RESUMO
Pulmonary dysfunction represents the most important cause of death in patients with paracoccidioidomycosis (PBM). In order to investigate the functional changes of the lungs in the early stages of PBM, a model of benign disease was developed by intratracheal challenge of 12-week old isogenic Wistar rats with 1 x 10(6) yeast forms of Paracoccidioides brasiliensis. Animals were studied 30 and 60 days after infection, when fully developed granulomas were demonstrable in the lungs. Measurements of airway reistance, lung elastance and tissue hysteresis were made during sinusoidal deformations (100 breaths/min, tidal volume = 2 ml) with direct measurement of alveolar pressure using the alveolar capsule technique. Infection caused a significant increase in hysteresis (infected: 1.69, N = 13; control: 1.13, N=12,P = 0.024, ANOVA), with no alterations in airway resitance or lung elastance. Histopathological analysis revealed the presence of fully developed granulomas located in the axial compartment of the lung interstitial space. These results suggest that alterations of tissue mechanics represent an early event in experimental PBM.
Assuntos
Ratos , Animais , Modelos Animais de Doenças , Pulmão/patologia , Paracoccidioidomicose/fisiopatologia , Paracoccidioides/patogenicidade , Ratos Endogâmicos WFRESUMO
O efeito imunomodulatorio da Cimetidine (CIM), um antagonista do receptor de histamina-tipo 2, foi avaliado na resposta blastogenica a Con A em celulas de ratos Wistar Furth (WF) infectados pela cepa Y de Trypanosoma cruzi (T.cruzi). Foi observado que apenas na concentracao de "10 POT. -3"M de Cimetidine houve amplificacao da resposta blastogenica de esplenocitos normais a Con A. Entretanto, a capacidade mitogenica de esplenocitos de animais infectados foi restaurada na presenca de molaridades da droga que variaram entre "10 POT. -8" a "10 POT. -3". Os resultados demonstraram que a CIM tem o potencial de modular a resposta mitogenica de celulas de animais infectados pelo T.cruzi, sugerindo um papel imunoregulatorio da histamina e/ou celulas que expressam receptores H2 nesta infeccao.