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Immuno
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GI Tract Immunology and Mucosal Immunity
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GI Tract Immunology and Mucosal Immunity

A special issue of Immuno (ISSN 2673-5601). This special issue belongs to the section "Mucosal Immunology".

Deadline for manuscript submissions: closed (10 March 2022) | Viewed by 20408

Special Issue Editors

Prof. Dr. Hiroshi Nakase

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Guest Editor
Department of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Minami 1-jo, Nishi 16-chome, Chuo-ku, Sapporo, Hokkaido, Japan
Interests: inflammation; macrophage; clinical trials; innate immunity; immunology; microbiology; ELISA; flow cytometry; cell culture; immunology of infectious diseases
Dr. Ken Sugimoto

E-Mail Website
Guest Editor
First Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan
Interests: inflammatory bowel disease
Prof. Masayuki Saruta

E-Mail Website
Guest Editor
Division of Gastroenterology and Hepatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan
Interests: Crohn's disease; gastroenterology; pancreatic cancer

Special Issue Information

Dear Colleagues,

The homeostasis of the intestinal immune system is maintained by intestinal bacteria, intestinal epithelial barrier function, and immune cells. Disruption of this homeostasis contributes to the induction of excessive pro-inflammatory cytokines and, consequently, developing autoinflammatory diseases, such as inflammatory bowel disease. This Special Issue will focus on the relationship between the intestinal immune system and various autoinflammatory diseases, including IBD, from multiple viewpoints, such as microbiome, immune cells, and cytokines, which play an important role in intestinal immunity, to broaden our understanding of the pathogenesis of these diseases. The scope of Immuno covers all aspects of immunological science and medicine from basic research to clinical research. We welcome submissions on translational research.

Prof. Dr. Hiroshi Nakase
Dr. Ken Sugimoto
Prof. Masayuki Saruta
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. Immuno is an international peer-reviewed open access quarterly 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 1000 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

  • mucosal immune system
  • autoinflammatory disease
  • microbiome
  • cytokines
  • inflammasome

Published Papers (6 papers)

