Browsing by Subject "Inflammatory bowel disease"
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- PublicationOpen AccessDual immune functions of IL-33 in inflammatory bowel disease.(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Chen, Jie; He, Yan; Tu, Lei; Duan, LihuaInterleukin-33 (IL-33) has emerged as a critical regulator in a variety of diseases, including inflammatory bowel disease (IBD). IL-33 can be produced by various tissues and cells, and typically induces Th2-type immune responses via binding to the receptor ST2. In addition, accumulated data have shown that IL-33 also plays a modulatory role in the function of regulatory T cells (Tregs), B cells, and innate immune cells such as macrophages and innate lymphoid cells (ILCs). IBD, including Crohn’s disease and ulcerative colitis, are characterized by aberrant immunological responses leading to intestinal tissue injury and destruction. Although IL-33 expression is increased in IBD patients and correlates with the patients’ disease activity index, mechanistic studies to date have demonstrated both pathogenic and protective roles in animal models of experimental colitis. In this review, we will summarize the roles and mechanisms of IL-33 in IBD, which is essential to understand the pathogenesis of IBD and determine potential therapies.
- PublicationOpen AccessEffect of pine bark extract and its phenolic compounds on selected pathogenic and probiotic bacterial strains(Frontiers, 2024-03-27) Sánchez Moya, Teresa; López Nicolás, Rubén; Peso Echarri, Patricia; González-Bermúdez, Carlos A.; Frontela-Saseta, Carmen; Tecnología de Alimentos, Nutrición y BromatologíaIntroduction: Inflammatory bowel disease (IBD) comprises a heterogeneous group of chronic diseases as ulcerative colitis (UC) and Crohn’s disease (CD). IBD is the result of a dysregulation of intestinal homeostasis with a host’s loss of tolerance toward normal enteric microflora. Plant-based extracts as phenolic compounds can play a role by modulating the intestinal inflammation response. Methods: The in vitro antimicrobial activity of French maritime pine bark extract (PBE) and its phenolic constituents has been investigated in this study. Furthermore, the ability of PBE and phenolic compounds (caffeic acid, chlorogenic acid, ferulic acid, gallic acid and taxifolin) to modulate the microbiota has been assessed. Results: Phenolic compounds and PBE showed a great inhibitory effect on the pathogens growth at the highest concentration assessed (1.25 mg/mL). The growth of E. sakazakii and E. faecalis were affected by the effect of caffeic acid and ferulic acid. Taxifolin showed a very strong activity against Listeria sp. (with a reduction ~98%). Gallic acid revealed antibacterial effect on S. aureus at different concentrations. The inhibitory effect of PBE was highly significant on the growth of E. coli O157:H7. PBE, caffeic acid and chlorogenic acid seem to provide the greatest beneficial effect on the probiotic bacteria. However, the highest concentrations of taxifolin may have impaired the growth of beneficial microbiota. Conclusion: Present findings could be of interest for considering PBE and/or its phenolic constituents as protectors against gastrointestinal disturbances which lead to ulcerative colitis and Crohn’s disease.
- PublicationOpen AccessExpression of WIF-1 in inflammatory bowel disease(Universidad de Murcia. Departamento de Biología Celular e Histología, 2019) Terry, Robert; Chintanaboina, JayaKrishna; Patel, Deep; Lippert, Brittany; Haner, Matthew; Price, Kimberly; Tracy, Amanda; Lalos, Alexander; Wakeley, Michelle; Gutierrez, Linda S.The WNT/β-catenin cellular network has been extensively studied in numerous diseases including inflammatory bowel disease (IBD). IBD is a condition that increases the risk of developing colorectal cancer. WIF-1 is an inhibitory protein that acts by blocking the interactions of WNT with its receptor complex, thus leading to downregulation of end products of this pathway. While WIF-1 has been characterized in several cancers, its relationship with IBD has yet to be elucidated. In this study, the expression of WIF-1 in patients with IBD was analyzed in order to provide insights into the pathophysiology and rationale for alternative therapies. Biopsies of both normal and inflamed colonic mucosa from patients with Crohn’s disease or ulcerative colitis were histologically examined for the degree of morphologic changes, immune cell infiltration and presence of WIF-1 through immunohistochemistry. No differences were observed in WIF-1 expression linked to a particular condition, but WIF-1 stain was significantly enhanced in the crypts and lamina propria as inflammation increased in biopsies from patients with both, ulcerative colitis and Crohn’s disease. These findings could give guidance to new therapeutic applications of the WNT/β-catenin system and WIF-1 in IBD.
