A human monoclonal anti-TNF alpha antibody (adalimumab) reduces airway inflammation and ameliorates lung histology in a murine model of acute asthma

• Autores: F. Catal, E. Mete, C. Tayman, E. Topal, A. Albayrak, H. Sert
• Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 43, Nº. 1, 2015, págs. 14-18
• Idioma: inglés
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• Resumen

  • Background A few experimental studies related to asthma have unveiled the beneficial effects of TNF alpha blocking agents on the airway histology, cytokine levels in bronchoalveolar lavage and bronchial hyper-responsiveness. In the current study, we aimed to assess the effect of adalimumab on the inflammation and histology of asthma in a murine model.

    Method Twelve-week-old BALB/c (H-2d/d) female rats (n = 18) were allocated into three groups, including (group I) control (phosphate-buffered saline was implemented), (group II) asthma induced with OVA (n = 6), and (group III) asthma induced with OVA + treated with adalimumab (n = 6). Rats were executed on the 28th day of the study. The lung samples were fixed in 10% neutral buffered formalin. Lung parenchyma, alveolus, peribronchial and perivascular inflammation were assessed. Lung pathological scoring was performed.

    Result Severity of lung damage was found to be reduced significantly in the asthma induced with OVA + treated with adalimumab group. When compared with the untreated group, adalimumab significantly reduced the inflammatory cells around the bronchi and bronchioles, and reduced inflammation of the alveolar wall and alveolar wall thickness as well (median score = 1, p = 0.52). Peribronchial smooth muscle hypertrophy and oedema were significantly reduced after adalimumab administration.

    Conclusion Adalimumab (a human monoclonal anti-TNF alpha antibody) therapy significantly reduced the severity of lung damage by decreasing cellular infiltration and improvement on the lung histology in a murine model of acute asthma.