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Recent data from human studies suggest that bacterial infections can alter susceptibility to anaphylaxis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>We examined the effect of <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> exposure on the induction of IgE\u2010mast cell (<jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>) mediated reactions in mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6 <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>,<jats:italic> tlr4<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> and <jats:italic><jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>10<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice were exposed to <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>, and serum cytokines (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010) were measured. Mice were subsequently treated with anti\u2010IgE, and the symptoms of passive IgE\u2010mediated anaphylaxis, <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content> activation, Ca<jats:sup>2+<\/jats:sup>\u2010mobilization and the expression of Fc\u03b5<jats:styled-content style=\"fixed-case\">RI<\/jats:styled-content> on peritoneal <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s were quantitated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We show that <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> exposure of C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6 <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice constraints IgE\u2010<jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>\u2013mediated reactions. <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced suppression of IgE\u2010<jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>\u2013mediated responses was <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\u20104\u2010dependent and associated with increased systemic <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 levels, decreased surface expression of Fc\u03b5<jats:styled-content style=\"fixed-case\">RI<\/jats:styled-content> on <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s and loss of sensitivity to IgE activation. Notably, <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced desensitization of <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s was short term with <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content> sensitivity to IgE reconstituted within 48\u00a0hours, which was associated with recapitulation of Fc\u03b5<jats:styled-content style=\"fixed-case\">RI<\/jats:styled-content> expression on the <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>s. Mechanistic analyses revealed a requirement for <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 in <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010mediated decrease in <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content> Fc\u03b5<jats:styled-content style=\"fixed-case\">RI<\/jats:styled-content> surface expression.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions &amp; Clinical Relevance<\/jats:title><jats:p>Collectively, these studies suggest that <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 promotes the down\u2010regulation of <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content> surface Fc\u03b5<jats:styled-content style=\"fixed-case\">RI<\/jats:styled-content> expression and leads to desensitization of mice to IgE\u2010mediated reactions. These studies indicate that targeting of the <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\u20104\u2010<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010 pathway may be used as a therapeutic approach to prevent adverse IgE\u2010mediated reactions.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cea.13013","type":"journal-article","created":{"date-parts":[[2017,8,21]],"date-time":"2017-08-21T14:42:39Z","timestamp":1503326559000},"page":"1574-1585","source":"Crossref","is-referenced-by-count":18,"title":["Lipopolysaccharide suppresses IgE\u2010mast cell\u2010mediated reactions"],"prefix":"10.1111","volume":"47","author":[{"given":"N.","family":"Wang","sequence":"first","affiliation":[{"name":"Division of Allergy and Immunology University of Cincinnati College of Medicine Cincinnati Children's Hospital Medical Center Cincinnati OH USA"},{"name":"Chongqing Health Center for 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