Infection of human monocytes by Chlamydia pneumoniae and Chlamydia trachomatis: an in vitro comparative study.
BACKGROUND
An increasing number of studies suggest that chlamydiae can infect immune cells. The altered immune cell function could contribute to the progression of several chronic inflammatory diseases.The aim of this study was to comparatively evaluate Chlamydia pneumoniae (CP) and Chlamydia trachomatis (CT) interactions with in vitro infected human blood monocytes.


RESULTS
Fresh isolated monocytes were infected with viable CP and CT elementary bodies and infectivity was evaluated by recultivating disrupted monocytes in permissive epithelial cells.The production of reactive oxygen and nitrogen species was studied in the presence of specific fluorescent probes. Moreover, TNF-α, INF-α, INF-β and INF-γ gene expression was determined. CT clearance from monocytes was complete at any time points after infection, while CP was able to survive up to 48 hours after infection. When NADPH oxydase or nitric oxide synthase inhibitors were used, CT infectivity in monocytes was restored, even if at low level, and CT recovery's rate was comparable to CP one.CT-infected monocytes produced significantly higher levels of reactive species compared with CP-infected monocytes, at very early time points after infection. In the same meanwhile, TNF-α and INF-γ gene expression was significantly increased in CT-infected monocytes.


CONCLUSIONS
Our data confirm that CP, but not CT, is able to survive in infected monocytes up to 48 hours post-infection. The delay in reactive species and cytokines production by CP-infected monocytes seems to be crucial for CP survival.
Microbiology, DIMES, University of Bologna, S,Orsola Hospital, via Massarenti 9, 40138 Bologna, Italy. antonella.marangoni@unibo.it.
Antonella
A
Marangoni
Christian
C
Bergamini
Romana
R
Fato
Claudia
C
Cavallini
Manuela
M
Donati
Paola
P
Nardini
Claudio
C
Foschi
Roberto
R
Cevenini
D002478:Cells, Cultured; D002692:Chlamydia trachomatis / Q000502:physiology*; D016993:Chlamydophila pneumoniae / Q000502:physiology*; D004791:Enzyme Inhibitors; D004847:Epithelial Cells / Q000378:metabolism / Q000382:microbiology*; D015870:Gene Expression; D006801:Humans; D016898:Interferon-alpha / Q000235:genetics / Q000378:metabolism; D016899:Interferon-beta / Q000235:genetics / Q000378:metabolism; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D050296:Microbial Viability; D009000:Monocytes / Q000378:metabolism / Q000382:microbiology*; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D013045:Species Specificity; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D004791:Enzyme Inhibitors; D016898:Interferon-alpha; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D016899:Interferon-beta; D007371:Interferon-gamma; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D019255:NADPH Oxidases