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Research

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13 pages, 2068 KiB  
Article
Macrophages and Epithelial Cells Mutually Interact through NLRP3 to Clear Infection and Enhance the Gastrointestinal Barrier
by Michael Bording-Jorgensen, Heather Armstrong, Madison Wickenberg, Paul LaPointe and Eytan Wine
Immuno 2022, 2(1), 13-25; https://doi.org/10.3390/immuno2010002 - 27 Dec 2021
Cited by 3 | Viewed by 3477
Abstract
Activation of the nod-like receptor protein 3 (NLRP3) leads to the release of the proinflammatory cytokine IL-1β, which then facilitates pathogen control by macrophages. The role of NLRPs in controlling infection of epithelial cells is not well understood. Our hypothesis was that activation [...] Read more.
Activation of the nod-like receptor protein 3 (NLRP3) leads to the release of the proinflammatory cytokine IL-1β, which then facilitates pathogen control by macrophages. The role of NLRPs in controlling infection of epithelial cells is not well understood. Our hypothesis was that activation of the NLRP3 inflammasome in colonic epithelial cells would promote macrophage-mediated epithelial recovery after infection with the pathogen Citrobacter rodentium. We devised a co-culture model using mouse colonic epithelial cells (CMT-93) and macrophages (J774A.1) during infection with C. rodentium. Inflammasome was activated using LPS and ATP and inhibited by YVAD. We assessed cytokine secretion (ELISA), macrophage recruitment and pathogen penetration (immunofluorescence), and epithelial barrier integrity (transepithelial electrical resistance). Macrophages were recruited to the apical membrane of epithelial cells, associated with tight junctions, promoted epithelial barrier recovery, and displaced C. rodentium. While NLRP3 was expressed in infected epithelial cells, IL-18 or IL-1β secretion remained unchanged. Supernatants from infected epithelial cells promoted infection clearance by macrophage; while this was inflammasome-independent, ATP significantly improved epithelial barrier recovery. The inflammasome appears to promote epithelial barrier function, independent of IL-18 and IL-1β secretion. Inflammasome activation in macrophages plays a dual role of promoting pathogen clearance and improving epithelial barrier integrity. Full article
(This article belongs to the Special Issue GI Tract Immunology and Mucosal Immunity)
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9 pages, 917 KiB  
Article
Lymphocyte-to-Monocyte Ratio as a Marker for Endoscopic Activity in Ulcerative Colitis
by Natsuki Ishida, Satoru Takahashi, Yusuke Asai, Takahiro Miyazu, Satoshi Tamura, Shinya Tani, Mihoko Yamade, Moriya Iwaizumi, Yasushi Hamaya, Satoshi Osawa, Takahisa Furuta and Ken Sugimoto
Immuno 2021, 1(4), 360-368; https://doi.org/10.3390/immuno1040024 - 03 Oct 2021
Viewed by 2435
Abstract
Leukocyte subtypes can be used to evaluate the severity of ulcerative colitis (UC). In this study, we examined the relationship between the lymphocyte-to-monocyte ratio (LMR) and the Mayo endoscopic score (MES) in assessing endoscopic activity in UC. Eighty-nine samples of leukocyte subtypes and [...] Read more.
Leukocyte subtypes can be used to evaluate the severity of ulcerative colitis (UC). In this study, we examined the relationship between the lymphocyte-to-monocyte ratio (LMR) and the Mayo endoscopic score (MES) in assessing endoscopic activity in UC. Eighty-nine samples of leukocyte subtypes and biomarkers, including fecal calprotectin (FC), the fecal immunochemical occult blood test (FIT), and C-reactive protein (CRP), from 71 patients with UC were retrospectively investigated, along with the MES. The MES was significantly correlated with the LMR, FC, the FIT, and CRP. There were significant differences in the LMR, FC, the FIT, and CRP between groups with an MES < 1 and >2 (p = 0.001, p = 0.003, p < 0.001, and p < 0.001, respectively). In the receiver operating characteristic (ROC) analysis for predicting mucosal healing (MES 0 or 1), the areas under the curve (AUCs) for the LMR, FC, the FIT, and CRP, were 0.712, 0.860, 0.908, and 0.796, respectively. In the analysis of patients without immunomodulators, the correlation of the MES with the LMR and CRP was significant. The LMR can be used to assess endoscopic activity in UC, particularly in patients without immunomodulators. Full article
(This article belongs to the Special Issue GI Tract Immunology and Mucosal Immunity)
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Review

