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Clearance of Pneumococcal Colonization in Infants Is Delayed through Altered Macrophage Trafficking

Steven J Siegel1, Edwin Tamashiro2, Jeffrey N Weiser3

  • 1Department of Microbiology, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.

Plos Pathogens
|June 25, 2015
PubMed

Insights

Infant mice show prolonged Streptococcus pneumoniae carriage due to delayed macrophage recruitment. This is linked to altered chemokine signaling, hindering clearance of the bacteria.

Area of Science:

  • Immunology
  • Microbiology
  • Pediatrics

Background:

  • Infections, particularly Streptococcus pneumoniae, are a leading cause of infant mortality globally.
  • Prolonged pneumococcal colonization in children precedes invasive disease, but underlying mechanisms remain unclear.

Purpose of the Study:

  • To investigate the mechanisms behind prolonged pneumococcal carriage in infants.
  • To understand the role of immune cell recruitment and chemokine signaling in infant susceptibility to pneumococcal colonization.

Main Methods:

  • Utilized infant mouse models to study Streptococcus pneumoniae colonization.
  • Analyzed macrophage recruitment into the nasopharyngeal lumen.
  • Measured chemokine (C-C) motif ligand 2 (Ccl2/Mcp-1) and Ccl7 expression.
  • Investigated the role of the infant microbiota.

Main Results:

  • Infant mice exhibited delayed macrophage recruitment and prolonged pneumococcal carriage compared to adults.
  • Failure to upregulate Ccl2/Mcp-1, a key chemoattractant for macrophages, was observed in infants.
  • Baseline Ccl2 and Ccl7 expression was higher in infant upper respiratory tracts, dependent on the microbiota.

Conclusions:

  • Altered baseline signals governing macrophage recruitment in infant mice impair innate immune responses to pneumococcal colonization.
  • This delay in immune cell infiltration contributes to prolonged bacterial carriage and increased susceptibility in infants.

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