Proteomics

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Synthetic Siglec-9 agonists inhibit neutrophil activation associated with COVID-19


ABSTRACT: Severe cases of coronavirus disease 2019 (COVID-19) are characterized by a hyperinflammatory immune response that leads to numerous complications. Production of proinflammatory neutrophil extracellular traps (NETs) has been suggested to be a key factor in inducing a hyperinflammatory signaling cascade, allegedly causing both pulmonary tissue damage and peripheral inflammation. If true, finding ways to inhibit NET production could provide therapeutic strategies to prevent respiratory damage and death from SARS-CoV-2 related inflammation. Here, we demonstrate that synthetic glycopolymers that activate signaling of the neutrophil checkpoint receptor Siglec-9 suppress NETosis induced by agonists of viral TLR receptors and COVID-19 plasma. Thus, Siglec-9 represents an attractive therapeutic target to curb neutrophilic hyperinflammation in COVID-19.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Neutrophil

DISEASE(S): Covid-19

SUBMITTER: Nicholas Riley  

LAB HEAD: Carolyn Bertozzi

PROVIDER: PXD022990 | Pride | 2021-07-28

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
2020_11_24_NeutPolymer_IMAC_1.raw Raw
2020_11_24_NeutPolymer_IMAC_2.raw Raw
2020_11_24_NeutPolymer_IMAC_3.raw Raw
2020_11_24_NeutPolymer_Prot_1.raw Raw
2020_11_24_NeutPolymer_Prot_2.raw Raw
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Publications

Synthetic Siglec-9 Agonists Inhibit Neutrophil Activation Associated with COVID-19.

Delaveris Corleone S CS   Wilk Aaron J AJ   Riley Nicholas M NM   Stark Jessica C JC   Yang Samuel S SS   Rogers Angela J AJ   Ranganath Thanmayi T   Nadeau Kari C KC   Blish Catherine A CA   Bertozzi Carolyn R CR  

ChemRxiv : the preprint server for chemistry 20201217


Severe cases of coronavirus disease 2019 (COVID-19), caused by infection with SARS-Cov-2, are characterized by a hyperinflammatory immune response that leads to numerous complications. Production of proinflammatory neutrophil extracellular traps (NETs) has been suggested to be a key factor in inducing a hyperinflammatory signaling cascade, allegedly causing both pulmonary tissue damage and peripheral inflammation. Accordingly, therapeutic blockage of neutrophil activation and NETosis, the cell d  ...[more]

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