Independent of bacterial clearance, Interleukin-17A acts to exacerbate pulmonary inflammation in BALB/c mice infected with Mycoplasma pulmonis




Mize, Maximillion T.
Simecka, Jerry


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Purpose: Accounting for >50,000 deaths per year, lung infections are a leading cause of mortality in the United States. Chronic lung diseases complicated by infectious disease result in an additional 140,000 deaths. As a leading cause of pneumonia in man and animals worldwide, mycoplasmas cause persistent infections that induce debilitating chronic lung inflammation. An incomplete understanding on the pathogenesis of disease has contributed to the absence of effective vaccines against these organisms. Using a naturally occurring murine model mirroring human and animal infections, interleukin-17A (IL-17A) was found to increase within the lungs of susceptible BALB/c and resistant C57BL/6 mice inoculated with M. pulmonis. In a previous study, C57BL/6 mice deficient in IL-17 receptor expression were shown to have impaired clearance of mycoplasma. We hypothesized that IL-17A may have a different role in susceptible BALB/c mice. Consistent with this idea, we report that injection of neutralizing antibodies against IL-17A reduced respiratory inflammation in BALB/c infected with M. pulmonis. This was seen through abrogated lymphoid and neutrophil recruitment when compared to littermate controls. In addition, both gross lung and alveolar lesions were significantly reduced upon IL-17A neutralization. Surprisingly, blocking IL-17A did not alter bacterial burden, thus solely influencing the inflammatory process during infection in BALB/c mice. Interestingly, anti-IL-17A antibody administration did not have an effect mycoplasma infection in resistant C57BL/6 mice, suggesting that the IL-17A pathways differ between susceptible and resistant strains of mice.


Research Appreciation Day Award Winner - 2015 Department of Cell Biology and Immunology - 2nd Place Oral Presentation