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Surfactant proteins A and D suppress alveolar macrophage phagocytosis via interaction with SIRP alpha

William J Janssen1, Kathleen A McPhillips, Matthew G Dickinson

  • 1Division of Pulmonary Medicine, Department of Medicine, National Jewish Medical and Research Center, K729, 1400 Jackson Street, Denver, CO 80206, USA. janssenw@njc.org

American Journal of Respiratory and Critical Care Medicine
|April 19, 2008
PubMed
Abstract

Insights

Surfactant proteins SP-A and SP-D inhibit the clearance of apoptotic cells by binding to SIRP alpha on macrophages. This suppression is overcome during inflammation by recruited phagocytes.

Area of Science:

  • Pulmonary immunology
  • Cellular biology
  • Inflammation resolution

Background:

  • Efficient clearance of apoptotic cells is crucial for resolving pulmonary inflammation.
  • Alveolar macrophages have a reduced capacity for apoptotic cell clearance at rest.
  • Surfactant proteins SP-A and SP-D may inhibit this clearance via SIRP alpha.

Purpose of the Study:

  • To determine if SP-A and SP-D binding to SIRP alpha suppresses apoptotic cell clearance by alveolar macrophages.
  • To investigate the mechanisms involved in this suppression.

Main Methods:

  • Assessed phagocytosis of apoptotic cells using macrophages treated with SP-A, SP-D, or C1q.
  • Confirmed SP-A and SP-D binding to SIRP alpha in vitro.
  • Studied downstream signaling molecules SHP-1 and RhoA.
  • Utilized SHP-1-deficient mice and chimeric mice for in vivo studies.

Main Results:

  • SP-A and SP-D suppressed macrophage phagocytosis of apoptotic cells.
  • Blocking SIRP alpha or inhibiting SHP-1 and RhoA reversed this suppression.
  • Macrophages from inflamed lungs showed enhanced apoptotic cell ingestion.
  • Recruited mononuclear phagocytes with low SP-A/SP-D levels mediated this enhanced clearance.

Conclusions:

  • SP-A and SP-D exert tonic inhibition on alveolar macrophage phagocytosis through SIRP alpha binding.
  • Recruited mononuclear phagocytes overcome apoptotic cell clearance defects during acute pulmonary inflammation.

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