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Volume 14 Supplement 2

Sepsis 2010

Chlamydophila pneumoniae infection in macrophages and in lung epithelial cells: IL-10 and the innate immunity response

Introduction

The genus of Chlamydiae comprises obligate intracellular pathogens that occasionally can disseminate and even cause septic infections. Chlamydophila pneumoniae causes acute and chronic respiratory tract infections from sinusitis to severe pneumonia, and phagocytes can transmit the bacteria from the lungs to the vasculature. We have previously shown in IL-10 knockout mice that IL-10 limits the severity of inflammation but prolongs the clearance of the C. pneumoniae pneumonia [1].

Objective

Although IL-10 could contribute to the resolution of C. pneumoniainfection by regulating the T-helper cell balance (Th1/Th2), we were interested in the direct effects of IL-10 and the IL-10-regulated genes in modulating C. pneumoniae growth in macrophages and in respiratory epithelial cells.

Methods

We investigated the effect of IL-10 and the expression of an IL-10-responsive anti-inflammatory factor on mRNA and protein level in C. pneumoniae infected human monocyte/macrophage (MonoMac6 and Thp-1) and in lung epithelial adenocarcinoma (A549) and in HL (human lung) cell lines. We also applied a luciferase promoter assay to study the regulation of the anti-inflammatory gene expression during the C. pneumoniae infection.

Results

In agreement with the previous studies, C. pneumoniae proliferated in epithelial cells, while in monocyte/macrophages the infection was often nonproductive and aberrant forms of bacteria were observed. The IL-10 responsive anti-inflammatory factor was differentially regulated at transcriptional level in A549 and MonoMac6 cells in response to C. pneumoniae infection, which could potentially affect the outcome of infection. The luciferase promoter assay showed that the transcription was mediated via the E-box regulatory element of the gene.

Conclusions

Our results imply that the anti-inflammatory response to intracellular C. pneumoniae infection varies in different cell types and ongoing studies are needed to clarify the role of IL-10 response in limiting Chlamydia growth in these cells.

References

  1. 1.

    Penttilä T, Haveri A, Tammiruusu A, Vuola JM, Lahesmaa R, Puolakkainen M: Chlamydia pneumoniae infection in IL-10 knock out mice: accelerated clearance but severe pulmonary inflammatory response. Microb Pathog 2008, 45: 25-29. 10.1016/j.micpath.2008.02.004

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Acknowledgements

JTK was financially supported by Drug Discovery Graduate School, Finland.

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Correspondence to JT Korhonen.

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Korhonen, J., Lahesmaa, R. & Puolakkainen, M. Chlamydophila pneumoniae infection in macrophages and in lung epithelial cells: IL-10 and the innate immunity response. Crit Care 14, P38 (2010). https://doi.org/10.1186/cc9141

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Keywords

  • Sinusitis
  • Lung Epithelial Cell
  • Respiratory Epithelial Cell
  • Chlamydophila Pneumoniae
  • Chronic Respiratory Tract Infection
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