Submitted on November 8, 2007
Accepted on August 14, 2008
Aerobic Conditioning and Allergic Pulmonary Inflammation in mice II: Effects on Lung Vascular and Parenchymal Inflammation and Remodeling
Rodolfo Paula Vieira1, Vanessa Ferreira de Andrade2, Anna Cecilia S. Duarte3, Angela B. G. dos Santos4, Thais Mauad1, Milton A. Martins5, Marisa Dolhnikoff1, and Celso R. F. Carvalho2*
1 Pathology (LIM 05), University of Sao Paulo, School of Medicine, Sao Paulo, Brazil
2 Physical Therapy, University of Sao Paulo, School of Medicine, Sao Paulo, Brazil
3 Physical Therapy, University of Sao Paulo, School of Medicine, Sao Paulo, Sao Paulo, Brazil
4 Pathology, University of Sao Paulo, School of Medicine, Sao Paulo, Brazil
5 Clinical Medicine (LIM 20), University of Sao Paulo, School of Medicine, Sao Paulo, Brazil
* To whom correspondence should be addressed. E-mail: cscarval{at}usp.br.
Rationale: Recent evidence suggests that asthma leads to inflammation and remodeling not only in the airways, but also in pulmonary vessels and parenchyma. In addition, some studies demonstrated that aerobic training decreases chronic allergic inflammation in the airways, however its effects on the pulmonary vessels and parenchyma has not been previously evaluated. Objectives: To test the hypothesis that aerobic conditioning reduces inflammation and remodeling in pulmonary vessels and parenchyma in a model of chronic allergic lung inflammation. Methods: Balb/c mice were sensitized in days 0, 14, 28 and 42 and challenged with ovalbumin from day 21st to day 50th. Aerobic training started in day 21 until day 50. Pulmonary vessel and parenchyma inflammation and remodeling were evaluated by quantitative analysis of eosinophils and mononuclear cells and by collagen and elastin contents and smooth muscle thickness. Immunohistochemistry was performed to quantify the density of positive cells to IL-2, IL-4, IL-5, IFN-
, IL-10, MCP-1, NF-
B p65 and IGF-1. Results: OVA exposure induced pulmonary vessel and parenchyma inflammation as well as increased expression of IL-4, IL-5, MCP-1, NF-B p65 and IGF-1 by inflammatory cells were reduced by aerobic conditioning. OVA exposure also induced an increase in smooth muscle thickness, elastic and collagen contents in pulmonary vessels, which were reduced by aerobic conditioning. Aerobic conditioning increased the expression of IL-10 in sensitized mice. Conclusions: Aerobic conditioning decreases pulmonary vascular and parenchymal inflammation and remodeling in this experimental model of chronic allergic lung inflammation in mice.
