Allergic Airway Sensitization Impairs Bacterial Specific IgG and Correlates with Increased Mycoplasma Pneumoniae Persistence
Sunday, March 6, 2016
South Exhibit Hall H (Convention Center)
Arthur H. Totten, Danlin Luo, Li Xiao, Donna M Crabb, Ken B Waites, T. Prescott Atkinson, MD PhD FAAAAI
Rationale: Mycoplasma pneumoniae (Mpn), an atypical human pathogen, has been associated with both asthma initiation and exacerbation. Asthmatics have been reported to have higher carriage rates of Mpn compared to non-asthmatic controls. We hypothesized that allergic airway sensitization would impair host immune responses to Mpn infection in a murine model.

Methods: BALB/cJ mice were sensitized and challenged with ovalbumin (OVA) to induce allergic airway disease and then infected with Mpn. Immune parameters were studied by analysis of cellular infiltrates in bronchioalveolar lavage fluid (BALF), ELISA of specific serum antibody levels for Mpn and OVA, and cytokine transcript levels in total lung RNA. Bacterial burden was determined by detection of bacterial 16S rRNA with qPCR.

Results: Mpn-specific IgG antibody levels were negatively correlated with OVA-specific IgE levels (r = -0.6732, p < 0.05). OVA-specific IgE and IgG levels were enhanced following Mpn infection, suggesting peripheral Th2 cytokine enhancement with infection (p < 0.001). Strikingly, Mpn-specific IgG antibody levels during allergic airway sensitization were negatively correlated with Mpn latency at 21 days post-infection (r = -0.6668, p < 0.01). 

Conclusions: Prior allergic sensitization results in impaired Mpn-specific antibody production and pathogen clearance following subsequent infection.  Mpn infection augments allergen-specific IgE production in sensitized mice.