Annexin-A1-Derived Peptide Ac2-26 Suppresses Allergic Airway Inflammation and Remodelling in Mice.
Tatiana Paula Teixeira FerreiraFernanda Verdini GuimarãesYago Amigo Pinho Jannini SáNatalia Barreto da Silva RibeiroAna Carolina Santos de ArantesVinicius de Frias CarvalhoLirlândia Pires SousaMauro PerrettiMarco Aurélio MartinsPatrícia Machado Rodrigues E SilvaPublished in: Cells (2022)
Annexin-A1 (AnxA1) and its N-terminal derived peptide Ac2-26 regulate the inflammatory response in several experimental models of disorders. This study evaluated the effect of endogenous AnxA1 and its N-terminal peptide Acetyl 2-26 (Ac2-26) on allergic asthma triggered by house dust mite (HDM) extract in mice. ANXA 1 -/- and wildtype (WT) mice were exposed to intranasal instillation of HDM every other day for 3 weeks, with analyses performed 24 h following the last exposure. Intranasal administration of peptide Ac2-26 was performed 1 h before HDM, beginning 1 week after the initial antigen application. ANXA 1 -/- mice stimulated with HDM showed marked exacerbations of airway hyperreactivity (AHR), eosinophil accumulation, subepithelial fibrosis, and mucus hypersecretion, all parameters correlating with overexpression of cytokines (IL-4, IL-13, TNF-α, and TGF-β) and chemokines (CCL11/eotaxin-1 and CCL2/MCP-1). Intranasal treatment with peptide Ac2-26 decreased eosinophil infiltration, peribronchiolar fibrosis, and mucus exacerbation caused by the allergen challenge. Ac2-26 also inhibited AHR and mediator production. Collectively, our findings show that the AnxA1-derived peptide Ac2-26 protects against several pathological changes associated with HDM allergic reaction, suggesting that this peptide or related AnxA1-mimetic Ac2-26 may represent promising therapeutic candidates for the treatment of allergic asthma.
Keyphrases
- allergic rhinitis
- chronic obstructive pulmonary disease
- inflammatory response
- high fat diet induced
- randomized controlled trial
- rheumatoid arthritis
- liver fibrosis
- intensive care unit
- type diabetes
- signaling pathway
- metabolic syndrome
- epithelial mesenchymal transition
- drug induced
- liver injury
- insulin resistance
- air pollution
- heavy metals
- study protocol
- atopic dermatitis
- smoking cessation