- PublicationOpen AccessHistological and immunohistochemical effects of L-arginine and silymarin on TNBS-induced inflammatory bowel disease in rats(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) Al-Drees, Abdul Majeed; Khalil, Mahmoud SalahInflammatory bowel disease (IBD) is a chronic disease that affects quality of life. Various mediators are involved in IBD pathogenesis including inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-κB), cytochrome c, heat shock protein 70 (HSP70) and tumor necrosis factor (TNF)-α. L-Arginine (L-Arg) can be depleted in IBD, and silymarin inhibits neutrophil infiltration, NF-κB, and TNF-α, which have crucial roles in inducing IBD. This study aimed to investigate whether silymarin and L-Arg supplementation decreases IBD progression in trinitrobenzinesulfonic acid (TNBS)-induced colitis. Fifty adult male albino rats were randomized into five groups (10 animals per group): Group I rats orally received 10 mg silymarin/100 g body weight once daily; Group II rats orally received 2 mg L-Arg/100 g body weight once daily; Group III rats rectally received 0.85 mL TNBS in 50% ethanol to induce colitis; Group IV rats were treated similar to group III and, on recovery from anesthesia, received silymarin as described for group I; and Group V rats were treated similar to group III and, on recovery from anesthesia, received L-Arg as described for group II. On day 7, the rats were anesthetized, and blood samples were collected to determine the serum concentrations of TNF-α. Laparotomy and total colectomy were performed for macroscopic, histological, and immunohistochemical investigations. The results showed that silymarin and L-Arg macroscopically and microscopically ameliorated TNBS-induced colitis; significantly decreased the serum levels of TNFα; inhibited the colonic expression of iNOS, NF-κB, and cytochrome c; and increased expression of HSP70. Our results suggest that these complementary medicines could be used to supplement current treatments for IBD.
- ItemOpen AccessITGAX promotes Th17-cell differentiation and drives pathogenesis in pediatric ulcerative colitis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Dong Zhan; Wanying Xie; Biología Celular e HistologíaBackground. Pediatric ulcerative colitis (UC) is an inflammatory bowel disease characterized by dysregulated immune responses and intestinal inflammation, often more severe than adult-onset UC. Th17 cells play a crucial role in UC pathogenesis but the mechanisms regulating their differentiation and recruitment in pediatric UC remain incompletely understood. Methods. Transcriptomic analysis of pediatric UC patients and weighted gene co-expression network analysis (WGCNA) were performed to identify key dysregulated genes. The functional role of the candidate gene ITGAX was investigated using in vitro Th17 differentiation assays with siRNA knockdown and an in vivo dextran sodium sulfate (DSS)-induced UC mouse model with intrarectal siRNA administration. Results. WGCNA identified ITGAX, SOCS3, CXCL1, CASP1, and CXCL11 as core upregulated genes in pediatric UC, with ITGAX being a novel candidate regulator of Th17 cells. ITGAX knockdown in naive CD4+ T cells impaired Th17 differentiation and IL-17A production in vitro. In the DSS-induced UC mouse model, intrarectal ITGAX siRNA ameliorated colonic inflammation and ulceration, suppressed IL-17A levels, and selectively reduced the expansion of IFNγ-IL-17+ Th17 cells in the colon. Conclusion. ITGAX is a key promoter of Th17-cell differentiation and expansion, contributing to the pathogenesis of pediatric UC. Targeting ITGAX may represent a potential therapeutic strategy for pediatric UC by modulating aberrant Th17 responses.
