Modulation of Allergic Airway Inflammation by the Oral Pathogen Porphyromonas gingivalis

Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA.
Infection and immunity (Impact Factor: 3.73). 03/2010; 78(6):2488-96. DOI: 10.1128/IAI.01270-09
Source: PubMed


Accumulating evidence suggests that bacteria associated with periodontal disease may exert systemic immunomodulatory effects. Although the improvement in oral hygiene practices in recent decades correlates with the increased incidence of asthma in developed nations, it is not known whether diseases of the respiratory system might be influenced by the presence of oral pathogens. The present study sought to determine whether subcutaneous infection with the anaerobic oral pathogen Porphyromonas gingivalis exerts a regulatory effect on allergic airway inflammation. BALB/c mice sensitized and subsequently challenged with ovalbumin exhibited airway hyperresponsiveness to methacholine aerosol and increased airway inflammatory cell influx and Th2 cytokine (interleukin-4 [IL-4], IL-5, and IL-13) content relative to those in nonallergic controls. Airway inflammatory cell and cytokine contents were significantly reduced by establishment of a subcutaneous infection with P. gingivalis prior to allergen sensitization, whereas serum levels of ovalbumin-specific IgE and airway responsiveness were not altered. Conversely, subcutaneous infection initiated after allergen sensitization did not alter inflammatory end points but did reduce airway responsiveness in spite of increased serum IgE levels. These data provide the first direct evidence of a regulatory effect of an oral pathogen on allergic airway inflammation and responsiveness. Furthermore, a temporal importance of the establishment of infection relative to allergen sensitization is demonstrated for allergic outcomes.

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Available from: Steven Offenbacher, Oct 02, 2015
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    • "While most studies of pulmonary bacterial infections and asthma are directed towards exacerbation, our investigations have been directed towards the development phase of the disease. Several other groups have investigated the role of bacterial infections on antigen sensitization, looking at Chlamydia muridarum, Streptococcus pneumoniae, or Porphyromonas gingivalis as their infection models [36], [37], [38]. However, all these models employ antigen sensitization via the intraperitoneal route using an adjuvant such as alum, and then examine the effects of bacterial infection on that sensitization. "
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