<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Bostanci N</submitter><funding>National Institute of Allergy and Infectious Diseases</funding><funding>NIDCR NIH HHS</funding><funding>FP7 Health</funding><funding>NIAID NIH HHS</funding><funding>National Institute of Dental and Craniofacial Research</funding><pagination>3153-3175</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6128774</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>17(9)</volume><pubmed_abstract>Periodontitis is a prevalent chronic inflammatory disease associated with dysbiosis. Although complement inhibition has been successfully used to treat periodontitis in animal models, studies globally analyzing inflamed tissue proteins to glean insight into possible mechanisms of action are missing. Using quantitative shotgun proteomics, we aimed to investigate differences in composition of inflammatory gingival tissue exudate ("gingival crevicular fluid"; GCF), before and after local administration of an inhibitor of the central complement component, C3, in nonhuman primates. The C3 inhibitor, Cp40 (also known as AMY-101) was administered locally in the maxillary gingival tissue of cynomolgus monkeys with established periodontitis, either once a week (1×-treatment; n = 5 animals) or three</pubmed_abstract><journal>Journal of proteome research</journal><pubmed_title>Gingival Exudatome Dynamics Implicate Inhibition of the Alternative Complement Pathway in the Protective Action of the C3 Inhibitor Cp40 in Nonhuman Primate Periodontitis.</pubmed_title><pmcid>PMC6128774</pmcid><funding_grant_id>DE024153</funding_grant_id><funding_grant_id>DE024716</funding_grant_id><funding_grant_id>AI068730</funding_grant_id><funding_grant_id>P01 AI068730</funding_grant_id><funding_grant_id>R01 DE024716</funding_grant_id><funding_grant_id>R01 DE015254</funding_grant_id><funding_grant_id>602699</funding_grant_id><funding_grant_id>R01 DE024153</funding_grant_id><funding_grant_id>DE015254</funding_grant_id><pubmed_authors>Garcia CAG</pubmed_authors><pubmed_authors>Maekawa T</pubmed_authors><pubmed_authors>Reis ES</pubmed_authors><pubmed_authors>Lambris JD</pubmed_authors><pubmed_authors>Tuplano JV</pubmed_authors><pubmed_authors>Grossmann J</pubmed_authors><pubmed_authors>Panse C</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Resuello RRG</pubmed_authors><pubmed_authors>Bao K</pubmed_authors><pubmed_authors>Bostanci N</pubmed_authors><pubmed_authors>Briones RA</pubmed_authors><pubmed_authors>Hajishengallis G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Gingival Exudatome Dynamics Implicate Inhibition of the Alternative Complement Pathway in the Protective Action of the C3 Inhibitor Cp40 in Nonhuman Primate Periodontitis.</name><description>Periodontitis is a prevalent chronic inflammatory disease associated with dysbiosis. Although complement inhibition has been successfully used to treat periodontitis in animal models, studies globally analyzing inflamed tissue proteins to glean insight into possible mechanisms of action are missing. Using quantitative shotgun proteomics, we aimed to investigate differences in composition of inflammatory gingival tissue exudate ("gingival crevicular fluid"; GCF), before and after local administration of an inhibitor of the central complement component, C3, in nonhuman primates. The C3 inhibitor, Cp40 (also known as AMY-101) was administered locally in the maxillary gingival tissue of cynomolgus monkeys with established periodontitis, either once a week (1×-treatment; n = 5 animals) or three</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Sep</publication><modification>2026-04-08T01:40:58.389Z</modification><creation>2019-09-12T07:00:33Z</creation></dates><accession>S-EPMC6128774</accession><cross_references><pubmed>30111112</pubmed><doi>10.1021/acs.jproteome.8b00263</doi></cross_references></HashMap>