A comparison of Streptococcus pneumoniae serotype 3 and serotype 14 infection in neonatal mice

Open Access
Author:
Bernardo, Tiffany Marie
Area of Honors:
Nutritional Sciences
Degree:
Bachelor of Science
Document Type:
Thesis
Thesis Supervisors:
  • A Catharine Ross, Thesis Supervisor
  • Rebecca L Corwin, Honors Advisor
Keywords:
  • pneumonia
  • streptococcus pneumoniae
  • serotype 3
  • serotype 14
  • vitamin A
  • retinoids
  • lung infection
  • neonates
  • leukocytes
Abstract:
Streptococcus pneumoniae, commonly referred to as the pneumococcus, is a Gram positive pathogen that colonizes the upper airways of humans (1). S. pneumoniae is the most frequent cause of community-acquired pneumonia, which occurs when the pneumococcus populates the lower bronchi, and is often the cause of otitis media in children (1, 2). This bacterium is also responsible for certain invasive diseases, such as sepsis and meningitis (3). S. pneumoniae colonization, pathogenesis, and clearance is well−documented in adults, but very few papers have characterized the effect of S. pneumoniae infection in neonates. Thus, the goal of the present study was to develop a model of pneumococcal disease in neonatal mice, and determine the efficacy of vitamin A (VA) supplementation on Streptococcus pneumoniae−induced pneumonia pathogenesis. Streptococcus pneumoniae serotype 3 (ST3) and serotype 14 (ST14) were chosen as a model of invasive and localized pneumococcal infection, respectively. We found that ST14 infection causes a large neutrophil influx to the lung 24 and 48 hours post−infection, while ST3 causes very little granulocyte migration. A myeloperoxidase (MPO) assay was used to confirm the increased levels of neutrophil activity during an acute infection with ST14. Furthermore, VA supplementation was found to have no effect on lung colonization, bacterial migration, or cellular infiltration, but VA supplementation significantly increased liver retinol levels. The data gathered in this study can be used to further knowledge regarding the complex interaction between diet, the host immune system, and bacterial pathogenesis.