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Biomedicines
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Inflammatory Bowel Disease: Pathomechanisms, Diagnostics, and Novel Therapeutic Strategies
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Inflammatory Bowel Disease: Pathomechanisms, Diagnostics, and Novel Therapeutic Strategies

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 July 2026 | Viewed by 2790

Editor

Dr. Ziming Zheng

E-Mail Website
Guest Editor
Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Interests: gastrointestinal disease; inflammatory bowel disease; gastrointestinal metabolism

Special Issue Information

Dear Colleagues,

This Special Issue, entitled “Inflammatory Bowel Disease: Pathomechanisms, Diagnostics, and Novel Therapeutic Strategies”, will present an in-depth exploration of the molecular pathogenesis and treatment prospects in inflammatory bowel disease (IBD). The recurrent nature of IBD means that no effective curative strategies are currently available in clinical practice. Owing to diagnostic challenges and a lack of specific biomarkers, diagnosis of IBD is often delayed, hindering timely clinical intervention. This Special Issue will systematically explore emerging biomarkers for clinical diagnosis, promising therapeutic compounds and novel therapeutic agents, newly identified pathogenic targets, and novel animal models to further elucidate clinical disease features. This Special Issue will also address IBD-induced secondary disorders, such as MAFLD, as well as challenges and opportunities in the translation of preclinical research into clinical applications. By incorporating cutting-edge research and expert perspectives, this Special Issue will advance our understanding of the pathogenesis of IBD and facilitate the development of more efficient diagnostic criteria and safer treatment regimens.

Dr. Ziming Zheng
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • inflammatory bowel disease
  • Crohn’s disease
  • bowel inflammation
  • targeted therapy

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Published Papers (3 papers)

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Research

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18 pages, 1445 KB  
Article
Reciprocal Serum Phosphatidylcholine Signatures Are Related to Intestinal Inflammation in Inflammatory Bowel Disease and Liver Fibrosis in Primary Sclerosing Cholangitis—An Exploratory Study
by Tanja Elger, Muriel Huss, Hauke Christian Tews, Marcus Höring, Johanna Loibl, Arne Kandulski, Martina Müller, Gerhard Liebisch and Christa Buechler
Biomedicines 2026, 14(7), 1485; https://doi.org/10.3390/biomedicines14071485 - 30 Jun 2026
Viewed by 337
Abstract
Background: Phosphatidylcholine (PC) is a major phospholipid that contributes to intestinal barrier protection and is essential for hepatic secretion of lipids and bile acids. Because inflammatory bowel disease (IBD) and primary sclerosing cholangitis (PSC) are closely linked, we hypothesized that individual serum PC [...] Read more.
Background: Phosphatidylcholine (PC) is a major phospholipid that contributes to intestinal barrier protection and is essential for hepatic secretion of lipids and bile acids. Because inflammatory bowel disease (IBD) and primary sclerosing cholangitis (PSC) are closely linked, we hypothesized that individual serum PC species would reflect disease activity. We therefore investigated whether serum PC profiling could identify clinically useful biomarkers across the gut–liver axis. Methods: Serum concentrations of 21 PC species were quantified by direct flow injection high-resolution mass spectrometry in 16 healthy controls, 57 patients with IBD, and 20 patients with PSC. Results: In IBD, multiple serum PC species were inversely associated with inflammatory activity, showing negative correlations with serum C-reactive protein and fecal calprotectin. Patients with fecal calprotectin concentrations above the diagnostic cut-off of 120 µg/g had lower levels of PC 34:3, 36:1, 36:2, 36:3, 36:4, 36:5, 38:3, 38:4, 38:5, 38:7, 40:5, and 40:6, as well as lower total PC. In contrast, in PSC, PC 30:0, 32:0, 32:1, and 34:1 were increased compared with IBD and correlated positively with gamma-glutamyltransferase and alkaline phosphatase. Furthermore, these shorter-chain PC species as well as PC 36:1 were markedly elevated in PSC with advanced liver fibrosis compared with PSC without fibrosis. Conclusions: Serum PC species show a reciprocal disease-associated pattern in IBD and PSC. In IBD, lower concentrations of predominantly unsaturated PC species are associated with active intestinal inflammation, whereas in PSC, higher concentrations of shorter-chain PC species are associated with cholestatic injury and advanced liver fibrosis. IBD and PSC exhibit opposing serum PC signatures, suggesting that dysregulated PC metabolism is a pathophysiological feature of intestinal inflammation and PSC-associated liver fibrosis. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: Pathomechanisms, Diagnostics, and Novel Therapeutic Strategies)
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20 pages, 4811 KB  
Article
Recombinant BMP9 Reinforces Gut Vascular Barrier in Experimental Colitis
by Shan Li, Xingyue Zhou, Yili Wang, Bingyue Yao, Siyuan Zhu, Ritian Lin, Qinjuan Sun, Jinlai Lu, Miao Hu, Wei Wang and Lan Zhong
Biomedicines 2026, 14(2), 288; https://doi.org/10.3390/biomedicines14020288 - 28 Jan 2026
Viewed by 704
Abstract
Background: Refractory ulcerative colitis (rUC) represents a critical therapeutic challenge, with emerging evidence implicating gut vascular barrier (GVB) dysfunction in disease persistence. We investigated whether dysregulation of the endothelial BMP9-ALK1 signaling axis—a pathway not previously studied in UC—is associated with GVB impairment and [...] Read more.
Background: Refractory ulcerative colitis (rUC) represents a critical therapeutic challenge, with emerging evidence implicating gut vascular barrier (GVB) dysfunction in disease persistence. We investigated whether dysregulation of the endothelial BMP9-ALK1 signaling axis—a pathway not previously studied in UC—is associated with GVB impairment and treatment resistance, and explored its therapeutic potential. Methods: Serum BMP9 and mucosal ALK1 levels were compared across rUC, non-rUC, and healthy cohorts. The therapeutic efficacy of BMP9 was evaluated in DSS-induced murine colitis by examining vascular permeability, histopathology, and inflammatory markers, while mechanistic roles were investigated using human intestinal microvascular endothelial cells. Results: Serum BMP9 levels were significantly reduced in rUC versus non-rUC patients, inversely correlating with post-treatment disease severity (Modified Mayo Score: r = −0.471, 95% CI: −0.618 to −0.293, p < 0.001; UCEIS: r = −0.495, 95% CI: −0.637 to −0.321, p < 0.001). Stratified analyses confirmed that BMP9 deficiency was associated with treatment-refractory status independent of baseline disease severity. Intestinal ALK1 was downregulated in rUC mucosa. In murine DSS-colitis, BMP9 attenuated disease severity, colon shortening, histopathological damage, inflammatory cytokines, and early pro-fibrotic markers (Col1a1, Col3a1, α-SMA). BMP9 activated SMAD1, restored VE-cadherin, and reduced hyperpermeability (FITC-dextran leakage decreased from 10.2-fold to 2.1-fold, p < 0.001). In vitro, BMP9 inhibited TNF-α-induced neutrophil migration and enhanced endothelial tube stability via ALK1. Conclusions: Dysregulated BMP9-ALK1 signaling may contribute to GVB dysfunction in UC. BMP9 supplementation attenuates vascular leakage and inflammation in experimental colitis, identifying a potential therapeutic target warranting further investigation. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: Pathomechanisms, Diagnostics, and Novel Therapeutic Strategies)
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Review

