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10.1053/j.gastro.2021.02.056

http://scihub22266oqcxt.onion/10.1053/j.gastro.2021.02.056
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suck abstract from ncbi


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pmid33676971      Gastroenterology 2021 ; 160 (7): 2435-2450.e34
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  • Intestinal Host Response to SARS-CoV-2 Infection and COVID-19 Outcomes in Patients With Gastrointestinal Symptoms #MMPMID33676971
  • Livanos AE; Jha D; Cossarini F; Gonzalez-Reiche AS; Tokuyama M; Aydillo T; Parigi TL; Ladinsky MS; Ramos I; Dunleavy K; Lee B; Dixon RE; Chen ST; Martinez-Delgado G; Nagula S; Bruce EA; Ko HM; Glicksberg BS; Nadkarni G; Pujadas E; Reidy J; Naymagon S; Grinspan A; Ahmad J; Tankelevich M; Bram Y; Gordon R; Sharma K; Houldsworth J; Britton GJ; Chen-Liaw A; Spindler MP; Plitt T; Wang P; Cerutti A; Faith JJ; Colombel JF; Kenigsberg E; Argmann C; Merad M; Gnjatic S; Harpaz N; Danese S; Cordon-Cardo C; Rahman A; Schwartz RE; Kumta NA; Aghemo A; Bjorkman PJ; Petralia F; van Bakel H; Garcia-Sastre A; Mehandru S
  • Gastroenterology 2021[Jun]; 160 (7): 2435-2450.e34 PMID33676971show ga
  • BACKGROUND & AIMS: Given that gastrointestinal (GI) symptoms are a prominent extrapulmonary manifestation of COVID-19, we investigated intestinal infection with SARS-CoV-2, its effect on pathogenesis, and clinical significance. METHODS: Human intestinal biopsy tissues were obtained from patients with COVID-19 (n = 19) and uninfected control individuals (n = 10) for microscopic examination, cytometry by time of flight analyses, and RNA sequencing. Additionally, disease severity and mortality were examined in patients with and without GI symptoms in 2 large, independent cohorts of hospitalized patients in the United States (N = 634) and Europe (N = 287) using multivariate logistic regressions. RESULTS: COVID-19 case patients and control individuals in the biopsy cohort were comparable for age, sex, rates of hospitalization, and relevant comorbid conditions. SARS-CoV-2 was detected in small intestinal epithelial cells by immunofluorescence staining or electron microscopy in 15 of 17 patients studied. High-dimensional analyses of GI tissues showed low levels of inflammation, including down-regulation of key inflammatory genes including IFNG, CXCL8, CXCL2, and IL1B and reduced frequencies of proinflammatory dendritic cells compared with control individuals. Consistent with these findings, we found a significant reduction in disease severity and mortality in patients presenting with GI symptoms that was independent of sex, age, and comorbid illnesses and despite similar nasopharyngeal SARS-CoV-2 viral loads. Furthermore, there was reduced levels of key inflammatory proteins in circulation in patients with GI symptoms. CONCLUSIONS: These data highlight the absence of a proinflammatory response in the GI tract despite detection of SARS-CoV-2. In parallel, reduced mortality in patients with COVID-19 presenting with GI symptoms was observed. A potential role of the GI tract in attenuating SARS-CoV-2-associated inflammation needs to be further examined.
  • |*Immunity, Mucosal[MESH]
  • |Aged[MESH]
  • |Aged, 80 and over[MESH]
  • |COVID-19/diagnosis/immunology/mortality/*virology[MESH]
  • |Case-Control Studies[MESH]
  • |Cells, Cultured[MESH]
  • |Cytokines/blood[MESH]
  • |Female[MESH]
  • |Gastrointestinal Diseases/diagnosis/immunology/mortality/*virology[MESH]
  • |Host-Pathogen Interactions[MESH]
  • |Humans[MESH]
  • |Inflammation Mediators/blood[MESH]
  • |Intestinal Mucosa/immunology/*virology[MESH]
  • |Italy[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |New York City[MESH]
  • |Prognosis[MESH]
  • |Risk Assessment[MESH]
  • |Risk Factors[MESH]
  • |SARS-CoV-2/immunology/*pathogenicity[MESH]


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