<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Magnaye KM</submitter><funding>NIAID NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>HHS | NIH | National Institute of Allergy and Infectious Diseases</funding><funding>HHS | NIH | National Heart, Lung, and Blood Institute</funding><funding>Division of Intramural Research, National Institute of Allergy and Infectious Diseases</funding><pagination>e2116467119</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9214527</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>119(24)</volume><pubmed_abstract>Maternal asthma (MA) is among the most consistent risk factors for asthma in children. Possible mechanisms for this observation are epigenetic modifications in utero that have lasting effects on developmental programs in children of mothers with asthma. To test this hypothesis, we performed differential DNA methylation analyses of 398,186 individual CpG sites in primary bronchial epithelial cells (BECs) from 42 nonasthma controls and 88 asthma cases, including 56 without MA (NMA) and 32 with MA. We used weighted gene coexpression network analysis (WGCNA) of 69 and 554 differentially methylated CpGs (DMCs) that were specific to NMA and MA cases, respectively, compared with controls. WGCNA grouped 66 NMA-DMCs and 203 MA-DMCs into two and five comethylation modules, respectively. The eigenvec</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>DNA methylation signatures in airway cells from adult children of asthmatic mothers reflect subtypes of severe asthma.</pubmed_title><pmcid>PMC9214527</pmcid><funding_grant_id>UM1 AI160040</funding_grant_id><funding_grant_id>U19 AI095230</funding_grant_id><funding_grant_id>F31 HL143891</funding_grant_id><pubmed_authors>Jackson DJ</pubmed_authors><pubmed_authors>Ober C</pubmed_authors><pubmed_authors>Clay SM</pubmed_authors><pubmed_authors>Nicodemus-Johnson J</pubmed_authors><pubmed_authors>Naureckas ET</pubmed_authors><pubmed_authors>Hogarth DK</pubmed_authors><pubmed_authors>Huffman J</pubmed_authors><pubmed_authors>Magnaye KM</pubmed_authors><pubmed_authors>White SR</pubmed_authors><pubmed_authors>Naughton KA</pubmed_authors><pubmed_authors>Gern JE</pubmed_authors><pubmed_authors>Altman MC</pubmed_authors></additional><is_claimable>false</is_claimable><name>DNA methylation signatures in airway cells from adult children of asthmatic mothers reflect subtypes of severe asthma.</name><description>Maternal asthma (MA) is among the most consistent risk factors for asthma in children. Possible mechanisms for this observation are epigenetic modifications in utero that have lasting effects on developmental programs in children of mothers with asthma. To test this hypothesis, we performed differential DNA methylation analyses of 398,186 individual CpG sites in primary bronchial epithelial cells (BECs) from 42 nonasthma controls and 88 asthma cases, including 56 without MA (NMA) and 32 with MA. We used weighted gene coexpression network analysis (WGCNA) of 69 and 554 differentially methylated CpGs (DMCs) that were specific to NMA and MA cases, respectively, compared with controls. WGCNA grouped 66 NMA-DMCs and 203 MA-DMCs into two and five comethylation modules, respectively. The eigenvec</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2025-04-04T03:06:30.81Z</modification><creation>2025-02-19T05:06:24.532Z</creation></dates><accession>S-EPMC9214527</accession><cross_references><pubmed>35666868</pubmed><doi>10.1073/pnas.2116467119</doi></cross_references></HashMap>