IL-10 Cytokine Responses in Chlamydia pneumoniae-Stimulated Human Peripheral Blood Mononuclear Cells

Chlamydia pneumoniae (C. pneumoniae) is a gram-negative intracellular bacterium that causes respiratory infections and may contribute to inflammatory responses in asthma. Cell-mediated immune responses are important for protective immunity against C. pneumoniae; however, these responses may be impaired in asthma. Interleukin (IL)-10 is a cytokine that modulates innate and adaptive immunity. IL-10 is necessary for resolution of acute infection, and maturation of memory T cells. The aim of this study sought to compare IL-10 responses between subjects with or without asthma, and according to C. pneumoniae IgG antibody (Ab) or serum IgE status.

Peripheral blood mononuclear cells (PBMC) (1×10⁶/mL) from stable adult asthmatic (N=6) and non-asthmatic subjects (N=6) were infected +/- C. pneumoniae TW-183 at a multiplicity of infection (MOI)=0.1, using dose responses (1:10, 1:100), and cultured 48 hrs. IL-10 responses were measured in supernatants (ELISA). C. pneumoniae-IgG Abs and total serum IgE levels were measured in serum (EIA, ELISA).

Cytokine responses (mean differences: unstimulated-stimulated cells) were significant for IL-10 (1:10, 1:100) (-618±443, -1405±155) (P=0.0005, 0.0005) in all subjects (Wilcoxon signed-rank test). When subjects were stratified according to asthma, C. pneumoniae IgG Ab or serum IgE status, no significant cytokine responses were observed.

C. pneumoniae stimulates IL-10 responses in subjects with or without asthma. These responses are not dependent on either asthma, C. pneumoniae IgG Ab or serum IgE status.