrangement of Membrane Proteins in the Formation of the Virulent Phenotype of Crohn’s Disease-Associated Adherent-Invasive Escherichia coli
by Olga V. Pobeguts, Maria A. Galyamina, Elena V. Mikhalchik, Sergey I. Kovalchuk, Igor P. Smirnov, Alena V. Lee, Lyubov Yu. Filatova, Kirill V. Sikamov, Oleg M. Panasenko and Alexey Yu. Gorbachev
Int. J. Mol. Sci. 2024, 25(18), 10118; https://doi.org/10.3390/ijms251810118 - 20 Sep 2024
Viewed by 1250
Abstract
Adhesive-invasive E. coli has been suggested to be associated with the development of Crohn’s disease (CD). It is assumed that they can provoke the onset of the inflammatory process as a result of the invasion of intestinal epithelial cells and then, due to [...] Read more.
Adhesive-invasive E. coli has been suggested to be associated with the development of Crohn’s disease (CD). It is assumed that they can provoke the onset of the inflammatory process as a result of the invasion of intestinal epithelial cells and then, due to survival inside macrophages and dendritic cells, stimulate chronic inflammation. In previous reports, we have shown that passage of the CD isolate ZvL2 on minimal medium M9 supplemented with sodium propionate (PA) as a carbon source stimulates and inhibits the adherent-invasive properties and the ability to survive in macrophages. This effect was reversible and not observed for the laboratory strain K12 MG1655. We were able to compare the isogenic strain AIEC in two phenotypes—virulent (ZvL2-PA) and non-virulent (ZvL2-GLU). Unlike ZvL2-GLU, ZvL2-PA activates the production of ROS and cytokines when interacting with neutrophils. The laboratory strain does not cause a similar effect. To activate neutrophils, bacterial opsonization is necessary. Differences in neutrophil NADH oxidase activation and ζ-potential for ZvL2-GLU and ZvL2-PA are associated with changes in membrane protein abundance, as demonstrated by differential 2D electrophoresis and LC-MS. The increase in ROS and cytokine production during the interaction of ZvL2-PA with neutrophils is associated with a rearrangement of the abundance of membrane proteins, which leads to the activation of Rcs and PhoP/Q signaling pathways and changes in the composition and/or modification of LPS. Certain isoforms of OmpA may play a role in the formation of the virulent phenotype of ZvL2-PA and participate in the activation of NADPH oxidase in neutrophils. Full article
(This article belongs to the Special Issue Advanced Research in Gut Inflammation and Gut-Mediated Disorders)
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26 pages, 6336 KiB  
Article
Endotoxin Inflammatory Action on Cells by Dysregulated-Immunological-Barrier-Linked ROS-Apoptosis Mechanisms in Gut–Liver Axis
by Andrei Dumitru, Elena Matei, Georgeta Camelia Cozaru, Anca Chisoi, Luana Alexandrescu, Răzvan Cătălin Popescu, Mihaela Pundiche Butcaru, Eugen Dumitru, Sorin Rugină and Cristina Tocia
Int. J. Mol. Sci. 2024, 25(5), 2472; https://doi.org/10.3390/ijms25052472 - 20 Feb 2024
Cited by 4 | Viewed by 2365
Abstract
Our study highlighted the immune changes by pro-inflammatory biomarkers in the gut–liver-axis-linked ROS-cell death mechanisms in chronic and acute inflammations when gut cells are exposed to endotoxins in patients with hepatic cirrhosis or steatosis. In duodenal tissue samples, gut immune barrier dysfunction was [...] Read more.
Our study highlighted the immune changes by pro-inflammatory biomarkers in the gut–liver-axis-linked ROS-cell death mechanisms in chronic and acute inflammations when gut cells are exposed to endotoxins in patients with hepatic cirrhosis or steatosis. In duodenal tissue samples, gut immune barrier dysfunction was analyzed by pro-inflammatory biomarker expressions, oxidative stress, and cell death by flow cytometry methods. A significant innate and adaptative immune system reaction was observed as result of persistent endotoxin action in gut cells in chronic inflammation tissue samples recovered from hepatic cirrhosis with the A-B child stage. Instead, in patients with C child stage of HC, the endotoxin tolerance was installed in cells, characterized by T lymphocyte silent activation and increased Th1 cytokines expression. Interesting mechanisms of ROS-cell death were observed in chronic and acute inflammation samples when gut cells were exposed to endotoxins and immune changes in the gut–liver axis. Late apoptosis represents the chronic response to injury induction by the gut immune barrier dysfunction, oxidative stress, and liver-dysregulated barrier. Meanwhile, necrosis represents an acute and severe reply to endotoxin action on gut cells when the immune system reacts to pro-inflammatory Th1 and Th2 cytokines releasing, offering protection against PAMPs/DAMPs by monocytes and T lymphocyte activation. Flow cytometric analysis of pro-inflammatory biomarkers linked to oxidative stress-cell death mechanisms shown in our study recommends laboratory techniques in diagnostic fields. Full article
(This article belongs to the Special Issue Advanced Research in Gut Inflammation and Gut-Mediated Disorders)
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14 pages, 2672 KiB  
Article
Promotion of Colitis in B Cell-Deficient C57BL/6 Mice Infected with Enterotoxigenic Bacteroides fragilis
by Minjeong Jo, Soonjae Hwang, Chang-Gun Lee, Ju-Eun Hong, Da-Hye Kang, Sang-Hyeon Yoo, Woo-Seung Kim, Jung-Yoon Yoo and Ki-Jong Rhee
Int. J. Mol. Sci. 2024, 25(1), 364; https://doi.org/10.3390/ijms25010364 - 27 Dec 2023
Cited by 2 | Viewed by 1937
Abstract
Enterotoxigenic Bacteroides fragilis (ETBF) causes colitis and is implicated in inflammatory bowel diseases and colorectal cancer. The ETBF-secreted B. fragilis toxin (BFT) causes cleavage of the adherence junction, the E-cadherin, resulting in the large intestine showing IL-17A inflammation in wild-type (WT) mice. However, [...] Read more.
Enterotoxigenic Bacteroides fragilis (ETBF) causes colitis and is implicated in inflammatory bowel diseases and colorectal cancer. The ETBF-secreted B. fragilis toxin (BFT) causes cleavage of the adherence junction, the E-cadherin, resulting in the large intestine showing IL-17A inflammation in wild-type (WT) mice. However, intestinal pathology by ETBF infection is not fully understood in B-cell-deficient mice. In this study, ETBF-mediated inflammation was characterized in B-cell-deficient mice (muMT). WT or muMT C57BL/6J mice were orally inoculated with ETBF and examined for intestinal inflammation. The indirect indicators for colitis (loss of body weight and cecum weight, as well as mortality) were increased in muMT mice compared to WT mice. Histopathology and inflammatory genes (Nos2, Il-1β, Tnf-α, and Cxcl1) were elevated and persisted in the large intestine of muMT mice compared with WT mice during chronic ETBF infection. However, intestinal IL-17A expression was comparable between WT and muMT mice during infection. Consistently, flow cytometry analysis applied to the mesenteric lymph nodes showed a similar Th17 immune response in both WT and muMT mice. Despite elevated ETBF colonization, the ETBF-infected muMT mice showed no histopathology or inflammation in the small intestine. In conclusion, B cells play a protective role in ETBF-induced colitis, and IL-17A inflammation is not attributed to prompted colitis in B-cell-deficient mice. Our data support the fact that B cells are required to ameliorate ETBF infection-induced colitis in the host. Full article
(This article belongs to the Special Issue Advanced Research in Gut Inflammation and Gut-Mediated Disorders)
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