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38 pages, 2491 KB  
Review
Current Perspectives on the Inflammatory Bowel Disease Pathogenesis of Microbiota and the Gut-Brain Axis, and Emerging Therapeutics
by Yujia Lin, Panpan Lu, Qiang Ding and Mei Liu
Biomedicines 2026, 14(4), 859; https://doi.org/10.3390/biomedicines14040859 - 9 Apr 2026
Cited by 1 | Viewed by 1352
Abstract
The pathogenesis of inflammatory bowel disease (IBD) is driven by an interplay among intestinal dysbiosis and aberrant mucosal immune responses. This review centers on the microbiota as a pivotal pathogenic hub, systematically dissecting how three hallmark features of dysbiosis—reduced microbial alpha diversity, depletion [...] Read more.
The pathogenesis of inflammatory bowel disease (IBD) is driven by an interplay among intestinal dysbiosis and aberrant mucosal immune responses. This review centers on the microbiota as a pivotal pathogenic hub, systematically dissecting how three hallmark features of dysbiosis—reduced microbial alpha diversity, depletion of immunomodulatory commensals, and expansion of pro-inflammatory pathobionts—collectively compromise epithelial barrier function, promote bacterial translocation, and sustain chronic mucosal inflammation. We further integrate emerging evidence implicating bidirectional gut-brain axis communication in amplifying both peripheral inflammation and central nervous system (CNS)-mediated behavioral comorbidities. Building on this mechanistic framework, we critically evaluate next-generation microbiota-targeted interventions: standardized fecal microbiota transplantation (FMT), rationally designed live biotherapeutic products (LBPs), precision phage cocktails targeting defined pathobionts, and microbiome-informed dietary strategies. Collectively, these approaches represent a paradigm shift—from broad-spectrum immunosuppression toward mechanism-guided, ecosystem-level modulation—thereby advancing the goal of precision medicine in IBD. Full article
(This article belongs to the Special Issue Inflammatory Bowel Disease: Pathomechanisms, Diagnostics, and Novel Therapeutic Strategies)
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