ArticleThe Journal of pharmacology and experimental therapeutics2026
Blocking interleukin 33 reduces joint, systemic, and lung inflammatory responses in the combined collagen-induced arthritis-inhalant endotoxin exposure model.
Article in The Journal of pharmacology and experimental therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Therapies capable of resolving rheumatoid arthritis (RA)-associated lung disease, particularly in the setting of environmental exposures, are lacking. This study sought to determine whether blocking interleukin (IL)-33 in a murine model of RA-associated lung disease induced by combined collagen-induced arthritis (CIA) and repeated inhalant lipopolysaccharide (LPS) exposures could be advantageous. Arthritis prone male DBA/1J mice received CIA (vs saline) injections (days 1 and 21) plus intranasal LPS (100 ng) or saline daily for 4 weeks and were subsequently treated with 5 doses of anti-IL-33 (10 mg/kg) or isotype over 11 days. Anti-IL-33 therapy significantly (P < .05) mitigated several CIA+LPS-induced effects. Anti-IL-33 reduced arthritis inflammatory score by 76% and serum acute phase reactant pentraxin-2 by 70% and reversed weight loss induced by CIA+LPS coexposure. Anti-IL-33 reduced CIA+LPS-induced antimalondialdehyde acetaldehyde but not anticitrullinated autoantibodies in serum and reduced serum levels of inflammatory mediators. Lung cell infiltrates induced by coexposure, including neutrophils, activated lung macrophages, transitional monocytes-macrophages, monocytic-like cells, and dendritic cells, were reduced with anti-IL-33. Anti-IL-33 also reduced CIA+LPS-induced lung levels of chemokines involved in monocyte-macrophage recruitment and fibrotic/repair mediators collagen deposition, IL-33 expression, inflammatory CC motif chemokine receptor 2
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