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1 Laboratory of Respiration Physiology, Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil
2 Laboratory of Immunopharmacology, FIOCRUZ, Sao Paulo, Sao Paulo, Brazil
3 Department of Thoracic Surgery, AC Camargo Cancer Hospital, Rio de Janeiro, Rio de Janeiro, Brazil
4 Department of Pathology, University of Sao Paulo, Sao Paulo, Sao Paulo, Brazil
5 Laboratory of Pulmonary Investigation; Carlos Chagas Filho Biophysics Insitute, Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil
* To whom correspondence should be addressed. E-mail: prmrocco{at}biof.ufrj.br.
To test whether pulmonary and extrapulmonary acute lung injury (ALI) of identical mechanical compromise would express diverse morphological patterns and immunological pathways. For this purpose, a model of pulmonary (p) and extra-pulmonary (exp) ALI with similar functional changes was developed and pulmonary morphology (light and electron microscopy), cytokines levels and neutrophilic infiltration in the bronchoalveolar lavage fluid (BALF), elastic and collagen fibers content in the alveolar septa, and neutrophil apoptosis in the lung parenchyma were analyzed. BALB/c mice were divided into four groups. In control groups (Cp and Cexp), saline was intratracheally (i.t., 0.05 ml) instilled and intraperitoneally (i.p., 0.5 ml) injected, respectively. In ALIp and ALIexp groups, mice received E. coli lipopolysaccharide (10 µg, i.t. and 125 µg, i.p., respectively). The changes in lung resistive and viscoelastic pressures, and static elastance, alveolar collapse and cells content in lung tissue were similar in ALIp and ALIexp groups. ALIp group presented a threefold increase in IL-8 and IL-10 levels in the BALF in relation to ALIexp, whereas IL-6 level showed a two-fold increase in ALIp. Neutrophils in the BALF were more frequent in ALIp than in ALIexp group. ALIp group showed more extensive injury of alveolar epithelium, intact capillary endothelium, and apoptotic neutrophils, while ALIexp group presented interstitial edema, intact type I and II cells and endothelial layer. In conclusion, given the same pulmonary mechanical dysfunction independently of the etiology of ALI, insult in pulmonary epithelium yielded more pronounced inflammatory responses, which induce ultrastructural morphological changes.
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