Rui Qin, Emma Kurz, Shuhui Chen, Briana Zeck, Luis Chiribogas, Dana Jackson, Alex Herchen, Tyson Attia, Michael Carlock, Amy Rapkiewicz, Dafna Bar-Sagi, Bruce Ritchie, Ted M Ross, Lara K Mahal
{"title":"α2,6-Sialylation在严重COVID-19中上调，暗示着补体级联。","authors":"Rui Qin, Emma Kurz, Shuhui Chen, Briana Zeck, Luis Chiribogas, Dana Jackson, Alex Herchen, Tyson Attia, Michael Carlock, Amy Rapkiewicz, Dafna Bar-Sagi, Bruce Ritchie, Ted M Ross, Lara K Mahal","doi":"10.1101/2022.06.06.22275981","DOIUrl":null,"url":null,"abstract":"<p><p>Better understanding of the mechanisms of COVID-19 severity is desperately needed in current times. Although hyper-inflammation drives severe COVID-19, precise mechanisms triggering this cascade and what role glycosylation might play therein is unknown. Here we report the first high-throughput glycomic analysis of COVID-19 plasma samples and autopsy tissues. We find α2,6-sialylation is upregulated in plasma of patients with severe COVID-19 and in the lung. This glycan motif is enriched on members of the complement cascade, which show higher levels of sialylation in severe COVID-19. In the lung tissue, we observe increased complement deposition, associated with elevated α2,6-sialylation levels, corresponding to elevated markers of poor prognosis (IL-6) and fibrotic response. We also observe upregulation of the α2,6-sialylation enzyme ST6GAL1 in patients who succumbed to COVID-19. Our work identifies a heretofore undescribed relationship between sialylation and complement in severe COVID-19, potentially informing future therapeutic development.</p>","PeriodicalId":35161,"journal":{"name":"Comparative Strategy","volume":"24 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9196116/pdf/","citationCount":"0","resultStr":"{\"title\":\"α2,6-Sialylation is Upregulated in Severe COVID-19 Implicating the Complement Cascade.\",\"authors\":\"Rui Qin, Emma Kurz, Shuhui Chen, Briana Zeck, Luis Chiribogas, Dana Jackson, Alex Herchen, Tyson Attia, Michael Carlock, Amy Rapkiewicz, Dafna Bar-Sagi, Bruce Ritchie, Ted M Ross, Lara K Mahal\",\"doi\":\"10.1101/2022.06.06.22275981\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Better understanding of the mechanisms of COVID-19 severity is desperately needed in current times. Although hyper-inflammation drives severe COVID-19, precise mechanisms triggering this cascade and what role glycosylation might play therein is unknown. Here we report the first high-throughput glycomic analysis of COVID-19 plasma samples and autopsy tissues. We find α2,6-sialylation is upregulated in plasma of patients with severe COVID-19 and in the lung. This glycan motif is enriched on members of the complement cascade, which show higher levels of sialylation in severe COVID-19. In the lung tissue, we observe increased complement deposition, associated with elevated α2,6-sialylation levels, corresponding to elevated markers of poor prognosis (IL-6) and fibrotic response. We also observe upregulation of the α2,6-sialylation enzyme ST6GAL1 in patients who succumbed to COVID-19. Our work identifies a heretofore undescribed relationship between sialylation and complement in severe COVID-19, potentially informing future therapeutic development.</p>\",\"PeriodicalId\":35161,\"journal\":{\"name\":\"Comparative Strategy\",\"volume\":\"24 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-06-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9196116/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Comparative Strategy\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1101/2022.06.06.22275981\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Social Sciences\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Comparative Strategy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2022.06.06.22275981","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Social Sciences","Score":null,"Total":0}
α2,6-Sialylation is Upregulated in Severe COVID-19 Implicating the Complement Cascade.
Better understanding of the mechanisms of COVID-19 severity is desperately needed in current times. Although hyper-inflammation drives severe COVID-19, precise mechanisms triggering this cascade and what role glycosylation might play therein is unknown. Here we report the first high-throughput glycomic analysis of COVID-19 plasma samples and autopsy tissues. We find α2,6-sialylation is upregulated in plasma of patients with severe COVID-19 and in the lung. This glycan motif is enriched on members of the complement cascade, which show higher levels of sialylation in severe COVID-19. In the lung tissue, we observe increased complement deposition, associated with elevated α2,6-sialylation levels, corresponding to elevated markers of poor prognosis (IL-6) and fibrotic response. We also observe upregulation of the α2,6-sialylation enzyme ST6GAL1 in patients who succumbed to COVID-19. Our work identifies a heretofore undescribed relationship between sialylation and complement in severe COVID-19, potentially informing future therapeutic development.
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