Open AccessExpression of bacterial genes and induction of INF‐γ in human myeloid dendritic cells during persistent infection with Chlamydophila pneumoniae
Author(s) -
Kis Zoltan,
Treso Balint,
Burian Katalin,
Endresz Valeria,
Pallinger Eva,
Nagy Agnes,
Toth Akos,
Takacs Maria,
Falus Andras,
Gonczol Eva
Publication year - 2008
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2007.00367.x
Subject(s) - biology , chlamydophila pneumoniae , cd11c , antigen , groel , microbiology and biotechnology , dendritic cell , monocyte , chlamydophila , cd40 , gene expression , immunology , population , immune system , virology , gene , chlamydiaceae , antibody , chlamydia , genetics , cytotoxic t cell , escherichia coli , demography , sociology , in vitro , phenotype
The interactions between human monocyte‐derived dendritic cells (DCs) and Chlamydophila pneumoniae ( Cpn ) infection were investigated. Cpn infection induced the maturation and functional activation of DCs, and Cpn antigens were present in all of the subpopulations during the maturation process. Chlamydial antigens were detected in DCs during an observation period of 28 days. The exponential production of infectious elementary bodies was not observed. Chlamydial transcripts of the 16S rRNA gene, groEL‐1 and omcB genes were expressed, as determined by a quantitative real‐time PCR, but the expression of the ftsK gene was limited. DC cultures produced IFN‐γ, but the presence of IFN‐γ in the culture medium was not the major factor that decreased the growth of Cpn , as was shown by neutralization of the IFN‐γ. A cell population identified as producing IFN‐γ had no markers for T, B, natural killer, monocyte cells or macrophages but displayed DC morphology and the expression of specific DC markers, such as CD11c and HLA‐DR. These results reveal a persistent infection of DCs with the expression of some, but not cell division‐related genes and the production of IFN‐γ that may contribute to the pathomechanism of chronic inflammatory diseases associated with persistent Cpn infection.