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Disparate Innate Immune Responses to Persistent and Acute Chlamydia pneumoniae Infection in Chronic Obstructive Pulmonary Disease

¹ Medical Clinic, Research Center Borstel, Borstel, Germany; ² Institute of Medical Microbiology and Hygiene, University of Schleswig-Holstein, Campus Lübeck, Lübeck, Germany; ³ Clinical and Experimental Pathology, Research Center Borstel, Borstel, Germany; ⁴ Division of Pulmonary Pharmacology, Research Center Borstel, Borstel, Germany; ⁵ Department of Thoracic Surgery, Krankenhaus Großhansdorf, Großhansdorf, Germany; ⁶ Department of Thoracic Surgery, University of Schleswig-Holstein, Campus Lübeck, Lübeck, Germany; and ⁷ Medical Clinic III, University of Schleswig-Holstein, Campus Lübeck, Lübeck, Germany

Correspondence and requests for reprints should be addressed to Daniel Droemann, M.D., Medical Clinic, Research Center Borstel, Parkallee 35, D-23845 Borstel, Germany. E-mail: ddroemann{at}fz-borstel.de

Rationale: Chlamydia pneumoniae (Cpn) infection may play a role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Few data are available comparing persistent and acute infection of this pathogen in the human respiratory tract.

Objectives: To study Cpn-induced innate immune responses in lung tissue from patients with COPD and control subjects ex vivo and in vitro.

Methods: Cpn detection was done by nested polymerase chain reaction, in situ hybridization, and immunohistochemistry ex vivo in unstimulated tissue and in vitro using an acute Cpn infection model. As main endpoints for the assessment of early cellular responses, nuclear factor (NF)-B activation and CXC chemokine ligand (CXCL)-8 expression were evaluated. The role of Toll-like receptors (TLRs) as recognition molecules in Cpn-induced innate responses was tested by blocking experiments.

Measurements and Main Results: Fifteen percent of patients with COPD were chronically infected with Cpn in contrast to 0% of control subjects (p < 0.05). There were no differences in CXCL-8 and NF-B expression between infected and noninfected COPD tissue ex vivo. In contrast, acute in vitro infection induced an intense innate immune response including up-regulation of TLR2. Blocking experiments demonstrated the predominant role of TLR2 in induction of the early immune response, whereas no influence on chlamydial infection rates was observed.

Conclusions: Acute in vitro infection of human lung tissue with Cpn elicited a marked innate response via TLR2, whereas chronic chlamydial infection in patients with COPD was not associated with enhanced cellular activation. These findings suggest different roles of Cpn during acute and chronic stages of pulmonary infection.

Key Words: Chlamydia pneumoniae • innate immunity • pulmonary host defense • Toll-like receptor 2 • chronic obstructive pulmonary disease

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Chlamydia pneumoniae (Cpn) infection may play a role in the pathogenesis of chronic obstructive pulmonary disease. Few data are available comparing persistent and acute infection of this pathogen in the human respiratory tract. What This Study Adds to the Field Although acute infection with Cpn elicited an inflammatory response via Toll-like receptor 2, chronic infection in patients with chronic obstructive pulmonary disease was not associated with enhanced lung pathology, suggesting different roles of Cpn.

 

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