{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T02:43:21Z","timestamp":1783997001520,"version":"3.55.0"},"reference-count":33,"publisher":"S. Karger AG","issue":"Suppl. 1","license":[{"start":{"date-parts":[[2011,1,1]],"date-time":"2011-01-01T00:00:00Z","timestamp":1293840000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/3.0\/"},{"start":{"date-parts":[[2011,1,1]],"date-time":"2011-01-01T00:00:00Z","timestamp":1293840000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Int Arch Allergy Immunol"],"published-print":{"date-parts":[[2011]]},"abstract":"<jats:p>&lt;i&gt;Background:&lt;\/i&gt; Interleukin (IL)-33, a new member of the IL-1 cytokine family, has been recognized as a key cytokine that enhances T helper 2-balanced immune regulation through its receptor ST2; however, the function and relationship of the IL-33 and ST2 pathways in bronchial asthma are still unclear. We investigated the cellular origin and regulation of IL-33 and ST2 in allergic bronchial asthma in vivo and in vitro. &lt;i&gt;Methods:&lt;\/i&gt; BALB\/c mice were sensitized by intraperitoneal injections of ovalbumin (OVA) with alum. Mice were exposed to aerosolized 1% OVA for 30 min a day for 7 days. These mice were then challenged with aerosolized 1% OVA 2 days after the last day of exposure. After the OVA challenge, the mice were sacrificed and their lung tissues were obtained. Mouse lung fibroblasts were cultured and treated with IL-33 or IL-13. &lt;i&gt;Results:&lt;\/i&gt; The levels of IL-33 mRNA and IL-33 protein in lung tissue increased after the OVA challenge. Most IL-33-expressing cells were CD11c+ cells and epithelial cells, and many ST2-expressing cells were stained lung fibroblasts and inflammatory cells. IL-33 induced eotaxin\/CCL11 production in lung fibroblasts. IL-33 and IL-13 synergistically induced eotaxin expression. &lt;i&gt;Conclusions:&lt;\/i&gt; IL-33 may contribute to the induction and maintenance of eosinophilic inflammation in the airways by acting on lung fibroblasts. IL-33 and ST2 may play important roles in allergic bronchial asthma.<\/jats:p>","DOI":"10.1159\/000327259","type":"journal-article","created":{"date-parts":[[2011,6,1]],"date-time":"2011-06-01T07:54:32Z","timestamp":1306914872000},"page":"12-20","source":"Crossref","is-referenced-by-count":46,"title":["Expression and Effects of IL-33 and ST2 in Allergic Bronchial Asthma: IL-33 Induces Eotaxin Production in Lung 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