IL-33, a member of IL-1 family cytokine, is synthesized as a full-length active form, stored in the nucleus of epithelial cells, and released when the cells are damaged mechanically or become necrotic. IL-33 has the capacity to stimulate Th2 cells, mast cells, basophils, eosinophils and ILC2s to produce Th2 cytokines. Thus, IL-33 plays an important role in induction of allergic diseases. We previously reported that Strongyloides venezuelensis (S. venezuelensis) infection induces production of IL-33 in the lungs, which induces ILC2s to proliferate and to produce IL-5 and IL-13. Thus, Rag2−/− mice infected with S. venezuelensis develop eosinophilic inflammation and goblet cell hyperplasia in their lungs (Loeffler’s syndrome). Therefore, IL-33 production in the lungs is important for induction of allergic responses, while the mechanism for induction of IL-33 production is totally unknown. We noticed massive hemorrhagic areas in the lungs at day 5 after S. venezuelensis infection. Thus, we speculated that such macroscopic or microscopic injury might induce production of damage associated molecular pattern (DAMP), which in turn increases the production of IL-33 in the lungs. Here, we demonstrated lung tissue extracts contain DAMP, which induces IL-33 production in the lungs. We performed purification of DAMP with IL-33-inducing activity (IL33ia) from the lung tissues. Highly purified DAMP is 20kDa protein. Intranasal administration of the DAMP induces an increase in the number of IL-33-expressing alveolar type II cells (ATII) in the lungs. DAMP also stimulates primary fibroblasts to produce IL-33 in vitro. We prepared recombinant DAMP, which recapitulates IL33ia of natural DAMP. Many organs constitutively express this DAMP. We can induce DAMP with IL33ia in the peritoneal cavity by injection of alum. At day 7 after alum injection, we can harvest IL33ia and IL-33 in alum/cells aggregate. We will present our current data about new DAMP with IL33ia.