Chlamydia pneumoniae modulates human monocyte-derived dendritic cells functions driving the induction of a Type 1/Type 17 inflammatory response.

Abstract:

:Chlamydia pneumoniae is a respiratory pathogen involved in the onset of chronic inflammatory pathologies. Dendritic cells (DC), are major players in spreading of C. pneumoniae from the lungs, a crucial step leading to disseminated infections. Less is known concerning modulation of DC functions consequent to encounter with the bacterium. In order to address this aspect, human monocyte-derived (MD)DC were infected with C. pneumoniae. After internalization bacterial counts increased in MDDC, as well as the expression of CPn1046, a gene involved in bacterial metabolism, with a peak 48 h after the infection. Infected MDDC switched to the mature stage, produced IL-12p70, IL-1β, IL-6, and IL-10, and drove a mixed Type 1/Type 17 polarization. Intracellular pathways triggered by C. pneumoniae involved Toll-like receptor (TLR) 2. Indeed, TLR2 was activated by C. pneumoniae in transfected HEK 293 cells, and C. pneumoniae-mediated phosphorylation of ERK1/2 was inhibited by an anti-TLR2 antibody in MDDC. When an ERK1/2 inhibitor was used, IL-12p70 and IL-10 release by MDDC was reduced and T cell polarization shifted towards a Type 2 profile. Overall, our findings unveiled the role played by TLR2 and ERK1/2 induced by C. pneumoniae to affect DC functions in a way that contributes to a Type 1/Type 17 pro-inflammatory response.

journal_name

Microbes Infect

journal_title

Microbes and infection

authors

Flego D,Bianco M,Quattrini A,Mancini F,Carollo M,Schiavoni I,Ciervo A,Ausiello CM,Fedele G

doi

10.1016/j.micinf.2012.11.004

subject

Has Abstract

pub_date

2013-02-01 00:00:00

pages

105-14

issue

2

eissn

1286-4579

issn

1769-714X

pii

S1286-4579(12)00275-4

journal_volume

15

pub_type

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