tetano
Editor, Senior Moderator
JCI Insight
. 2021 Jul 9;151551.
doi: 10.1172/jci.insight.151551. Online ahead of print.
SARS-CoV-2 infection of the pancreas promotes thrombo-fibrosis and is associated with new-onset diabetes
Mirza Muhammad Fahd Qadir[SUP] 1 [/SUP], Manika Bhondeley[SUP] 1 [/SUP], Wandy Beatty[SUP] 2 [/SUP], Dina D Gaupp[SUP] 3 [/SUP], Lara A Doyle-Meyers[SUP] 4 [/SUP], Tracy Fischer[SUP] 4 [/SUP], Ishitri Bandyopadhyay[SUP] 1 [/SUP], Robert V Blair[SUP] 4 [/SUP], Rudolf Bohm[SUP] 4 [/SUP], Jay Rappaport[SUP] 4 [/SUP], Eric Lazartigues[SUP] 5 [/SUP], Richard S Vander Heide[SUP] 6 [/SUP], Jay K Kolls[SUP] 7 [/SUP], Xuebin Qin[SUP] 4 [/SUP], Franck Mauvais-Jarvis[SUP] 1 [/SUP]
Affiliations
Abstract
Evidence suggests an association between severe acute respiratory syndrome-cornavirus-2 (SARS-CoV-2) infection and the occurrence of new-onset diabetes. We examined pancreatic expression of angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2), the cell entry factors for SARS-CoV-2, using public single cell RNA sequencing datasets, and pancreas tissue from control male and female non-human primates (NHPs) and humans. We also examined SARS-CoV-2 immunolocalization in pancreas cells of SARS-CoV-2-infected NHPs, and patients deceased from coronavirus disease 2019 (COVID-19). We report expression of ACE2 in pancreatic islet, ductal, and endothelial cells in NHPs and humans. In pancreata from SARS-CoV-2-infected NHPs and COVID-19 patients, SARS-CoV-2 infected ductal, endothelial and islet cells. These pancreata also exhibited generalized fibrosis associated with multiple vascular thrombi. Two out of eight NHPs developed new onset diabetes following SARS-CoV-2 infection. Two out of five COVID-19 patients exhibited new onset diabetes at admission. These results suggest that SARS-CoV-2 infection of the pancreas may promote acute and especially chronic pancreatic dysfunction that could potentially lead to new-onset diabetes.
Keywords: COVID-19; Diabetes; Endothelial cells; Thrombosis.
. 2021 Jul 9;151551.
doi: 10.1172/jci.insight.151551. Online ahead of print.
SARS-CoV-2 infection of the pancreas promotes thrombo-fibrosis and is associated with new-onset diabetes
Mirza Muhammad Fahd Qadir[SUP] 1 [/SUP], Manika Bhondeley[SUP] 1 [/SUP], Wandy Beatty[SUP] 2 [/SUP], Dina D Gaupp[SUP] 3 [/SUP], Lara A Doyle-Meyers[SUP] 4 [/SUP], Tracy Fischer[SUP] 4 [/SUP], Ishitri Bandyopadhyay[SUP] 1 [/SUP], Robert V Blair[SUP] 4 [/SUP], Rudolf Bohm[SUP] 4 [/SUP], Jay Rappaport[SUP] 4 [/SUP], Eric Lazartigues[SUP] 5 [/SUP], Richard S Vander Heide[SUP] 6 [/SUP], Jay K Kolls[SUP] 7 [/SUP], Xuebin Qin[SUP] 4 [/SUP], Franck Mauvais-Jarvis[SUP] 1 [/SUP]
Affiliations
- PMID: 34241597
- DOI: 10.1172/jci.insight.151551
Abstract
Evidence suggests an association between severe acute respiratory syndrome-cornavirus-2 (SARS-CoV-2) infection and the occurrence of new-onset diabetes. We examined pancreatic expression of angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2), the cell entry factors for SARS-CoV-2, using public single cell RNA sequencing datasets, and pancreas tissue from control male and female non-human primates (NHPs) and humans. We also examined SARS-CoV-2 immunolocalization in pancreas cells of SARS-CoV-2-infected NHPs, and patients deceased from coronavirus disease 2019 (COVID-19). We report expression of ACE2 in pancreatic islet, ductal, and endothelial cells in NHPs and humans. In pancreata from SARS-CoV-2-infected NHPs and COVID-19 patients, SARS-CoV-2 infected ductal, endothelial and islet cells. These pancreata also exhibited generalized fibrosis associated with multiple vascular thrombi. Two out of eight NHPs developed new onset diabetes following SARS-CoV-2 infection. Two out of five COVID-19 patients exhibited new onset diabetes at admission. These results suggest that SARS-CoV-2 infection of the pancreas may promote acute and especially chronic pancreatic dysfunction that could potentially lead to new-onset diabetes.
Keywords: COVID-19; Diabetes; Endothelial cells; Thrombosis.