scholarly journals Innate Immunity: A Potent Target for Management of Inflammatory Bowel Disease

Colitis ◽  
10.5772/27617 ◽  
2012 ◽  
Author(s):  
Masayuki Fukata
Keyword(s):  
Inflammatory Bowel Disease ◽  
Innate Immunity ◽  
Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Chemical and cytokine features of innate immunity characterize serum and tissue profiles in inflammatory bowel disease

2013 ◽  
Vol 110 (26) ◽  
pp. E2332-E2341 ◽  
Author(s):  
C. G. Knutson ◽  
A. Mangerich ◽  
Y. Zeng ◽  
A. R. Raczynski ◽  
R. G. Liberman ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Innate Immunity ◽  
Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Immunopathophysiology of inflammatory bowel disease: how genetics link barrier dysfunction and innate immunity to inflammation

2017 ◽  
Vol 23 (6) ◽  
pp. 497-505 ◽  
Author(s):  
Minesh Mehta ◽  
Shifat Ahmed ◽  
Gerald Dryden
Keyword(s):  
Inflammatory Bowel Disease ◽  
Innate Immunity ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Inflammatory Responses ◽  
Clinical Symptoms ◽  
Barrier Dysfunction ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Chronic Intestinal Inflammation

Inflammatory bowel diseases (IBD) comprise a distinct set of clinical symptoms resulting from chronic or relapsing immune activation and corresponding inflammation within the gastrointestinal (GI) tract. Diverse genetic mutations, encoding important aspects of innate immunity and mucosal homeostasis, combine with environmental triggers to create inappropriate, sustained inflammatory responses. Recently, significant advances have been made in understanding the interplay of the intestinal epithelium, mucosal immune system, and commensal bacteria as a foundation of the pathogenesis of inflammatory bowel disease. Complex interactions between specialized intestinal epithelial cells and mucosal immune cells determine different outcomes based on the environmental input: the development of tolerance in the presence of commensal bacterial or the promotion of inflammation upon recognition of pathogenic organisms. This article reviews key genetic abnormalities involved in inflammatory and homeostatic pathways that enhance susceptibility to immune dysregulation and combine with environmental triggers to trigger the development of chronic intestinal inflammation and IBD.

Vedolizumab is associated with changes in innate rather than adaptive immunity in patients with inflammatory bowel disease

Gut ◽  
2018 ◽  
Vol 68 (1) ◽  
pp. 25-39 ◽  
Author(s):  
Sebastian Zeissig ◽  
Elisa Rosati ◽  
C Marie Dowds ◽  
Konrad Aden ◽  
Johannes Bethge ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Innate Immunity ◽  
T Cell ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Photon Emission ◽  
Emission Computed Tomography ◽  
Antibody Treatment ◽  
Inflammatory Bowel

ObjectiveVedolizumab, a monoclonal antibody directed against the integrin heterodimer α4β7, is approved for the treatment of Crohn’s disease and ulcerative colitis. The efficacy of vedolizumab has been suggested to result from inhibition of intestinal T cell trafficking although human data to support this conclusion are scarce. We therefore performed a comprehensive analysis of vedolizumab-induced alterations in mucosal and systemic immunity in patients with inflammatory bowel disease (IBD), using anti-inflammatory therapy with the TNFα antibody infliximab as control.DesignImmunophenotyping, immunohistochemistry, T cell receptor profiling and RNA sequencing were performed using blood and colonic biopsies from patients with IBD before and during treatment with vedolizumab (n=18) or, as control, the anti-TNFα antibody infliximab (n=20). Leucocyte trafficking in vivo was assessed using single photon emission computed tomography and endomicroscopy.ResultsVedolizumab was not associated with alterations in the abundance or phenotype of lamina propria T cells and did not affect the mucosal T cell repertoire or leucocyte trafficking in vivo. Surprisingly, however, α4β7 antibody treatment was associated with substantial effects on innate immunity including changes in macrophage populations and pronounced alterations in the expression of molecules involved in microbial sensing, chemoattraction and regulation of the innate effector response. These effects were specific to vedolizumab, not observed in response to the TNFα antibody infliximab, and associated with inhibition of intestinal inflammation.ConclusionOur findings suggest that modulation of innate immunity contributes to the therapeutic efficacy of vedolizumab in IBD.Trial registration numberNCT02694588

