Age, Inflammation, and Disease Location Are Critical Determinants of Intestinal Expression of SARS-CoV-2 Receptor ACE2 and TMPRSS2 in Inflammatory Bowel Disease

Nowak, Jan Krzysztof; Lindstrøm, Jonas Christoffer; Kalla, Rahul; Ricanek, Petr; Halfvarson, Jonas; Satsangi, Jack

doi:10.1053/j.gastro.2020.05.030

Cited by 61 publications

(72 citation statements)

References 5 publications

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“…There are conflicting data on changes in the expression of ACE-2 in ileal and colonic mucosa of patients with active IBD. 3,4 In addition, the therapeutic agents used in IBD could affect ACE-2 expression. 4 Therefore, a complex interplay of receptors, physiological processes and therapies may define the risk of acquisition and clinical outcomes in these patients.…”

Section: Introductionmentioning

confidence: 99%

Risk and outcomes of coronavirus disease in patients with inflammatory bowel disease: A systematic review and meta‐analysis

et al. 2021

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Background The risk of severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) infection and clinical outcomes of coronavirus disease (COVID-19) in inflammatory bowel disease are unclear. Methods We searched PubMed and Embase with the keywords: inflammatory bowel disease, Crohn’s disease, ulcerative colitis and COVID-19, novel coronavirus and SARS-CoV-2. We included studies reporting the frequency of COVID-19 infection and outcomes (hospitalisation, need for intensive care unit care and mortality) in patients with inflammatory bowel disease. We estimated the pooled incidence of COVID-19 in inflammatory bowel disease and comparative risk vis-a-vis the general population. We also estimated the pooled frequency of outcomes and compared them in patients who received and did not receive drugs for inflammatory bowel disease. Results Twenty-four studies were included. The pooled incidence rate of COVID-19 per 1000 patients of inflammatory bowel disease and the general population were 4.02 (95% confidence interval (CI) 1.44–11.17) and 6.59 (3.25–13.35), respectively, with no increase in relative risk (0.47, 0.18–1.26) in inflammatory bowel disease. The relative risk of the acquisition of COVID-19 was not different between ulcerative colitis and Crohn’s disease (1.03, 0.62–1.71). The pooled proportion of COVID-19-positive inflammatory bowel disease patients requiring hospitalisation and intensive care unit care was 27.29% and 5.33% while pooled mortality was 4.27%. The risk of adverse outcomes was higher in ulcerative colitis compared to Crohn’s disease. The relative risks of hospitalisation, intensive care unit admission and mortality were lower for patients on biological agents (0.34, 0.19–0.61; 0.49, 0.33–0.72 and 0.22, 0.13–0.38, respectively) but higher with steroids (1.99, 1.64–2.40; 3.41, 2.28–5.11 and 2.70, 1.61–4.55) or 5-aminosalicylate (1.59, 1.39–1.82; 2.38, 1.26–4.48 and 2.62, 1.67–4.11) use. Conclusion SARS-CoV-2 infection risk in patients with inflammatory bowel disease is comparable to the general population. Outcomes of COVID-19-positive inflammatory bowel disease patients are worse in ulcerative colitis, those on steroids or 5-aminosalicylates but outcomes are better with biological agents.

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Section: Introductionmentioning

confidence: 99%

Risk and outcomes of coronavirus disease in patients with inflammatory bowel disease: A systematic review and meta‐analysis

et al. 2021

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“…It was shown that the susceptibility to the SARS-CoV-2-inflicted GI damage of the inflammatory bowel disease (IBD) patients is determined by the dysregulated mucosal ACE2 and TMPRSS2 expression in the colon and ileum in IBD [186]. This deregulation was further enhanced by advanced age, smoking, and active disease that served as potential additional risk factors defining the vulnerability of IBD patients to COVID-19 through alterations of receptor expression [186].…”

Section: Peripheral Nerve or Neuronal Retrograde Route: Accessing Cnsmentioning

confidence: 99%

SARS-CoV-2 Infection Reaches the Human Nervous System: How?

Uversky¹,

Elrashdy²,

Aljadawi³

et al. 2020

Preprint

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Without protective and/or therapeutic agents the SARS-CoV-2 infection known as coronavirus disease 2019 (COVID-19) is quickly spreading worldwide. It has surprising transmissibility potential, since it could infect all ages, gender, and human sectors. It attacks respiratory, gastrointestinal, urinary, hepatic, and endovascular systems and can reach the peripheral nervous system (PNS) and central nervous system (CNS) through known and unknown mechanisms. The reports on the neurological manifestations and complications of the SARS-CoV-2 infection are increasing exponentially. Herein, we enumerate seven candidate routes, which the mature or immature SARS-CoV-2 components could use to reach the CNS and PNS, utilizing the within-body crosstalk between organs. The majority of SARS-CoV-2 infected patients suffer from some neurological manifestations (e.g., confusion, anosmia, and ageusia). It seems that although the mature virus did not reach the CNS or PNS of the majority of patients, its unassembled components and/or the accompanying immune-mediated responses may be responsible for the observed neurological symptoms. The viral particles and/or its components have been specifically documented in endothelial cells of lung, kidney, skin, and CNS. This means that the blood-endothelial-barrier may be considered as the main route for SARS-CoV-2 entry into the nervous system, with the barrier disruption being more logical than barrier permeability, as evidenced by postmortem analyses.

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“…Авторы считают, что это свидетельствует, во-первых, в пользу системного воспалительного ответа, запускаемого SARS-CoV-2, который, по-видимому, протекает в 2 волны (на первой идет активное вирусовыделение, но симптоматика не выражена, на второй -симптомы определяются воспалительными изменениями в разных органах и системах -«цитокиновым штормом», но вирусовыделение в этот момент уже может минимизироваться), а во-вторых, в пользу применения антицитокиновой терапии. Кстати, у пациентов с ВЗК в фазе активного воспаления (без лечения) уровни ACE2 резко повышены, что делает их уязвимыми для SARS-CoV-2в отличие от пациентов с БА и аллергией [34].…”

Section: иммуногенез/патогенезunclassified