<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Loeser RF</submitter><funding>Arthritis Foundation</funding><funding>National Institute of Arthritis and Musculoskeletal and Skin Diseases</funding><funding>National Center for Advancing Translational Sciences</funding><funding>NCATS NIH HHS</funding><funding>NCCDPHP CDC HHS</funding><funding>Crohn's &amp; Colitis Foundation of America</funding><funding>National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>NIH Office of the Director</funding><funding>Office of the Director, NIH</funding><funding>Centers for Disease Control and Prevention</funding><funding>NIDDK NIH HHS</funding><funding>NIAMS NIH HHS</funding><funding>NIH HHS</funding><funding>Nutrition Obesity Resource Core of the National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>CDC HHS</funding><pagination>227-236</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8795472</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>74(2)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>To test the hypothesis that an altered gut microbiota (dysbiosis) plays a role in obesity-associated osteoarthritis (OA).&lt;h4>Methods&lt;/h4>Stool and blood samples were collected from 92 participants with a body mass index (BMI) ≥30 kg/m&lt;sup>2&lt;/sup> , recruited from the Johnston County Osteoarthritis Project. OA patients (n = 50) had hand and knee OA (Kellgren/Lawrence [K/L] grade ≥2 or arthroplasty). Controls (n = 42) had no hand OA and a K/L grade of 0-1 for the knees. Compositional analysis of stool samples was carried out by 16S ribosomal RNA amplicon sequencing. Alpha- and beta-diversity and differences in taxa relative abundances were determined. Blood samples were used for multiplex cytokine analysis and measures of lipopolysaccharide (LPS) and LPS binding protein. Ge</pubmed_abstract><journal>Arthritis &amp; rheumatology (Hoboken, N.J.)</journal><pubmed_title>Association of Increased Serum Lipopolysaccharide, But Not Microbial Dysbiosis, With Obesity-Related Osteoarthritis.</pubmed_title><pmcid>PMC8795472</pmcid><funding_grant_id>UL1-TR-002489</funding_grant_id><funding_grant_id>P30 DK056350</funding_grant_id><funding_grant_id>P30-DK-034987</funding_grant_id><funding_grant_id>UL1 TR002489</funding_grant_id><funding_grant_id>P30-DK-056350</funding_grant_id><funding_grant_id>U01‐DP‐006266</funding_grant_id><funding_grant_id>P40 OD010995</funding_grant_id><funding_grant_id>U01-DP-006266</funding_grant_id><funding_grant_id>U01 DP006266</funding_grant_id><funding_grant_id>P40‐OD‐010995</funding_grant_id><funding_grant_id>P30‐DK‐056350</funding_grant_id><funding_grant_id>718285</funding_grant_id><funding_grant_id>P40-OD-010995</funding_grant_id><funding_grant_id>P30‐AR‐072580</funding_grant_id><funding_grant_id>P30 DK034987</funding_grant_id><funding_grant_id>UL1‐TR‐002489</funding_grant_id><funding_grant_id>P30-AR-072580</funding_grant_id><funding_grant_id>P30‐DK‐034987</funding_grant_id><funding_grant_id>P30 AR072580</funding_grant_id><pubmed_authors>Arbeeva L</pubmed_authors><pubmed_authors>Jordan JM</pubmed_authors><pubmed_authors>Azcarate-Peril MA</pubmed_authors><pubmed_authors>Kelley K</pubmed_authors><pubmed_authors>Longobardi L</pubmed_authors><pubmed_authors>Renner JB</pubmed_authors><pubmed_authors>Carroll IM</pubmed_authors><pubmed_authors>Cui Y</pubmed_authors><pubmed_authors>Sartor RB</pubmed_authors><pubmed_authors>Sun S</pubmed_authors><pubmed_authors>Fodor AA</pubmed_authors><pubmed_authors>Nelson AE</pubmed_authors><pubmed_authors>Ulici V</pubmed_authors><pubmed_authors>Stewart DA</pubmed_authors><pubmed_authors>Sumner SJ</pubmed_authors><pubmed_authors>Loeser RF</pubmed_authors></additional><is_claimable>false</is_claimable><name>Association of Increased Serum Lipopolysaccharide, But Not Microbial Dysbiosis, With Obesity-Related Osteoarthritis.</name><description>&lt;h4>Objective&lt;/h4>To test the hypothesis that an altered gut microbiota (dysbiosis) plays a role in obesity-associated osteoarthritis (OA).&lt;h4>Methods&lt;/h4>Stool and blood samples were collected from 92 participants with a body mass index (BMI) ≥30 kg/m&lt;sup>2&lt;/sup> , recruited from the Johnston County Osteoarthritis Project. OA patients (n = 50) had hand and knee OA (Kellgren/Lawrence [K/L] grade ≥2 or arthroplasty). Controls (n = 42) had no hand OA and a K/L grade of 0-1 for the knees. Compositional analysis of stool samples was carried out by 16S ribosomal RNA amplicon sequencing. Alpha- and beta-diversity and differences in taxa relative abundances were determined. Blood samples were used for multiplex cytokine analysis and measures of lipopolysaccharide (LPS) and LPS binding protein. Ge</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2025-04-05T09:03:13.597Z</modification><creation>2025-04-05T09:03:13.597Z</creation></dates><accession>S-EPMC8795472</accession><cross_references><pubmed>34423918</pubmed><doi>10.1002/art.41955</doi></cross_references></HashMap>