Innate immunity in inflammatory bowel disease: state of the art

2008 ◽  
Vol 24 (4) ◽  
pp. 448-454 ◽  
Author(s):  
Tadakazu Hisamatsu ◽  
Haruhiko Ogata ◽  
Toshifumi Hibi
Keyword(s):  
Inflammatory Bowel Disease ◽  
Innate Immunity ◽  
Bowel Disease ◽  
State Of The Art ◽  
Disease State ◽  
Inflammatory Bowel

scholarly journals The protein C pathway in tissue inflammation and injury: pathogenic role and therapeutic implications

Blood ◽  
2010 ◽  
Vol 115 (6) ◽  
pp. 1121-1130 ◽  
Author(s):  
Silvio Danese ◽  
Stefania Vetrano ◽  
Li Zhang ◽  
Victoria A. Poplis ◽  
Francis J. Castellino
Keyword(s):  
Inflammatory Bowel Disease ◽  
Innate Immunity ◽  
Bowel Disease ◽  
Protein C ◽  
Inflammatory Diseases ◽  
Pathogenic Role ◽  
Chronic Inflammatory Diseases ◽  
Therapeutic Implications ◽  
Inflammatory Bowel ◽  
Cellular Components

Abstract Inflammation and coagulation are closely linked interdependent processes. Under physiologic conditions, the tissue microcirculation functions in anticoagulant and anti-inflammatory fashions. However, when inflammation occurs, coagulation is also set in motion and actively participates in enhancing inflammation. Recently, novel and unexpected roles of hemostasis in the humoral and cellular components of innate immunity have been described. In particular, the protein C system, besides its well-recognized role in anticoagulation, plays a crucial role in inflammation. Indeed, the protein C system is now emerging as a novel participant in the pathogenesis of acute and chronic inflammatory diseases, such as sepsis, asthma, inflammatory bowel disease, atherosclerosis, and lung and heart inflammation, and may emerge as unexpected therapeutic targets for intervention.

scholarly journals The Role of Innate Immunity Receptors in the Pathogenesis of Inflammatory Bowel Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Paula Peruzzi Elia ◽  
Yolanda Faia M. Tolentino ◽  
Claudio Bernardazzi ◽  
Heitor Siffert Pereira de Souza
Keyword(s):  
Inflammatory Bowel Disease ◽  
Innate Immunity ◽  
Bowel Disease ◽  
Critical Role ◽  
Innate Immune ◽  
Gastrointestinal Mucosa ◽  
Persistent Inflammation ◽  
Nucleotide Oligomerization ◽  
Inflammatory Bowel ◽  
Molecular Patterns

Innate immunity constitutes the first line of defense, fundamental for the recognition and the initiation of an inflammatory response against microorganisms. The innate immune response relies on the sensing of microbial-associated molecular patterns through specialized structures such as toll-like receptors (TLRs) and the nucleotide oligomerization domain- (NOD-) like receptors (NLRs). In the gut, these tasks are performed by the epithelial barrier and the presence of adaptive and innate immune mechanisms. TLRs and NLRs are distributed throughout the gastrointestinal mucosa, being more expressed in the epithelium, and in lamina propria immune and nonimmune cells. These innate immunity receptors exhibit complementary biological functions, with evidence for pathways overlapping. However, as tolerance is the predominant physiological response in the gastrointestinal mucosa, it appears that the TLRs are relatively downregulated, while NLRs play a critical role in mucosal defense in the gut. Over the past two decades, genetic polymorphisms have been associated with several diseases including inflammatory bowel disease. Special emphasis has been given to the susceptibility to Crohn’s disease, in association with abnormalities in the NOD2 and in the NLRP3/inflammasome. Nevertheless, the mechanisms underlying innate immune receptors dysfunction that result in the persistent inflammation in inflammatory bowel disease remain to be clarified.

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