<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li H</submitter><funding>National Natural Science Foundation of China</funding><funding>“Ten thousand plan” innovation leader of Zhejiang Province</funding><pagination>2127456</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9542615</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(1)</volume><pubmed_abstract>Severe acute pancreatitis (SAP) is a critical illness characterized by a severe systemic inflammatory response resulting in persistent multiple organ failure and sepsis. The intestinal microbiome is increasingly appreciated to play a crucial role in modulation of AP disease outcome, but limited information is available about the identity and mechanism of action for specific commensal bacteria involved in AP-associated inflammation. Here we show that &lt;i>Bifidobacteria&lt;/i>, particularly &lt;i>B. animalis&lt;/i>, can protect against AP by regulating pancreatic and systemic inflammation in germ-free (GF) and oral antibiotic-treated (Abx) mouse models. Colonization by &lt;i>B. animalis&lt;/i> and administration of its metabolite lactate protected Abx and GF mice from AP by reducing serum amylase concentrat</pubmed_abstract><journal>Gut microbes</journal><pubmed_title>&lt;i>Bifidobacterium&lt;/i> spp. and their metabolite lactate protect against acute pancreatitis via inhibition of pancreatic and systemic inflammatory responses.</pubmed_title><pmcid>PMC9542615</pmcid><funding_grant_id>U21A20261</funding_grant_id><funding_grant_id>2020R52007</funding_grant_id><funding_grant_id>82002073</funding_grant_id><funding_grant_id>3217864</funding_grant_id><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Yang G</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Guo X</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Wang D</pubmed_authors><pubmed_authors>Yue M</pubmed_authors><pubmed_authors>Wang G</pubmed_authors><pubmed_authors>Yu H</pubmed_authors><pubmed_authors>Liu W</pubmed_authors><pubmed_authors>Cai B</pubmed_authors><pubmed_authors>Zheng H</pubmed_authors><pubmed_authors>Zhu SJ</pubmed_authors><pubmed_authors>Guo J</pubmed_authors><pubmed_authors>Qi X</pubmed_authors><pubmed_authors>Xie J</pubmed_authors><pubmed_authors>Guo F</pubmed_authors><pubmed_authors>Chen S</pubmed_authors><pubmed_authors>Tang Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>&lt;i>Bifidobacterium&lt;/i> spp. and their metabolite lactate protect against acute pancreatitis via inhibition of pancreatic and systemic inflammatory responses.</name><description>Severe acute pancreatitis (SAP) is a critical illness characterized by a severe systemic inflammatory response resulting in persistent multiple organ failure and sepsis. The intestinal microbiome is increasingly appreciated to play a crucial role in modulation of AP disease outcome, but limited information is available about the identity and mechanism of action for specific commensal bacteria involved in AP-associated inflammation. Here we show that &lt;i>Bifidobacteria&lt;/i>, particularly &lt;i>B. animalis&lt;/i>, can protect against AP by regulating pancreatic and systemic inflammation in germ-free (GF) and oral antibiotic-treated (Abx) mouse models. Colonization by &lt;i>B. animalis&lt;/i> and administration of its metabolite lactate protected Abx and GF mice from AP by reducing serum amylase concentrat</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jan-Dec</publication><modification>2025-04-04T14:34:28.467Z</modification><creation>2025-04-04T14:34:28.467Z</creation></dates><accession>S-EPMC9542615</accession><cross_references><pubmed>36195972</pubmed><doi>10.1080/19490976.2022.2127456</doi></cross_references></HashMap>