Inflammatory bowel diseases in patients with adaptive and complement immunodeficiency disorders

Marks, Daniel; Seymour, Craig R.; Sewell, Gavin W.; Rahman, Farooq; Smith, Andrew M.; McCartney, Sara; Bloom, Stuart

doi:10.1002/ibd.21280

Cited by 15 publications

(9 citation statements)

References 125 publications

(151 reference statements)

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“…Reducing the production of IgA has important consequences for the host. For instance sIgA deficient mice show an increase in segmented filamentous bacteria [ 48 ] and in humans it has been associated with the development of inflammatory bowel disease-like inflammation [ 49 ]. It is important to note however that absence of IgA is at least partly compensated by adaptive measures such as an increased production of IgG and IgM antibodies [ 50 ].…”

Section: Mucusmentioning

confidence: 99%

“…Reciprocally, a defect in the immune system may ultimately result in inflammation by weakening of IBF. For instance, inflammatory bowel disease-like inflammation has been described in a number of disorders associated with impaired lymphocyte function in humans [ 49 ]. Mice deficient in multiple components of the mucosal immune system are almost invariably prone to colitis or even develop spontaneous inflammation, including several TLRs and cytokines.…”

Section: Mucosal Immune Systemmentioning

confidence: 99%

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Food Derived Bioactive Peptides and Intestinal Barrier Function

Martínez‐Augustin

Rivero-Gutiérrez

Mascaraque

et al. 2014

IJMS

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A wide range of food-derived bioactive peptides have been shown to exert health-promoting actions and are therefore considered functional foods or nutraceuticals. Some of these actions are related to the maintenance, reinforcement or repairment of the intestinal barrier function (IBF) whose role is to selectively allow the absorption of water, nutrients and ions while preventing the influx of microorganisms from the intestinal lumen. Alterations in the IBF have been related to many disorders, such as inflammatory bowel disease or metabolic syndrome. Components of IBF are the intestinal epithelium, the mucus layer, secretory immunoglobulin A and cells of the innate and adaptive immune systems. Here we review the effects of food derived bioactive peptides on these IBF components. In vitro and in vivo effects, both in healthy and disease states, have been reviewed. Although limited, the available information indicates a potential for food-derived peptides to modify IBF and to contribute to disease treatment, but further research is needed to better isolate responsible peptides, and to help define their mode of action.

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Section: Mucusmentioning

confidence: 99%

Section: Mucosal Immune Systemmentioning

confidence: 99%

Food Derived Bioactive Peptides and Intestinal Barrier Function

Martínez‐Augustin

Rivero-Gutiérrez

Mascaraque

et al. 2014

IJMS

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“…The role of Entamoeba CRT in pathogenicity is less clear. In intestinal amoebiasis, trophozoites are not totally exposed to complement system; apparently, the complement system only crosses to the mucosa membrane in conditions of disease as cancer, inflammatory bowel diseases, or autoimmune inflammatory intestinal diseases [33]. In amoebiasis infection, only in the case of invasive intestinal amoebiasis trophozoites are exposed to serum complement system.…”

Section: Discussionmentioning

confidence: 99%

Entamoeba histolyticaandE. disparCalreticulin: Inhibition of Classical Complement Pathway and Differences in the Level of Expression in Amoebic Liver Abscess

Ximénez

González

Nieves

et al. 2014

BioMed Research International

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The role of calreticulin (CRT) in host-parasite interactions has recently become an important area of research. Information about the functions of calreticulin and its relevance to the physiology of Entamoeba parasites is limited. The present work demonstrates that CRT of both pathogenic E. histolytica and nonpathogenic E. dispar species specifically interacted with human C1q inhibiting the activation of the classical complement pathway. Using recombinant EhCRT protein, we demonstrate that CRT interaction site and human C1q is located at the N-terminal region of EhCRT. The immunofluorescence and confocal microscopy experiments show that CRT and human C1q colocalize in the cytoplasmic vesicles and near to the surface membrane of previously permeabilized trophozoites or are incubated with normal human serum which is known to destroy trophozoites. In the presence of peripheral mononuclear blood cells, the distribution of EhCRT and C1q is clearly over the surface membrane of trophozoites. Nevertheless, the level of expression of CRT in situ in lesions of amoebic liver abscess (ALA) in the hamster model is different in both Entamoeba species; this molecule is expressed in higher levels in E. histolytica than in E. dispar. This result suggests that EhCRT may modulate some functions during the early moments of the host-parasite relationship.

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“…The most commonly described pathogenetic association between SIgAD and IBD concerns primary abnormalities underlying SIgAD: A deficit of IgA, especially the secretory component. On the one hand, a lack of secretory IgA can impair the local immune mechanism in the gut and thus weaken the mucous barrier, which might translate into increased permeability of the mucosa and enhanced exposure to bowel antigens, subsequently leading to sustained inflammation within the gut mucosa [ 286 , 287 ]. The described mechanism might contribute to the development of autoimmunity within the GI tract, which is conclusive with the observation of an increased prevalence of autoimmune diseases in patients with SIgAD [ 40 ].…”

Section: Inflammatory Bowel Disease In Selective Iga Deficiencymentioning

confidence: 99%

Primary Humoral Immune Deficiencies: Overlooked Mimickers of Chronic Immune-Mediated Gastrointestinal Diseases in Adults

Malesza

Krela‐Kaźmierczak

et al. 2020

IJMS

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In recent years, the incidence of immune-mediated gastrointestinal disorders, including celiac disease (CeD) and inflammatory bowel disease (IBD), is increasingly growing worldwide. This generates a need to elucidate the conditions that may compromise the diagnosis and treatment of such gastrointestinal disorders. It is well established that primary immunodeficiencies (PIDs) exhibit gastrointestinal manifestations and mimic other diseases, including CeD and IBD. PIDs are often considered pediatric ailments, whereas between 25 and 45% of PIDs are diagnosed in adults. The most common PIDs in adults are the selective immunoglobulin A deficiency (SIgAD) and the common variable immunodeficiency (CVID). A trend to autoimmunity occurs, while gastrointestinal disorders are common in both diseases. Besides, the occurrence of CeD and IBD in SIgAD/CVID patients is significantly higher than in the general population. However, some differences concerning diagnostics and management between enteropathy/colitis in PIDs, as compared to idiopathic forms of CeD/IBD, have been described. There is an ongoing discussion whether CeD and IBD in CVID patients should be considered a true CeD and IBD or just CeD-like and IBD-like diseases. This review addresses the current state of the art of the most common primary immunodeficiencies in adults and co-occurring CeD and IBD.

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Inflammatory bowel diseases in patients with adaptive and complement immunodeficiency disorders

Cited by 15 publications

References 125 publications

Food Derived Bioactive Peptides and Intestinal Barrier Function

Food Derived Bioactive Peptides and Intestinal Barrier Function

Entamoeba histolyticaandE. disparCalreticulin: Inhibition of Classical Complement Pathway and Differences in the Level of Expression in Amoebic Liver Abscess

Primary Humoral Immune Deficiencies: Overlooked Mimickers of Chronic Immune-Mediated Gastrointestinal Diseases in Adults

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