Abstract
Introduction - Whether and how T cells actually contribute to COPD pathogenesis remains undefined. The protein Lck (p56LcK) is a Src family tyrosine kinase expressed at all stages of thymocyte development and is required for maturation of T cells. The targeted disruption of p56LcK gene (p56LcK –/–) in mice results in severe block in thymocyte maturation with substantial reduction of CD4+CD8+ thymocytes and peripheral T cells, and disruption of TCR signaling with defective function of T cell responses.
Aims & Objectives - To investigate the role of T lymphocytes- in the development of cigarette smoke (CS) induced pulmonary changes in p56LcK –/– and their congenic wild type mice.
Methods – At 7 months after chronic exposure,lungs of air- and CS-exposed mice were analysed by biochemical, immunological and morphometric methods.
Results - Smoking mice from both genotypes showed disseminated foci of emphysema and large areas of goblet cell metaplasia in bronchial and bronchiolar epithelium. Evaluation of lung mean linear intercepts and internal surface areas, as well as lung elastin confirms that mice from both genotypes show the same degree of emphysematous lesions. These changes are accompanied by the same degree of inflammation and by a significant increase of Il-6, MCP-1, KC, and TNF-α. No difference in the expression levels of perforin and granzyme b, the two major cytolytic effector proteins of NK and CD8 T cells are observed. Macrophages show a M1 pattern of polarization in peripheral zones and a M2 pattern in peribronchiolar areas.
Conclusions – CS exposure in presence of a severe reduction in number and function of peripheral T cells does not influence the development of pulmonary changes in mice.
- Copyright ©the authors 2016
