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Biomedicines
Special Issues
Molecular Research on Colitis
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Molecular Research on Colitis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 11861

Special Issue Editor

Dr. Fu-Chen Huang

E-Mail Website
Guest Editor
Department of Anatomic Pathology, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung 833, Taiwan
Interests: probiotics; prebiotics; postbiotics; gut microbiota
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

An experimental colitis that resembles infectious colitis or inflammatory bowel diseases (IBDs) in many important ways has been found. A goal of research in the field is to explore the pathogenesis of colitis and search for alternative therapies to antibiotics or anti-inflammatory reagents. Immune responses to infection include innate and adaptive immunity. Pathogen-associated molecular patterns (PAMPs) from Salmonella, recognized by extracellular and intracellular receptors, induce innate immunity involving intestinal epithelial cells, neutrophils, macrophages, dendric cells, and lymphocytes, including natural killer (NK) and natural killer T (NKT) cells. The cytokines, mostly interleukins (ILs), produced by the cells involved in innate immunity, stimulate adaptive immunity involving T and B cells. Increasing studies have linked autophagy to host defense against several intracellular bacterial pathogens that use different strategies to establish infection. The abnormalities in the handling of intracellular bacteria through autophagy might play a role in IBD pathogenesis, like Crohn’s disease. The interaction between ILs and autophagy has been increasingly reported. For example, loss of the autophagy protein enhances responses to endotoxin-induced ILs production, and ILs regulate the autophagy of immune cells to ameliorate experimental colitis in mice. Shifting the balance to favor the inhibition of inflammation and the enhancement of autophagy may lead to the identification of novel drug candidates to treat or prevent Salmonella infection or IBD. Therefore, it is important to explore the role of ILs and autophagy in immune responses to experimental colitis.

Dr. Fu-Chen Huang
Guest Editor

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Keywords

  • immune response
  • intestine
  • innate immunity
  • infection
  • colitis
  • autophagy
  • interleukins

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Published Papers (3 papers)

