Chlamydia pneumoniae induces interleukin-6 and interleukin-10 in human gingival fibroblasts

Authors

  • Antonietta Rizzo,

    1. Department of Experimental Medicine, Section of Microbiology and Clinical Microbiology, Faculty of Medicine and Surgery
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  • Rossella Paolillo,

    1. Department of Experimental Medicine, Section of Microbiology and Clinical Microbiology, Faculty of Medicine and Surgery
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  • Alfonso Galeota Lanza,

    1. Department of Experimental Medicine, Section of Microbiology and Clinical Microbiology, Faculty of Medicine and Surgery
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  • Luigi Guida,

    1. Department of Odontostomatological, Orthodontic and Surgical Disciplines, Faculty of Medicine and Surgery, Second University of Naples, Naples, Italy
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  • Marco Annunziata,

    1. Department of Odontostomatological, Orthodontic and Surgical Disciplines, Faculty of Medicine and Surgery, Second University of Naples, Naples, Italy
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  • Caterina Romano Carratelli

    1. Department of Experimental Medicine, Section of Microbiology and Clinical Microbiology, Faculty of Medicine and Surgery
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Correspondence
Caterina Romano Carratelli, Via Santa Maria di Costantinopoli,16, 80138 Napoli, Italy.
Tel: +39 081 566 5658; fax +39 081 566 5668; email: caterina.romanocarratelli@unina2.it

ABSTRACT

Chlamydia pneumoniae is an obligate intracellular Gram-negative bacterium with a unique biphasic developmental cycle that can cause persistent infections. In humans, Chlamydia causes airway infection and has been implicated in chronic inflammatory diseases, such as asthma and atherosclerosis. In addition, recent studies demonstrated that patients with severe periodontitis can harbor C. pneumoniae, which can increase the risk for a host inflammatory response with weighty clinical sequelae. Previous studies have established that periodontal pathogenic bacteria (i.e. Gram-negative bacteria) can induce the synthesis and release of cytokines and other inflammatory mediators in human gingival fibroblasts. HGF are resident cells of the periodontium that respond to receptor stimulation by producing a variety of substances including cytokines and growth factors. Our results demonstrate that after 48 hr of incubation with viable C. pneumoniae HGF showed a proliferative response, as seen by both colorimetric MTT assay and direct cell count (30% and 35%, respectively). In addition, HGF incubated with viable or UV light-inactivated C. pneumoniae organisms showed an increase in the levels of IL-6 and IL-10, but not IL-4; on the contrary, HGF infected with heat-killed bacteria did not show a significant production of any of the cytokines considered. In conclusion, the present study suggests that C. pneumoniae may modulate the expression of IL-6 and IL-10 by human gingival fibroblasts. Further studies are warranted to clarify the molecular mechanisms of C. pneumoniae in the regulation of cytokine expression by host cells and to elaborate the relevant clinical implications.

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