Interleukin-5 production by peripheral blood monocytes from asthmatic patients: effect of alveolar macrophages

ABSTRACT

This study aimed to assess the role of ALM in the pathogenesis of bronchial asthma by studying the effect of ALM derived from bronchoalveolar lavage [BAL] on IL-5 production by peripheral blood monocytes PBMC [including T lymphocytes] in cocultures in patients with bronchial asthma as compared to that in non asthmatic individuals. Nineteen patients with bronchial asthma were enrolled in this study. Ten normal non-smoker subjects were considered as controls. Patients were subjected to broncoalveolar lavage [BAL]. The lavage fluid was cultured in 3 wells; one with peripheral blood monocytes [PBMC], another with PBMC with mitogen stimulation and the third with PBMC with BAL cells and stimulation. Cultures were incubated and the supernatants were assayed for IL-5 by EL1SA. The mean [SD] age for the asthmatic patients was 37.67[9.66] years with a mean [SD] body mass index of 28.3[6.12]. Male constituted 53% [11/19] of the studied asthmatic patients. The levels of 1L-5 in the supernatant of resting PBMN cultures were significantly higher in patients with asthma in all three states [basal state, after PHA stimulation, in cocultures with ALM [mean [SD] = 219.45[68.34] ng/ml, range [100-320 ng/ml], 484.85[115048.01], range [170-670 ng/ml], 1118 [336.59], range [530-1800 ng/ml], respectively. The respective levels in the nonatopic normal subjects was [mean [SD] 21.20[8.97], 26.8[10.10], 29.30[7.87]]. The differences between the three states in the asthmatic patients were highly significant. The changes between the three states in the non-asthmatic patients were insignificant. IL5 production by PBMN is markedly increased in asthmatic patients versus non-asthmatic subjects, furthermore, IL-5 production was markedly amplified by co-culturing PBMN with autologous ALM derived from BAL in the asthmatics patients. This is in contrast to the finidings in non-asthmatic subjects where IL5 production was not augmented by autologous ALM. The fact that ALM from non-asthmatic subjects functioned poorly as APC may represent a local inhibitory protective mechanism in the airways