- PublicationRestrictedKiller immunoglobulin-like receptor repertoire analysis in a Caucasian Spanish cohort with inflammatory bowel disease(Wiley, 2016-11) López Hernández, Ruth; Campillo, Jose Antonio; Valdés, Mariano; Salama, Hortensia; Boix, Francisco; Hernández Martínez, AM; Eguia, Jorge; González Martínez, G; Moya Quiles, María R.; Minguela, Alfredo; García Alonso, Ana; Carballo, Fernando; Muro, Manuel; Legaz Pérez, Isabel; Ciencias SociosanitariasImmunological molecules are implicated in inflammatory disorders, including inflammatory bowel disease (IBD; Crohn disease [CD] and ulcerative colitis [UC]). Killer cell immunoglobulin-like receptors (KIRs) are also genetically variable proteins involved in immune function. They are expressed by NK cells and certain T lymphocytes, regulate specificity and function by interaction with HLA Class I molecules, may be either inhibitory or activating and are polymorphic both in terms of alleles and haplotype gene content. Genetic associations between activating KIRs and certain autoimmune and inflammatory diseases have been reported; however, a possible association between KIR and IBD remains unclear. The aim of this study was to determine the relationship between KIR repertoire and IBD pathologies in a Spanish cohort. KIR variability was analyzed using PCR–sequence specific oligonucleotide probes (SSOP). Inhibitory KIR2DL5 was found more frequently in UC and IBD patient groups than in healthy controls (P = 0.028 and P = 0.01, respectively), as was activating KIR2DS1 (P = 0.02, Pc > 0.05, UC vs. Controls; P = 0.001, Pc = 0.01, IBD vs Controls; P = 0.01, Pc > 0.05, Controls vs CR), KIR2DS5 (P = 0.0028, Pc = 0.04, Controls vs UC; P = 0.0001, Pc = 0.0017, Controls vs IBD; P = 0.01, Pc > 0.05, Controls vs CD) and KIR3DS1 (P = 0.012, Pc > 0.05, Controls vs IBD). Our data suggest that imbalance between activating and inhibitory KIR may partially explain the different pathogeneses of these IBDs and that there is a hypothetical role for the telomeric B region (which contains both KIR2DS5 and KIR2DS1) in these diseases.
- PublicationOpen AccessPotential pitfalls in reporting non- neoplastic gastrointestinal mucosal biopsies(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Al Qudah, Mohammad; Murshed, Khaled; Haddad, Husam K.; Haboubi, NajibBiopsies taken from the gastrointestinal tract (GIT) comprise a significant percentage of the pathologists’ routine work. The variable histology and normal components of each organ along the GIT, as well as the different ways of responding to injury among these organs, can cause morphological changes that could result in potential diagnostic pitfalls. Herein, we review the pathological conditions of the GIT that could cause these diagnostic pitfalls. Our aim was to increase awareness among pathologists and trainees regarding these conditions and provide a pragmatic approach to prevent them and achieve a correct diagnosis.
- PublicationOpen AccessPotential role of chitinases and chitin-binding proteins in host-microbial interactions during the development of intestinal inflammation(F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Tran, Hoa T.; Barnich, Nicolas; Mizoguchi, EmikoThe small and large intestines contain an abundance of luminal antigens derived from food products and enteric microorganisms. The function of intestinal epithelial cells is tightly regulated by several factors produced by enteric bacteria and the epithelial cells themselves. Epithelial cells actively participate in regulating the homeostasis of intestine, and failure of this function leads to abnormal and host-microbial interactions resulting in the development of intestinal inflammation. Major determinants of host susceptibility against luminal commensal bacteria include genes regulating mucosal immune responses, intestinal barrier function and microbial defense. Of note, it has been postulated that commensal bacterial adhesion and invasion on/into host cells may be strongly involved in the pathogenesis of inflammatory bowel disease (IBD). During the intestinal inflammation, the composition of the commensal flora is altered, with increased population of aggressive and detrimental bacteria and decreased populations of protective bacteria. In fact, some pathogenic bacteria, including Adherent-Invasive Escherichia coli, Listeria monocytogenes and Vibrio cholerae are likely to initiate their adhesion to the host cells by expressing accessory molecules such as chitinases and/or chitin-binding proteins on themselves. In addition, several inducible molecules (e.g., chitinase 3-like 1, CEACAM6) are also induced on the host cells (e.g. epithelial cells, lamina proprial macrophages) under inflammatory conditions, and are actively participated in the host-microbial interactions. In this review, we will summarize and discuss the potential roles of these important molecules during the development of acute and chronic inflammatory conditions.
