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Zuo, F., Kaminski, N., Eugui, E,, Allard, J., Yakhini, Z., Ben-Dor, A., Lollini, L., Morris D., Kim, Y. and De Lustro, B. (2002) Gene expression analysis reveals matrilysin as a key regulator of pulmonary fibrosis in mice and humans. Proceedings of the National Academy of Sciences, 99, 6292. doi:10.1073/pnas.092134099

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• TITLE: IL13-induced lung fibrosis in meconium aspiration

  AUTHORS: A. Zagariya, S. Navale, O. Zagariya, K. McClain, D. Vidyasagar

  KEYWORDS: Meconium Aspiration Syndrome, IL-13 Cytokine, Newborn Lungs, Fibrosis

  JOURNAL NAME: Journal of Biomedical Science and Engineering, Vol.4 No.9, September 30, 2011

  ABSTRACT: We demonstrated previously that inflammatory cy-tokines TNF, IL-1, IL-6 and IL-8 are signifi-cantly expressed in meconium-instilled lungs. Capto-pril was a strong inhibitor of meconium-induced lung injury, inflammation and apoptosis and reduces lung alveolar and airway epithelial cell damage. Presently we demonstrate that IL-13 expression in the me-conium aspiration syndrome (MAS). IL-13 was maximally expressed 8 hrs after meconium instilla-tion. It was previously described that IL-13 plays a major role in degradation of airway epithelial cells and inducing of lung fibrosis by activating collagen production that is a major point in identification of lung fibrosis. We also showed that Captopril treat-ment significantly inhibits IL-13 expression in the lungs. We believe it reduces meconium-induced lung injury and has a therapeutic effect on histological and biochemical functions of the lungs and possibly pulmonary fibrosis. Captopril treatment significantly reduced the number of neuprophils and macrophages which express IL13 and levels of other inflammatory cytokines after meconium instillation. Selective neu-tralization of IL-13 ameliorated lung injury, airway hyper responsiveness, eosinophil recruitment and mucus overproduction.