Outcomes of inflammatory bowel disease in patients with eosinophil-predominant colonic inflammation

Alhmoud, Tarik; Gremida, Anas; Steele, Diego Colom; Fallahi, Imaneh; Tuqan, Wael; Nandy, Nina; Ismail, Mahmoud; Altamimi, Barakat Aburajab; Xiong, Meng; Kerwin, Audra A.; Martín, David

doi:10.1136/bmjgast-2020-000373

Cited by 20 publications

(20 citation statements)

References 26 publications

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“…In inflammatory bowel disease, comprising ulcerative colitis and Crohn’s disease, eosinophils have been considered as pro-inflammatory cells associated with increased tissue damage. However, a recent study suggested that inflammatory bowel disease patients with eosinophil-predominant inflammation might have a reduced risk of disease flares and hospitalization [ 52 ].…”

Section: Cellular Mechanism Underlying Eosinophilic Inflammationmentioning

confidence: 99%

Role of Short Chain Fatty Acids and Apolipoproteins in the Regulation of Eosinophilia-Associated Diseases

Sturm

Knuplez

Marsche

2021

IJMS

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Eosinophils are key components of our host defense and potent effectors in allergic and inflammatory diseases. Once recruited to the inflammatory site, eosinophils release their cytotoxic granule proteins as well as cytokines and lipid mediators, contributing to parasite clearance but also to exacerbation of inflammation and tissue damage. However, eosinophils have recently been shown to play an important homeostatic role in different tissues under steady state. Despite the tremendous progress in the treatment of eosinophilic disorders with the implementation of biologics, there is an unmet need for novel therapies that specifically target the cytotoxic effector functions of eosinophils without completely depleting this multifunctional immune cell type. Recent studies have uncovered several endogenous molecules that decrease eosinophil migration and activation. These include short chain fatty acids (SCFAs) such as butyrate, which are produced in large quantities in the gastrointestinal tract by commensal bacteria and enter the systemic circulation. In addition, high-density lipoprotein-associated anti-inflammatory apolipoproteins have recently been shown to attenuate eosinophil migration and activation. Here, we focus on the anti-pathogenic properties of SCFAs and apolipoproteins on eosinophil effector function and provide insights into the potential use of SCFAs and apolipoproteins (and their mimetics) as effective agents to combat eosinophilic inflammation.

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Section: Cellular Mechanism Underlying Eosinophilic Inflammationmentioning

confidence: 99%

Role of Short Chain Fatty Acids and Apolipoproteins in the Regulation of Eosinophilia-Associated Diseases

Sturm

Knuplez

Marsche

2021

IJMS

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“…Apart from monocyte-derived macrophages, other polymorphonuclear cells such as neutrophils and eosinophils are recruited into the inflamed mucosa in IBD [ 165 , 166 ], but their role in promoting IBD-associated cancer has not yet been well addressed. Interestingly, expression of the transcription factor BATF3 in intestinal epithelial cells promoted the transcription of CXCL5, which together with CXC chemokine receptor (CXCR)- 2 stimulate neutrophil recruitment, which was associated with increased CAC development in AOM/DSS-treated mice [ 167 ].…”

Section: The Role Of the Immune System In Ibd-associated Cancermentioning

confidence: 99%

The Role of the Immune System in IBD-Associated Colorectal Cancer: From Pro to Anti-Tumorigenic Mechanisms

Frigerio

Lartey

D’Haens

et al. 2021

IJMS

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Patients with inflammatory bowel disease (IBD) have increased incidence of colorectal cancer (CRC). IBD-associated cancer follows a well-characterized sequence of intestinal epithelial changes, in which genetic mutations and molecular aberrations play a key role. IBD-associated cancer develops against a background of chronic inflammation and pro-inflammatory immune cells, and their products contribute to cancer development and progression. In recent years, the effect of the immunosuppressive microenvironment in cancer development and progression has gained more attention, mainly because of the unprecedented anti-tumor effects of immune checkpoint inhibitors in selected groups of patients. Even though IBD-associated cancer develops in the background of chronic inflammation which is associated with activation of endogenous anti-inflammatory or suppressive mechanisms, the potential role of an immunosuppressive microenvironment in these cancers is largely unknown. In this review, we outline the role of the immune system in promoting cancer development in chronic inflammatory diseases such as IBD, with a specific focus on the anti-inflammatory mechanisms and suppressive immune cells that may play a role in IBD-associated tumorigenesis.

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“…However, there are conflicting results regarding the association of eosinophil numbers and disease severity in humans. This is revealed by a recent study reporting that patients with eosinophil-predominant inflammation have a lower risk of disease flares and hospitalization than those with a neutrophil-predominant inflammation [ 87 ]. It is worth noting that an increased number of eosinophils is a hallmark not only of IBD but also of a different disease, known as eosinophilic colitis (EC) [ 88 ].…”

Section: Type 2 Associated Immune Cells In Ibdmentioning

confidence: 99%

The Regulation of Intestinal Inflammation and Cancer Development by Type 2 Immune Responses

Gámez‐Belmonte

Erkert

Wirtz

et al. 2020

IJMS

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The gut is among the most complex organs of the human body. It has to exert several functions including food and water absorption while setting up an efficient barrier to the outside world. Dysfunction of the gut can be life-threatening. Diseases of the gastrointestinal tract such as inflammatory bowel disease, infections, or colorectal cancer, therefore, pose substantial challenges to clinical care. The intestinal epithelium plays an important role in intestinal disease development. It not only establishes an important barrier against the gut lumen but also constantly signals information about the gut lumen and its composition to immune cells in the bowel wall. Such signaling across the epithelial barrier also occurs in the other direction. Intestinal epithelial cells respond to cytokines and other mediators of immune cells in the lamina propria and shape the microbial community within the gut by producing various antimicrobial peptides. Thus, the epithelium can be considered as an interpreter between the microbiota and the mucosal immune system, safeguarding and moderating communication to the benefit of the host. Type 2 immune responses play important roles in immune-epithelial communication. They contribute to gut tissue homeostasis and protect the host against infections with helminths. However, they are also involved in pathogenic pathways in inflammatory bowel disease and colorectal cancer. The current review provides an overview of current concepts regarding type 2 immune responses in intestinal physiology and pathophysiology.

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Outcomes of inflammatory bowel disease in patients with eosinophil-predominant colonic inflammation

Cited by 20 publications

References 26 publications

Role of Short Chain Fatty Acids and Apolipoproteins in the Regulation of Eosinophilia-Associated Diseases

Role of Short Chain Fatty Acids and Apolipoproteins in the Regulation of Eosinophilia-Associated Diseases

The Role of the Immune System in IBD-Associated Colorectal Cancer: From Pro to Anti-Tumorigenic Mechanisms

The Regulation of Intestinal Inflammation and Cancer Development by Type 2 Immune Responses

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