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11 pages, 1041 KiB  
Review
Uptake and Advanced Therapy of Butyrate in Inflammatory Bowel Disease
by Shinji Ota and Hirotake Sakuraba
Immuno 2022, 2(4), 692-702; https://doi.org/10.3390/immuno2040042 - 25 Nov 2022
Cited by 6 | Viewed by 3759
Abstract
The pathogenesis and refractory nature of inflammatory bowel disease (IBD) are related to multiple factors, including genetic factors, environmental factors, and abnormalities in gut microbial diversity, which lead to decreased levels of short-chain fatty acids (SCFAs). Among SCFAs, butyrate plays an important role [...] Read more.
The pathogenesis and refractory nature of inflammatory bowel disease (IBD) are related to multiple factors, including genetic factors, environmental factors, and abnormalities in gut microbial diversity, which lead to decreased levels of short-chain fatty acids (SCFAs). Among SCFAs, butyrate plays an important role in mucosal barrier maintenance, serves as an energy source in intestinal epithelial cells (IECs), and exhibits anti-inflammatory effects; therefore, it is a particularly important factor in gut homeostasis. Changes in gut microbiota and butyrate levels affect the outcomes of drug therapy for IBD. Butyrate is mainly absorbed in the large intestine and is transported by monocarboxylate transporter 1 (MCT1) and sodium-coupled monocarboxylate transporter 1 (SMCT1). During gut inflammation, butyrate utilization and uptake are impaired in IECs. Dysbiosis and low abundance of butyrate affect fecal microbiota transplantation and anticancer immunotherapy. Although butyrate administration has been reported as a treatment for IBD, its effects remain controversial. In this review, we discuss butyrate absorption and metabolism in patients with IBD and their relationship with drug therapy. Full article
(This article belongs to the Special Issue GI Tract Immunology and Mucosal Immunity)
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12 pages, 891 KiB  
Review
The Multifaceted Effects of Gut Microbiota on the Immune System of the Intestinal Mucosa
by Takehiro Hirano and Hiroshi Nakase
Immuno 2021, 1(4), 583-594; https://doi.org/10.3390/immuno1040041 - 13 Dec 2021
Cited by 1 | Viewed by 4475
Abstract
The gut microbiota has diverse microbial components, including bacteria, viruses, and fungi. The interaction between gut microbiome components and immune responses has been studied extensively over the last decade. Several studies have reported the potential role of the gut microbiome in maintaining gut [...] Read more.
The gut microbiota has diverse microbial components, including bacteria, viruses, and fungi. The interaction between gut microbiome components and immune responses has been studied extensively over the last decade. Several studies have reported the potential role of the gut microbiome in maintaining gut homeostasis and the development of disease. The commensal microbiome can preserve the integrity of the mucosal barrier by acting on the host immune system. Contrastingly, dysbiosis-induced inflammation can lead to the initiation and progression of several diseases through inflammatory processes and oxidative stress. In this review, we describe the multifaceted effects of the gut microbiota on several diseases from the perspective of mucosal immunological responses. Full article
(This article belongs to the Special Issue GI Tract Immunology and Mucosal Immunity)
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9 pages, 890 KiB  
Review
Current Topics of the Mechanism of Intestinal Fibrosis in Crohn’s Disease
by Yusuke Honzawa, Shuji Yamamoto, Makoto Okabe, Hiroshi Seno and Hiroshi Nakase
Immuno 2021, 1(4), 574-582; https://doi.org/10.3390/immuno1040040 - 07 Dec 2021
Cited by 2 | Viewed by 2852
Abstract
Intestinal fibrosis is one of the most common intestinal complications observed in inflammatory bowel disease, especially Crohn’s disease (CD). Intestinal fibrosis in CD is associated with chronic inflammation resulting from immunologic abnormalities and occurs as a form of tissue repair during the anti-inflammatory [...] Read more.
Intestinal fibrosis is one of the most common intestinal complications observed in inflammatory bowel disease, especially Crohn’s disease (CD). Intestinal fibrosis in CD is associated with chronic inflammation resulting from immunologic abnormalities and occurs as a form of tissue repair during the anti-inflammatory process. Various types of immune cells and mesenchymal cells, including myofibroblasts, are intricately involved in causing intestinal fibrosis. It is often difficult to treat intestinal fibrosis as intestinal stricture may develop despite treatment aimed at controlling inflammation. Detailed analysis of the pathogenesis of intestinal fibrosis is critical towards advancing the development of future therapeutic applications. Full article
(This article belongs to the Special Issue GI Tract Immunology and Mucosal Immunity)
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16 pages, 2083 KiB  
Review
Role of microRNAs in the Pathophysiology of Ulcerative Colitis
by Takahiko Toyonaga and Masayuki Saruta
Immuno 2021, 1(4), 558-573; https://doi.org/10.3390/immuno1040039 - 03 Dec 2021
Cited by 1 | Viewed by 2601
Abstract
Ulcerative colitis (UC) is an intractable disorder characterized by a chronic inflammation of the colon. Studies have identified UC as a multifactorial disorder affected by both genetic and environmental factors; however, the precise mechanism remains unclear. Recent advances in the field of microRNA [...] Read more.
Ulcerative colitis (UC) is an intractable disorder characterized by a chronic inflammation of the colon. Studies have identified UC as a multifactorial disorder affected by both genetic and environmental factors; however, the precise mechanism remains unclear. Recent advances in the field of microRNA (miRNA) research have identified an association between this small non-coding RNA in the pathophysiology of UC and altered miRNA expression profiles in patients with UC. Nevertheless, the roles of individual miRNAs are uncertain due to heterogeneity in both research samples and clinical backgrounds. In this review, we focus on miRNA expression in colonic mucosa where inflammation occurs in UC and discuss the potential roles of individual miRNAs in disease development, outlining the pathophysiology of UC. Full article
(This article belongs to the Special Issue GI Tract Immunology and Mucosal Immunity)
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