Chlamydia pneumoniae enhances the Th2 profile of stimulated peripheral blood mononuclear cells from asthmatic patients

Chlamydia pneumoniae is a cause of respiratory infection in adults and children. There is evidence for an association between atypical bacterial respiratory pathogens and the pathogenesis of asthma. We compared T helper (Th) responses in C. pneumoniae – infected peripheral blood mononuclear cells (PBMC) in patients with or without asthma. PBMC (1 × 106/mL) from asthmatic patients (N = 11) and non-asthmatic controls (N = 12) were infected or mock-infected for 1 h +/− C. pneumoniae TW-183 at a multiplicity of infection (MOI) = 1 and MOI = 0.1, or cultured for 24 h +/− Lactobacillus rhamnosus GG (LGG). Interleukin (IL)-4, IL-10, IL-12, Interferon (IFN)-gamma and total IgE levels were measured in supernatants (ELISA). C. pneumoniae infection led to an increase (>50%) of IgE levels in PBMC from asthmatics, compared with mock-infected on day 10; IgE wasn’t detected in non-asthmatics. C. pneumoniae – infected PBMC from asthmatics increased levels of IL-4 and IFN-gamma after 24 h, compared with PBMC alone; levels of IL-10 and IL-12 were low. When uninfected-PBMC from asthmatics were LGG-stimulated, after 24 h, IL-4 was undetectable, but IL-10, IL-12, and IFN-gamma increased, compared with PBMC alone. Thus, C. pneumoniae infection has the ability to induce allergic responses in PBMC of asthmatics, as evidenced by production of Th2 responses and IgE.