Abstract
Cathelicidin is a family of cationic antimicrobial peptide acts as immunomodulator of the innate immune system and CRAMP is the homologous molecule in mice. Cathelicidin stimulates airway proliferation and inhibits inflammatory cytokine release. Because emphysema and cathelicidin are related to inflammation and destruction, we postulated that cathelicidin might be involved in reducing severity of emphysema. The quantification of emphysema severity is performed by measuring the mean linear intercept (Lm) in lungs taken from both elastase-induced emphysema in CRAMP-deficient and WT control mice. BALF and cytospin were performed for the inflammatory cell fractions and inflammatory cytokine (ELISA). For the healing role of endogenous cathelicidin, selective injury was induced to Clara cells with naphthalene. Mice were sacrificed and lung sections were used for immunohistochemistry using monoclonal antibodies (antiCC10 protein). The healing was evaluated by counting clara cells in one millimeter of basement membrane (index). Our results showed that the presence of cathelicidin minimized significantly severity of emphysema in mice. The Lm for WT mice was (85,51µm± 3,15µm, n=8) and for CRAMP-KO was (111,7 µm± 6,850µm, n=8) markedly increased compared with the PBS groups. The number of inflammatory cells and the concentration of TNF-a and IL-1B in response to elastase were significantly higher in BALF of CRAMP-KO than WT mice. The healing of CRAMP-ko lung was significantly lower than wild type mice after 15 days of naphthalene administration. Based on our results, it can be concluded that the endogenous cathelicidin in mice reduces severity of emphysema and this may relate to anti-inflammatory and healer role of cathelicidin.
- © 2014 ERS