International Journal of Molecular Sciences

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Dr. Soonjae Hwang

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Guest Editor

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 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

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Keywords

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

Published Papers (2 papers)

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Research

26 pages, 6336 KiB

Open AccessArticle

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

Viewed by 864

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 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

Open AccessArticle

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 1 | Viewed by 942

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, 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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