<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Patton JB</submitter><funding>HHS | National Institutes of Health</funding><funding>Howard Hughes Medical Institute</funding><funding>NIDDK NIH HHS</funding><funding>NIAID NIH HHS</funding><pagination>204-209</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5776800</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>115(1)</volume><pubmed_abstract>&lt;i>Strongyloides stercoralis&lt;/i> hyperinfection causes high mortality rates in humans, and, while hyperinfection can be induced by immunosuppressive glucocorticoids, the pathogenesis remains unknown. Since immunocompetent mice are resistant to infection with &lt;i>S. stercoralis&lt;/i>, we hypothesized that NSG mice, which have a reduced innate immune response and lack adaptive immunity, would be susceptible to the infection and develop hyperinfection. Interestingly, despite the presence of large numbers of adult and first-stage larvae in &lt;i>S. stercoralis&lt;/i>-infected NSG mice, no hyperinfection was observed even when the mice were treated with a monoclonal antibody to eliminate residual granulocyte activity. NSG mice were then infected with third-stage larvae and treated for 6 wk with methylpr</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Methylprednisolone acetate induces, and Δ7-dafachronic acid suppresses, &lt;i>Strongyloides stercoralis&lt;/i> hyperinfection in NSG mice.</pubmed_title><pmcid>PMC5776800</pmcid><funding_grant_id>R01 AI050668</funding_grant_id><funding_grant_id>N/A</funding_grant_id><funding_grant_id>DK067158</funding_grant_id><funding_grant_id>R01 DK067158</funding_grant_id><funding_grant_id>AI105856</funding_grant_id><funding_grant_id>R21 AI105856</funding_grant_id><funding_grant_id>OD P40-10939</funding_grant_id><funding_grant_id>R33 AI105856</funding_grant_id><funding_grant_id>R01 AI022662</funding_grant_id><pubmed_authors>Patton JB</pubmed_authors><pubmed_authors>Bonne-Annee S</pubmed_authors><pubmed_authors>Eberhard ML</pubmed_authors><pubmed_authors>Deckman J</pubmed_authors><pubmed_authors>Mangelsdorf DJ</pubmed_authors><pubmed_authors>Lok JB</pubmed_authors><pubmed_authors>Kliewer SA</pubmed_authors><pubmed_authors>Abraham D</pubmed_authors><pubmed_authors>Torigian A</pubmed_authors><pubmed_authors>Durham AC</pubmed_authors><pubmed_authors>Hess JA</pubmed_authors><pubmed_authors>Lee JJ</pubmed_authors><pubmed_authors>Nolan TJ</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Methylprednisolone acetate induces, and Δ7-dafachronic acid suppresses, &lt;i>Strongyloides stercoralis&lt;/i> hyperinfection in NSG mice.</name><description>&lt;i>Strongyloides stercoralis&lt;/i> hyperinfection causes high mortality rates in humans, and, while hyperinfection can be induced by immunosuppressive glucocorticoids, the pathogenesis remains unknown. Since immunocompetent mice are resistant to infection with &lt;i>S. stercoralis&lt;/i>, we hypothesized that NSG mice, which have a reduced innate immune response and lack adaptive immunity, would be susceptible to the infection and develop hyperinfection. Interestingly, despite the presence of large numbers of adult and first-stage larvae in &lt;i>S. stercoralis&lt;/i>-infected NSG mice, no hyperinfection was observed even when the mice were treated with a monoclonal antibody to eliminate residual granulocyte activity. NSG mice were then infected with third-stage larvae and treated for 6 wk with methylpr</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Jan</publication><modification>2026-05-06T00:27:04.232Z</modification><creation>2019-03-26T23:44:09Z</creation></dates><accession>S-EPMC5776800</accession><cross_references><pubmed>29203662</pubmed><doi>10.1073/pnas.1712235114</doi></cross_references></HashMap>