Gastroduodenal Injury: Role of Protective Factors

Galura, Gian; Chavez, Luis; Robles, Alejandro; McCallum, Richard W.

doi:10.1007/s11894-019-0701-x

Cited by 23 publications

(13 citation statements)

References 36 publications

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“…The ingestion of ethanol causes microvascular endothelium impairment, reduces gastric mucosal blood flow (GMBF), and weakens the mucosal resistance, making it susceptible to damaging factors, even heightening the intensity of gastric damage [ 42 ]. Continuous blood flow lined with endothelial cells forms an endothelial “barrier” in gastric stomach [ 43 ]. In addition, nitric oxide (NO) and prostaglandin E2 (PGE2), which are endogenous molecules, are described as the second major mucosal defense mechanism, regulating the gastric mucosal acidity [ 44 , 45 ].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Wheat Peptides against Ethanol-Induced Gastric Mucosal Lesions in Rats: Vasodilation and Anti-Inflammation

Liu

et al. 2020

Nutrients

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Alcohol consumption increases the risk of gastritis and gastric ulcer. Nutritional alternatives are considered for relieving the progression of gastric mucosal lesions instead of conventional drugs that produce side effects. This study was designed to evaluate the gastroprotective effects and investigate the defensive mechanisms of wheat peptides against ethanol-induced acute gastric mucosal injury in rats. Sixty male Sprague–Dawley rats were divided into six groups and orally treated with wheat peptides (0.1, 0.2, 0.4 g/kgbw) and omeprazole (20 mg/kgbw) for 4 weeks, following absolute ethanol administration for 1 h. Pretreatment with wheat peptides obviously enhanced the vasodilation of gastric mucosal blood vessels via improving the gastric mucosal blood flow and elevating the defensive factors nitric oxide (NO) and prostaglandin E2 (PGE2), and lowering the level of vasoconstrictor factor endothelin (ET)-1. Wheat peptides exhibited anti-inflammatory reaction through decreasing inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, and increasing trefoil factor 1 (TFF1) levels. Moreover, wheat peptides significantly down-regulated the expression of phosphorylated nuclear factor kappa-B (p-NF-κB) p65 proteins in the NF-κB signaling pathway. Altogether, wheat peptides protect gastric mucosa from ethanol-induced lesions in rats via improving the gastric microcirculation and inhibiting inflammation mediated by the NF-κB signaling transduction pathway.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Wheat Peptides against Ethanol-Induced Gastric Mucosal Lesions in Rats: Vasodilation and Anti-Inflammation

Liu

et al. 2020

Nutrients

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“…Host tissue repair would be advantageous for the parasite, as helminth survival depends on the host’s survival. TFF proteins are also critical for mucosal tissue repair [51], and may act upstream or in parallel with type 2 immune responses. Although our work in mouse models of hookworm infection suggests that both TFF2 and TFF3 contribute to worm clearance, tissue repair, and the suppression of proinflammatory cytokines [32-35], we found that TFF2 is specifically increased in the context of human hookworm infection and can reduce secretion of proinflammatory cytokine by human PMBCs.…”

Section: Discussionmentioning

confidence: 99%

Parasitic helminth infections in humans modulate Trefoil Factor levels in a manner dependent on the species of parasite and age of the host

Adewale

Pastore

Rossi

et al. 2021

Preprint

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Helminth infections, including hookworms and Schistosomes, can cause severe disability and death. Infection management and control would benefit from identification of biomarkers for early detection and prognosis. While animal models suggest that Trefoil Factor Family proteins (TFF2 and TFF3) and interleukin-33 (IL-33)-driven type 2 immune responses are critical mediators of tissue repair and worm clearance in the context of hookworm infection, very little is known about how they are modulated in the context of human helminth infection. We measured TFF2, TFF3, and IL-33 levels in serum from patients in Brazil infected with Hookworm and/or Schistosomes, and compared them to endemic and non-endemic controls. TFF2 was specifically elevated by Hookworm infection, not Schistosoma or co-infection. This elevation was more strongly correlated with age than with worm burden. To determine if this might apply more broadly to other species or regions, we measured TFFs and cytokine levels in both the serum and urine of Nigerian school children infected with S. haematobium. We found that serum levels of TFF2 and 3 were reduced by infection, but urine cytokine levels were increased (IL-1β, TNFα, IL-13, and IL-10). Finally, to determine if TFF2 and 3 might have immunosuppressive effects, we treated stimulated or unstimulated PMBCs with recombinant human TFF2 or TFF3 and measured proinflammatory cytokine levels. We found that rhTFF2, but not rhTFF3, was able to suppress TNF alpha and IFN gamma release from stimulated human PMBCs. Taken together, these data support a role for TFF proteins in human helminth infection.

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“…The factors which permit ulcers to persist are unknown, but healing (restitution) of wounds in epithelial monolayers in vitro has been well studied. Once a monolayer is wounded, cell migration from the margins, accompanied by increased cell turnover, permits the breach to be covered and integrity to be restored [26]. In vivo, injury is associated by dedifferentiation and emergence of injuryassociated cell types, including surface mucosal cells, ulcer-associated cells, mucosal neck cells, spasmolytic polypeptide-expressing metaplasia (SPEM), and pyloric metaplasia [27].…”

Section: Gastrointestinal Repair Mechanismsmentioning

confidence: 99%

Colostrum Therapy for Human Gastrointestinal Health and Disease

Chandwe

Kelly

2021

Nutrients

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There is increasing awareness that a broad range of gastrointestinal diseases, and some systemic diseases, are characterized by failure of the mucosal barrier. Bovine colostrum is a complex biological fluid replete with growth factors, nutrients, hormones, and paracrine factors which have a range of properties likely to contribute to mucosal healing in a wide range of infective, inflammatory, and injury conditions. In this review, we describe the anatomy and physiology of the intestinal barrier and how it may fail. We survey selected diseases in which disordered barrier function contributes to disease pathogenesis or progression, and review the evidence for or against efficacy of bovine colostrum in management. These disorders include enteropathy due to non-steroidal anti-inflammatory drugs (NSAIDs), inflammatory bowel disease (IBD), necrotizing enterocolitis, infectious diarrhea, intestinal failure, and damage due to cancer therapy. In animal models, bovine colostrum benefits NSAID enteropathy, IBD, and intestinal failure. In human trials, there is substantial evidence of efficacy of bovine colostrum in inflammatory bowel disease and in infectious diarrhea. Given the robust scientific rationale for using bovine colostrum as a promoter of mucosal healing, further work is needed to define its role in therapy.

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Gastroduodenal Injury: Role of Protective Factors

Cited by 23 publications

References 36 publications

Protective Effects of Wheat Peptides against Ethanol-Induced Gastric Mucosal Lesions in Rats: Vasodilation and Anti-Inflammation

Protective Effects of Wheat Peptides against Ethanol-Induced Gastric Mucosal Lesions in Rats: Vasodilation and Anti-Inflammation

Parasitic helminth infections in humans modulate Trefoil Factor levels in a manner dependent on the species of parasite and age of the host

Colostrum Therapy for Human Gastrointestinal Health and Disease

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