Source: Annual Congress 2002 - Cellular reactions in allergy in humans and animals
Disease area: Airway diseases

Abstract

Persistent infection with Chlamydia pneumoniae (Cpn) is implicated in the pathogenesis of asthma. The mechanisms are not known but there is evidence for involvement of T cells and monocytes. Adequate T cell activation requires antigen presentation via expression of major histocompatibility complex (MHC) molecules on antigen presenting cells, (eg monocytes) and a second costimulatory signal. We aimed to investigate monocyte expression of MHC and costimulatory molecules in response to Cpn stimulation. Methods Whole blood from healthy volunteers was obtained and incubated overnight in the presence of sonicated Cpn or E. coli LPS. Surface expression of costimulatory (CD80 and CD86) and MHC molecules was determined using flow cytometry. Results After exposure to Cpn or E. coli LPS, mean fluorescence intensity of cells expressing MHC molecules, CD80 and CD86, was increased, compared to baseline levels. Monocytes constitutively expressed CD86 and MHC molecules. CD80 was not expressed constitutively but was induced by Cpn or E. coli LPS. E. coli LPS increased CD80 expression in a dose dependent fashion. Conversely, Cpn initially caused a smaller increase and with higher doses a progressive decrease in CD80 expression, although this still remained above baseline. Conclusion Cpn is a relatively poor stimulator of CD80 compared with E. coli LPS. We have previously shown that Cpn promotes a Th2 cytokine response pattern in monocytes by upregulating IL10 production, which in turn may be responsible for decreased CD80 expression. We hypothesise that Cpn may not only promote asthma (increased Th2 response) but also induce its own persistent infection (decreased Th1 response).

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T. R. McNamara, G. L. Hodge, R. Scicchitano, M. D. Holmes (Adelaide, Australia). C. pneumoniae alters CD80 expression in monocytes: implications in asthma. Eur Respir J 2002; 20: Suppl. 38, 308

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