scholarly journals The Functions and Therapeutic Potential of Heat Shock Proteins in Inflammatory Bowel Disease—An Update

2019 ◽  
Vol 20 (21) ◽  
pp. 5331 ◽  
Author(s):  
Abdullah Hoter ◽  
Hassan Y. Naim
Keyword(s):  
Inflammatory Bowel Disease ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Bowel Disease ◽  
Therapeutic Potential ◽  
Inflammatory Bowel ◽  
Targeted Inhibition ◽  
Shock Proteins ◽  
Lines Of Evidence

Inflammatory bowel disease (IBD) is a multifactorial human intestinal disease that arises from numerous, yet incompletely defined, factors. Two main forms, Crohn’s disease (CD) and ulcerative colitis (UC), lead to a chronic pathological form. Heat shock proteins (HSPs) are stress-responsive molecules involved in various pathophysiological processes. Several lines of evidence link the expression of HSPs to the development and prognosis of IBD. HSP90, HSP70 and HSP60 have been reported to contribute to IBD in different aspects. Moreover, induction and/or targeted inhibition of specific HSPs have been suggested to ameliorate the disease consequences. In the present review, we shed the light on the role of HSPs in IBD and their targeting to prevent further disease progression.

Heat shock proteins peptides as regulators of autoimmune inflammation in inflammatory bowel disease

2003 ◽  
Vol 124 (4) ◽  
pp. A326
Author(s):  
Silvia Buratti ◽  
Gisela Y. Puga ◽  
Erica Cox ◽  
Robert Newbury ◽  
Ranjan Dohil ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Bowel Disease ◽  
Autoimmune Inflammation ◽  
Inflammatory Bowel ◽  
Shock Proteins

Heat-shock proteins (HSP) and HSP70 antibodies in the mucosa of inflammatory bowel disease

1995 ◽  
Vol 108 (4) ◽  
pp. A866 ◽  
Author(s):  
D. Ludwig ◽  
M. Ibrahim ◽  
C. Pfister ◽  
K. Schwarting ◽  
E.F. Stange
Keyword(s):  
Inflammatory Bowel Disease ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Shock Proteins

The Role of Peroxisome Proliferator–Activated Receptor γ in Colon Cancer and Inflammatory Bowel Disease

2003 ◽  
Vol 127 (9) ◽  
pp. 1121-1123
Author(s):  
Arthur W. Bull
Keyword(s):  
Inflammatory Bowel Disease ◽  
Colon Cancer ◽  
Bowel Disease ◽  
Cell Function ◽  
Therapeutic Potential ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Inflammatory Bowel

Abstract Objective.—Review the role and therapeutic potential of peroxisome proliferator–activated receptor (PPAR) γ in colonic disorders. Data Sources.—Recent peer-reviewed scientific literature focusing on PPAR γ in the colon. Study Selection.—Research reports using animal models, cultured cell lines, and clinical material were examined for content related to the role of PPAR γ in normal colon cell function, colon cancer, and inflammatory bowel disease. Issues concerned with potential therapeutic use were also considered. Data Synthesis.—Key points pertaining to PPAR function and involvement in colon pathology were extracted and noted. Potential compromises to therapeutic utility are identified. Conclusions.—The emerging important role of PPAR γ in normal tissue homeostasis and pathologic outcomes suggests this receptor is a good candidate as a drug target. Several potential problems with this approach will require further investigation prior to widespread recommendations for modulation of PPAR as an efficacious therapy for cancer, chemoprevention of colon cancer, or treatment of inflammatory bowel disease. The widespread use of PPAR γ ligands for management of type 2 diabetes (such as the glitazone class of drugs including rosiglitazone and pioglitazone) may provide a fortuitous assessment of the efficacy of long-term PPAR modulation.

scholarly journals Inflammasome Regulation: Therapeutic Potential for Inflammatory Bowel Disease

Molecules ◽  
2021 ◽  
Vol 26 (6) ◽  
pp. 1725
Author(s):  
Qiuyun Xu ◽  
Xiaorong Zhou ◽  
Warren Strober ◽  
Liming Mao
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Therapeutic Potential ◽  
Experimental Colitis ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Genetic Abnormalities ◽  
Inflammatory Bowel ◽  
Inflammatory Caspases