- PublicationOpen AccessProspective evaluation of the learning curve of confocal laser endomicroscopy in patients with IBD(F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Neumann, Helmut; Vieth, Michael; Atreya, Raja; Neurath, Markus F.; Mudter, JonasBackground and aims: Confocal laser endomicroscopy (CLE) represents a novel endoscopic imaging technique which enables the in vivo microscopic imaging within the mucosal layer of the gut at subcellular resolution. Currently, there are no data available on the learning curve of CLE, which was therefore the aim of our study. Methods: Twenty-six consecutive patients with inflammatory bowel disease (IBD) underwent total colonoscopy and were examined by fluorescein-aided CLE. Image data were collected and reviewed by two endoscopists in a blinded fashion. CLE images were compared to endoscopical and histological findings. Prospectively, the following performance parameters were documented: total duration of the procedure, confocal imaging time, time to receive a confocal image in focus, number of confocal images, number of confocal images in focus, CLE diagnosis and final histopathological diagnosis. Results: A significance decrease of CLE duration was detected between the first 8 and the subsequent cases (p=0.002). Confocal imaging time and the time to receive an image in focus declined significantly over time (p=0.0001), while number of images in focus significantly increased (p=0.0007). Agreement between CLE and histopathology improved over time with kappa values of 0.81 after twenty-six cases. Conclusions: There was a significant improvement in CLE performance over time, including decreased confocal imaging time, successful CLE diagnosis and decline in procedural time. These parameters improved significantly after the initial three cases. Therefore, CLE represents an easy to learn and apply novel diagnostic method for in vivo analysis and diagnosis in IBD.
- PublicationOpen AccessQuantitative phase microscopy for evaluation of intestinal inflammation and wound healing utilizing label-free biophysical markers(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Bettenworth, Dominik; Bokemeyer, Arne; Poremba, Christopher; Ding, Nik Sheng; Ketelhut, Steffi; Lenz, Philipp; Kemper, BjörnInflammatory bowel diseases (IBD) are inflammatory disorders of the gastrointestinal tract characterized by a chronic relapsing disease course. As uncontrolled intestinal inflammation can result in severe disease complications, recent treatment targets of IBD evolved toward seeking the absence of mucosal and histological inflammation. However, this approach requires adequate histological evaluation of IBD disease activity. The diagnostic challenge of histological examination of intestinal inflammation is documented by the multitude of proposed histological scoring systems. In this context, we review quantitative phase imaging (QPI) techniques such as digital holographic microscopy (DHM) for characterizing intestinal inflammation. DHM determines optical path-length delays in a stain-free manner, thereby providing the tissue refractive index as a biophysical marker that directly correlates to tissue density. Recently, DHM has been successfully applied in cell biology, cancer cell research and infectious-induced cellular alterations. We summarized the capabilities of DHM and related QPI techniques to assess the severity of intestinal inflammation in experimental colitis as well as in colonic samples from human IBD patients. Moreover, we illustrate major advantages of DHM facilitated multimodal evaluation of epithelial wound healing processes as assessed by physical parameters like cell volume, density, thickness and dry mass in vitro. Furthermore, potential limitations of DHM and future utilities of QPI are discussed. In conclusion, DHM represents a promising, easy-to-use quantitative tool to provide accurate and objective assessment of intestinal inflammation and may pave the way towards automated label-free digital pathology and related in vitro cell culture analysis in future.
- PublicationOpen AccessRole of cannabinoid receptors and RAGE in inflammatory bowel disease(F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología., 2011) Stintzing, Sebastian; Wissniowski, Till Th.; Lohwasser, Christina; Alinger, Beate; Neureiter, Daniel; Ocker, MatthiasBackground: The endocanabinoid system is involved in many inflammatory diseases, such as Crohn’s disease (CD) and ulcerative colitis (UC). The distribution and expression of cannabinoid receptors 1 (CNR1) and 2 (CNR2) in combination with inflammatory cytokines and RAGE (receptor of advanced glycation end products), which is also overactive in these diseases, in dependency of the extent of inflammation and alteration of the colon barrier is still unclear and needs to be elucidated. Material and Methods: 10 specimens of CD patients who underwent colectomy and 14 colectomy specimens of patients suffering from UC were investigated histologically for inflammatory infiltrate, extent of fibrosis and for disturbance of the intestinal barrier. Immunohistochemistry was carried out to examine the distribution and localization of CNR1, CNR2 and RAGE. Additionally, qRT-PCR was performed to study the expression of CNR1, CNR2, RAGE and inflammatory cytokines (TNFα, TGFß, CTGF, IL12, IFNγ). 35 morphological and histological normal specimens of colectomy cases served as controls. Results: The expression level of CNR2 did not differ between the control group and the group of patients with IBD, while CNR1 displayed a significant up regulation, especially in cases of CD. A differential association between the expression of CNR1/CNR2 and RAGE with morphological changes and expression of molecular markers of inflammation could be established. Conclusion: We showed that cannabinoid receptors are expressed differentially in inflammatory bowel disease and that the expression seems to be influenced by the underlying disease and by localized inflammation.