CD11b regulates recruitment of alveolar macrophages but not pulmonary dendritic cells after pneumococcal challenge

Alun C Kirby1, John G Raynes, Paul M Kaye

  • 1Immunology Unit, Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom. ak510@york.ac.uk

Insights

Alveolar macrophages (AMs) and pulmonary dendritic cells (pulDCs) show distinct responses during pneumonia. CD11b expression is crucial for AM recruitment, but not pulDC recruitment, into the lung.

Area of Science:

  • Immunology
  • Pulmonary Medicine
  • Infectious Disease

Background:

  • Alveolar macrophages (AMs) and pulmonary dendritic cells (pulDCs) are key immune cells in the lungs.
  • Their distinct roles and responses during infection, particularly pneumonia, remain under-investigated.

Purpose of the Study:

  • To investigate and compare the distinct characteristics and recruitment kinetics of AMs and pulDCs during Streptococcus pneumoniae-induced pneumonia.
  • To elucidate the role of CD11b expression in the inflammatory response and cellular recruitment.

Main Methods:

  • Utilized a nonlethal, resolving mouse model of pneumonia induced by intranasal Streptococcus pneumoniae.
  • Analyzed cell populations using flow cytometry, focusing on CD11b expression on AMs and pulDCs.
  • Employed antibody blockade to assess the functional significance of CD11b in cellular recruitment.

Main Results:

  • AMs and pulDCs exhibited differential recruitment kinetics during pulmonary inflammation.
  • A distinct subset of CD11b(High) AMs contributed significantly to the increased AM numbers.
  • CD11b expression was upregulated on AMs by granulocyte-macrophage colony-stimulating factor and was critical for AM recruitment, but not pulDC recruitment.

Conclusions:

  • AMs and pulDCs display significantly different responses to pathogenic stimuli in vivo.
  • CD11b plays a critical role in the recruitment of AMs to the lungs during pneumococcal challenge.
  • These findings highlight the distinct immune mechanisms employed by AMs and pulDCs in resolving pneumonia.