{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Keshari RS"],"funding":["HHS | NIH | National Institute of General Medical Sciences","HHS | NIH | National Institute of Allergy and Infectious Diseases"],"pagination":["e2104347118"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8449412"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["118(37)"],"pubmed_abstract":["Late-stage anthrax infections are characterized by dysregulated immune responses and hematogenous spread of Bacillus anthracis, leading to extreme bacteremia, sepsis, multiple organ failure, and, ultimately, death. Despite the bacterium being nonhemolytic, some fulminant anthrax patients develop a secondary atypical hemolytic uremic syndrome (aHUS) through unknown mechanisms. We recapitulated the pathology in baboons challenged with cell wall peptidoglycan (PGN), a polymeric, pathogen-associated molecular pattern responsible for the hemostatic dysregulation in anthrax sepsis. Similar to aHUS anthrax patients, PGN induces an initial hematocrit elevation followed by progressive hemolytic anemia and associated renal failure. Etiologically, PGN induces erythrolysis through direct excessive act"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Complement C5 inhibition protects against hemolytic anemia and acute kidney injury in anthrax peptidoglycan-induced sepsis in baboons."],"pmcid":["PMC8449412"],"funding_grant_id":["U19AI062629","GM122775","GM121601","AI157037"],"pubmed_authors":["Regmi G","Lupu F","Ricardo A","Popescu NI","Silasi R","Lupu C","Simmons JH","Coggeshall KM","Keshari RS"],"additional_accession":[]},"is_claimable":false,"name":"Complement C5 inhibition protects against hemolytic anemia and acute kidney injury in anthrax peptidoglycan-induced sepsis in baboons.","description":"Late-stage anthrax infections are characterized by dysregulated immune responses and hematogenous spread of Bacillus anthracis, leading to extreme bacteremia, sepsis, multiple organ failure, and, ultimately, death. Despite the bacterium being nonhemolytic, some fulminant anthrax patients develop a secondary atypical hemolytic uremic syndrome (aHUS) through unknown mechanisms. We recapitulated the pathology in baboons challenged with cell wall peptidoglycan (PGN), a polymeric, pathogen-associated molecular pattern responsible for the hemostatic dysregulation in anthrax sepsis. Similar to aHUS anthrax patients, PGN induces an initial hematocrit elevation followed by progressive hemolytic anemia and associated renal failure. Etiologically, PGN induces erythrolysis through direct excessive act","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2025-05-31T23:31:34.342Z","creation":"2025-05-31T23:31:34.342Z"},"accession":"S-EPMC8449412","cross_references":{"pubmed":["34507997"],"doi":["10.1073/pnas.2104347118"]}}