Crohn's disease

Ballester, María Pilar; Boscá-Watts, Marta Maia; Pérez, Manuel Asensi

doi:10.1016/j.medcle.2018.05.006

Cited by 20 publications

(22 citation statements)

References 67 publications

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“…CD has unknown etiology associated with an impaired immune response. It is characterized by periods of activity and remission and shows patchy and transmural lesions which can affect the entire gastrointestinal tract [ 7 ]. UC is another chronic inflammatory bowel disease that affects the colon and rectum and like CD its etiology is unknown.…”

Section: Tissue Hypoxia: Pathological Consequencesmentioning

confidence: 99%

Hypoxia: molecular pathophysiological mechanisms in human diseases

et al. 2022

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Hypoxia, a low O2 tension, is a fundamental feature that occurs in physiological events as well as pathophysiological conditions, especially mentioned for its role in the mechanism of angiogenesis, glucose metabolism, and cell proliferation/survival. The hypoxic state through the activation of specific mechanisms is an aggravating circumstance commonly noticed in multiple sclerosis, cancer, heart disease, kidney disease, liver disease, lung disease, and in inflammatory bowel disease. On the other hand, hypoxia could play a key role in tissue regeneration and repair of damaged tissues, especially by acting on specific tissue stem cells, but their features may result as a disadvantage when it is concerned for neoplastic stem cells. Furthermore, hypoxia could also have a potential role in tissue engineering and regenerative medicine due to its capacity to improve the performance of biomaterials. The current review aims to highlight the hypoxic molecular mechanisms reported in different pathological conditions to provide an overview of hypoxia as a therapeutic agent in regenerative and molecular therapy. Graphical abstract

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Section: Tissue Hypoxia: Pathological Consequencesmentioning

confidence: 99%

Hypoxia: molecular pathophysiological mechanisms in human diseases

et al. 2022

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“…Inflammatory bowel diseases (IBD) is an umbrella term that comprises the chronic inflammatory conditions of gastrointestinal tract, which are categorized as Crohn's disease (CD) and ulcerative colitis (UC) [1,2].…”

Section: Introductionmentioning

confidence: 99%

“…Though the exact mechanisms underlying the pathophysiology of UC are not clearly understood, it is a multifactorial disease where an interplay between environmental factors and genetic susceptibility, together with a dysregulated immune response, could be the major cause for the onset of this inflammatory condition [3,4]. CD is categorized as inappropriate immune response of Th1 pathway and involvement of various mechanisms in different periods of disease progression [1]. UC is associated with impairment of gut barrier integrity [5], inflammatory and immune responses in the mucosa, and elevated oxidative stress [6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Nerolidol Mitigates Colonic Inflammation: An Experimental Study Using both In Vivo and In Vitro Models

et al. 2020

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Nerolidol (NED) is a naturally occurring sesquiterpene alcohol present in various plants with potent anti-inflammatory effects. In the current study, we investigated NED as a putative anti-inflammatory compound in an experimental model of colonic inflammation. C57BL/6J male black mice (C57BL/6J) were administered 3% dextran sodium sulfate (DSS) in drinking water for 7 days to induce colitis. Six groups received either vehicle alone or DSS alone or DSS with oral NED (50, 100, and 150 mg/kg body weight/day by oral gavage) or DSS with sulfasalazine. Disease activity index (DAI), colonic histology, and biochemical parameters were measured. TNF-α-treated HT-29 cells were used as in vitro model of colonic inflammation to study NED (25 µM and 50 µM). NED significantly decreased the DAI and reduced the inflammation-associated changes in colon length as well as macroscopic and microscopic architecture of the colon. Changes in tissue Myeloperoxidase (MPO) concentrations, neutrophil and macrophage mRNA expression (CXCL2 and CCL2), and proinflammatory cytokine content (IL-1β, IL-6, and TNF-α) both at the protein and mRNA level were significantly reduced by NED. The increase in content of the proinflammatory enzymes, COX-2 and iNOS induced by DSS were also significantly inhibited by NED along with tissue nitrate levels. NED promoted Nrf2 nuclear translocation dose dependently. NED significantly increased antioxidant enzymes activity (Superoxide dismutase (SOD) and Catalase (CAT)), Hemeoxygenase-1 (HO-1), and SOD3 mRNA levels. NED treatment in TNF-α-challenged HT-29 cells significantly decreased proinflammatory chemokines (CXCL1, IL-8, CCL2) and COX-2 mRNA levels. NED supplementation attenuates colon inflammation through its potent antioxidant and anti-inflammatory activity both in in vivo and in vitro models of colonic inflammation.

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“…Aluminium, a neurotoxicant that affects diverse metabolic reactions, can enter and accumulate in the brain from the systemic circulation or the site of absorption (Igbokwe et al, 2019 ), has been proven to be involved in aluminium‐mediated neurodegeneration resulting in cognitive dysfunction, and may cause Alzheimer's disease (Yokel et al, 2002 ). Additionally, aluminium has been suspected as an adjuvant for the induction of Crohn's disease (Lerner, 2012 ), a highly debilitating disease characterized by excessive uncontrolled intestinal inflammation (Ballester Ferré et al, 2018 ). Recently, it has been demonstrated that ingestion of excessive aluminium worsened intestinal inflammation in mice with chemical induction (Djouina et al, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

Dietary aluminium intake disrupts the overall structure of gut microbiota in Wistar rats

Wang

Cui

et al. 2022

Food Science & Nutrition

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Approximately, 40% of ingested dietary aluminium accumulates in the intestine, which has been considered a target organ for dietary aluminium exposure. The gut microbiota may be the first protective barrier against the toxic metal aluminium and a crucial mediator of the bioavailability of metal aluminium. We previously evaluated dietary aluminium intake and its health risks in a population from Jilin Province, China, and found that the average daily intake of aluminium in the diet of residents in Jilin Province was 0.163 mg/kg after the total diet survey. In the present study, the equivalent concentration of aluminium in rats was extrapolated by the average dietary aluminium intake in the population of Jilin Province based on body surface area. Furthermore, healthy adult Wistar rats were randomly divided into four groups (n = 15 for each group): a control group and three groups treated with aluminium solution (1, 10, and 100 mg/kg/day, intragastrically) for 28 days. Following treatment, necrosis of renal tubular epithelial cells, hyperplasia of bile ducts and hyperplasia of heart tissue, as well as fiber in the liver, kidney, and heart tissues of aluminium‐treated rats were observed, although there were no significant changes in the spleen and brain. Subsequently, fecal samples were withdrawn for 16S rRNA gene sequence analysis. It was found that aluminium decreased the microbiota diversity and changed the overall community structure of the gut microbiota, including three phyla and four genera, together with the regulation of 12 signaling pathways. Collectively, treatment with aluminium markedly altered the structure of the gut microbiota, suggesting that the disorders of intestinal flora induced by aluminium may be an important mechanism for aluminium toxicity.

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Crohn's disease

Cited by 20 publications

References 67 publications

Hypoxia: molecular pathophysiological mechanisms in human diseases

Hypoxia: molecular pathophysiological mechanisms in human diseases

Nerolidol Mitigates Colonic Inflammation: An Experimental Study Using both In Vivo and In Vitro Models

Dietary aluminium intake disrupts the overall structure of gut microbiota in Wistar rats

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