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20 pages, 37650 KiB  
Article
Nicotine Exerts a Stronger Immunosuppressive Effect Than Its Structural Analogs and Regulates Experimental Colitis in Rats
by Kohki Okada and Kano Matsuo
Biomedicines 2023, 11(3), 922; https://doi.org/10.3390/biomedicines11030922 - 16 Mar 2023
Cited by 6 | Viewed by 6070
Abstract
Ulcerative colitis (UC) is an intractable disease that causes persistent colonic inflammation. Numerous studies have reported that smoking can afford clinical benefits in UC. This study aimed to elucidate whether nicotine, the main component in cigarettes, can exert pharmacological effects against experimental UC. [...] Read more.
Ulcerative colitis (UC) is an intractable disease that causes persistent colonic inflammation. Numerous studies have reported that smoking can afford clinical benefits in UC. This study aimed to elucidate whether nicotine, the main component in cigarettes, can exert pharmacological effects against experimental UC. To achieve this objective, we compared the effects of nicotine with those of structural nicotine analogs in a UC rodent model (Slc: Wistar rats, male, 9-week-old, and 220–250 g/rat). Nicotine, or a respective structural analog (nornicotine, cotinine, anabasine, myosmine, and anatabine), was administered intraperitoneally daily to rats (n = 6/group) exhibiting dextran sulfate sodium-induced experimental colitis. Examining the colon tissues of model rats, we compared disease severity, cytokine secretion, and α7 nicotine acetylcholine receptor (nAChR7) expression. We observed that nicotine administration induced weight loss at 2.35% in 10 days. Notably, the reduction in histological severity (score) of UC was more pronounced in rats treated with nicotine (score = 4.83, p = 0.042) than in untreated rats (score = 8.17). Nicotine administration increased nAChR7 expression 6.88-fold (p = 0.022) in inflammatory sites of the colon, mainly by suppressing the production of interleukin (IL)-1β and IL-6. Moreover, the secretion of these cytokines was suppressed in lipopolysaccharide-stimulated rat macrophages (MΦ) treated with nicotine. In conclusion, nicotine better alleviates experimental UC than the examined structural analogs by activating nAChR7 expression and suppressing proinflammatory cytokines in MΦ. Full article
(This article belongs to the Special Issue Molecular Research on Colitis)
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15 pages, 2728 KiB  
Article
The Critical Role of Acyl Hydrocarbon Receptor on the Combined Benefits of Postbiotic Propionate on Active Vitamin D3-Orchestrated Innate Immunity in Salmonella Colitis
by Fu-Chen Huang and Shun-Chen Huang
Biomedicines 2023, 11(1), 195; https://doi.org/10.3390/biomedicines11010195 - 12 Jan 2023
Cited by 2 | Viewed by 1676
Abstract
Our recent study observed the combined beneficial effects of postbiotic butyrate on active vitamin D3-orchestrated innate immunity to Salmonella Colitis. There is increasing interest in the role of acyl hydrocarbon receptor (AhR) on colitis and innate immunity. Therefore, we investigated the involvement of [...] Read more.
Our recent study observed the combined beneficial effects of postbiotic butyrate on active vitamin D3-orchestrated innate immunity to Salmonella Colitis. There is increasing interest in the role of acyl hydrocarbon receptor (AhR) on colitis and innate immunity. Therefore, we investigated the involvement of AhR in the effects. Salmonella colitis model is conducted with 6–8 w/o male C57BL/6 mice: Streptomycin (20 mg/mouse p.o.)-pretreated C57BL/6 mice were mock infected with sterile PBS or infected orally with 1 × 108 CFU of an S. typhimurium wild-type strain SL1344 for 48 h. Before and after the colitis induction, mice were oral gavage with active vitamin D3 0.2 μg/25 g mice (VD3) and/or postbiotics propionate (PP), in the absence of the presence of intraperitoneal injection of AhR inhibitor for 4 and 7 days, respectively. We observed AhR inhibitor counteracted the synergistic effects of PP and VD3 on reducing the severity of Salmonella colitis and body weight loss in C57BL/6 mice, reducing the cecal inflammatory but enhancing antimicrobial peptide mRNAs expression, and reducing the bacterial translocation in liver/spleen, compared to single treatment. It suggests the involvement of AhR on the synergistic effects of postbiotics PP and VD3 on the antibacterial and anti-inflammatory responses in Salmonella colitis and the potential biological treatment of Salmonella colitis. Full article
(This article belongs to the Special Issue Molecular Research on Colitis)
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14 pages, 2474 KiB  
Article
Bacteroides fragilis Toxin Induces Intestinal Epithelial Cell Secretion of Interleukin-8 by the E-Cadherin/β-Catenin/NF-κB Dependent Pathway
by Chang-Gun Lee, Soonjae Hwang, Sun-Yeong Gwon, Chanoh Park, Minjeong Jo, Ju-Eun Hong and Ki-Jong Rhee
Biomedicines 2022, 10(4), 827; https://doi.org/10.3390/biomedicines10040827 - 31 Mar 2022
Cited by 16 | Viewed by 3526
Abstract
Enterotoxigenic Bacteroides fragilis (ETBF) has emerged as a gut microbiome pathogen that can promote colitis associated cancer in humans. ETBF secretes the metalloprotease, B. fragilis toxin (BFT), which can induce ectodomain cleavage of E-cadherin and IL-8 secretion through the β-catenin, NF-κB, and MAPK [...] Read more.
Enterotoxigenic Bacteroides fragilis (ETBF) has emerged as a gut microbiome pathogen that can promote colitis associated cancer in humans. ETBF secretes the metalloprotease, B. fragilis toxin (BFT), which can induce ectodomain cleavage of E-cadherin and IL-8 secretion through the β-catenin, NF-κB, and MAPK pathways in intestinal epithelial cells. However, it is still unclear whether E-cadherin cleavage is required for BFT induced IL-8 secretion and the relative contribution of these signaling pathways to IL-8 secretion. Using siRNA knockdown and CRISPR knockout studies, we found that E-cadherin cleavage is required for BFT mediated IL-8 secretion. In addition, genetic ablation of β-catenin indicates that β-catenin is required for the BFT induced increase in transcriptional activity of NF-κB, p65 nuclear localization and early IL-8 secretion. These results suggest that BFT induced β-catenin signaling is upstream of NF-κB activation. However, despite β-catenin gene disruption, BFT still activated the MAPK pathway, suggesting that the BFT induced activation of the MAPK signaling pathway is independent from the E-cadherin/β-catenin/NF-κB pathway. These findings show that E-cadherin and β-catenin play a critical role in acute inflammation following ETBF infection through the inflammatory response to BFT in intestinal epithelial cells. Full article
(This article belongs to the Special Issue Molecular Research on Colitis)
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