The effect of ammonia exposure on pulmonary surfactant and chronic murine mycoplasmosis

Open Access
Booth, Jennifer Lynn
Graduate Program:
Laboratory Animal Medicine
Master of Science
Document Type:
Master Thesis
Date of Defense:
Committee Members:
  • Zissis C Chroneos, Thesis Advisor
  • mouse
  • housing
  • husbandry
  • static cage
  • individually ventilated cage
  • mycoplasma pulmonis
  • surfactant
  • ammonia
Within various animal and industrial settings there are concerns about air quality related to animal manure and by-products. Ammonia (NH¬¬3) is an air pollutant and irritant that has been recognized to cause various clinical signs in people and animals, including the development of respiratory disease. Ammonia concentrations in the microenvironment of laboratory rodents can be altered based upon housing and husbandry practices. These differences could potentially serve as a variable in certain research models, especially those involving respiratory investigations. In this study, female C57BL/6J mice were separated into groups that were either housed in individually ventilated or filter-topped caging without forced ventilation (hereafter referred to as static caging), and cages changed at either 1 or 2 week intervals. Within 5 days, static cages reached a significantly higher concentration of NH¬¬3 than the ventilated cages. The effect of this ammonia exposure on pulmonary inflammation, pathogen clearance, and surfactant levels after intranasal challenge with Mycoplasma pulmonis infection was then assessed. Baseline levels of inflammation, prior to infection, tended to be higher in mice housed in static cages and for mice that had their cages changed at 2 week intervals, however these differences were not statistically significant. Exposure to higher concentrations of ammonia exacerbated the mycoplasmal infection in mice housed in static cages, causing them to have higher CFU counts in the earlier stages of infection when compared to mice in ventilated cages. Mice in static cages also experienced a rapid decrease in pulmonary mycoplasma burden, while mice in ventilated cages had a much slower rate of clearance. The effect of mycoplasma on pulmonary surfactant proteins was characterized by a significant increase of surfactant protein A (SP-A) at 3 days post-infection. SP-A levels resolved back to baseline by 14 days post-infection. The observed variation in mycoplasma infection and fluctuation of local humoral immunity may have confounding effects on mice used as models of respiratory disease. When institutions or facilities consider changing housing and husbandry practices of laboratory rodents, it is critical to consider physiological and pathologic effects and its potential impact on research.