Inflammasomes are multiprotein complexes formed to regulate the maturation of pro-inflammatory caspases, in response to intracellular or extracellular stimulants. Accumulating studies showed that the inflammasomes are implicated in the pathogenesis of inflammatory bowel disease (IBD), although their activation is not a decisive factor for the development of IBD. Inflammasomes and related cytokines play an important role in the maintenance of gut immune homeostasis, while its overactivation might induce excess immune responses and consequently cause tissue damage in the gut. Emerging studies provide evidence that some genetic abnormalities might induce enhanced NLRP3 inflammasome activation and cause colitis. In these cases, the colonic inflammation can be ameliorated by blocking NLRP3 activation or its downstream cytokine IL-1β. A number of natural products were shown to play a role in preventing colon inflammation in various experimental colitis models. On the other hand, lack of inflammasome function also causes intestinal abnormalities. Thus, an appropriate regulation of inflammasomes might be a promising therapeutic strategy for IBD intervention. This review aims at summarizing the main findings in these studies and provide an outline for further studies that might contribute to our understanding of the role of inflammasomes in the pathogenesis and therapeutic treatment of IBD.

scholarly journals Role of MicroRNA in Inflammatory Bowel Disease: Clinical Evidence and the Development of Preclinical Animal Models

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2204
Author(s):  
Kanika Suri ◽  
Jason A. Bubier ◽  
Michael V. Wiles ◽  
Leonard D. Shultz ◽  
Mansoor M. Amiji ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Animal Models ◽  
Mirna Expression ◽  
Bowel Disease ◽  
Therapeutic Potential ◽  
Genetically Engineered ◽  
Complex Interactions ◽  
Inflammatory Bowel ◽  
Preclinical Animal Models

The dysregulation of microRNA (miRNA) is implicated in cancer, inflammation, cardiovascular disorders, drug resistance, and aging. While most researchers study miRNA’s role as a biomarker, for example, to distinguish between various sub-forms or stages of a given disease of interest, research is also ongoing to utilize these small nucleic acids as therapeutics. An example of a common pleiotropic disease that could benefit from miRNA-based therapeutics is inflammatory bowel disease (IBD), which is characterized by chronic inflammation of the small and large intestines. Due to complex interactions between multiple factors in the etiology of IBD, development of therapies that effectively maintain remission for this disease is a significant challenge. In this review, we discuss the role of dysregulated miRNA expression in the context of clinical ulcerative colitis (UC) and Crohn’s disease (CD)—the two main forms of IBD—and the various preclinical mouse models of IBD utilized to validate the therapeutic potential of targeting these miRNA. Additionally, we highlight advances in the development of genetically engineered animal models that recapitulate clinical miRNA expression and provide powerful preclinical models to assess the diagnostic and therapeutic promise of miRNA in IBD.

Regulation of Antimicrobial Pathways by Endogenous Heat Shock Proteins in Gastrointestinal Disorders

2018 ◽  
Vol 1 (1) ◽  
pp. 39-56 ◽  
Author(s):  
Emma Finlayson-Trick ◽  
Jessica Connors ◽  
Andrew Stadnyk ◽  
Johan Van Limbergen
Keyword(s):  
Heat Shock ◽  
Heat Shock Proteins ◽  
Host Immunity ◽  
Gastrointestinal Disorders ◽  
Complex Interplay ◽  
Disease Phenotypes ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Shock Proteins

Heat shock proteins (HSPs) are essential mediators of cellular homeostasis by maintaining protein functionality and stability, and activating appropriate immune cells. HSP activity is influenced by a variety of factors including diet, microbial stimuli, environment and host immunity. The overexpression and down-regulation of HSPs is associated with various disease phenotypes, including the inflammatory bowel diseases (IBD) such as Crohn’s disease (CD). While the precise etiology of CD remains unclear, many of the putative triggers also influence HSP activity. The development of different CD phenotypes therefore may be a result of the disease-modifying behavior of the environmentally-regulated HSPs. Understanding the role of bacterial and endogenous HSPs in host homeostasis and disease will help elucidate the complex interplay of factors. Furthermore, discerning the function of HSPs in CD may lead to therapeutic developments that better reflect and respond to the gut environment.

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