Endotoxin-stimulated alveolar macrophage recruitment of neutrophils and modulation with exogenous surfactant

Crit Care Med. 1998 Aug;26(8):1414-8. doi: 10.1097/00003246-199808000-00029.

Abstract

Objective: To determine whether endotoxin-stimulated alveolar macrophages would attract neutrophils and whether exogenous surfactant treatment would modulate this chemoattraction.

Design: Alveolar macrophages were harvested from bronchoalveolar lavage fluid and neutrophils from the blood of anesthetized guinea pigs.

Subjects: Hartley guinea pigs.

Interventions: Alveolar macrophages were suspended in RPMI 1640 and stimulated with 1 microg/mL of lipopolysaccharide (LPS), the supernatant removed and the alveolar macrophages were incubated in either RPMI or RPMI with surfactant at two different doses (292 microg/mL or 875 microg/mL) for 16 hrs.

Measurements and main results: The supernatant was extracted from the alveolar macrophages and placed in a chemotaxis plate and the migration of neutrophils was measured. Chemotaxis of all cell types to be tested was measured by a change of absorbance on a microplate reader set at 492 nm. Results were compared with alveolar macrophages not stimulated with LPS, RPMI alone, and N formyl-methionyl-leucyl-phenylalanine (FMLP). The supernatant of the stimulated alveolar macrophages increased neutrophil chemotaxis as compared with unstimulated alveolar macrophages, and RPMI (p < .05). Surfactant treatment with 292 microg/mL significantly decreased LPS-stimulated alveolar macrophages induced neutrophil chemotaxis. Treatment with 875 microg/mL of surfactant did not alter neutrophil chemotaxis.

Conclusions: Alveolar macrophages stimulation with LPS increased the chemotaxis of neutrophils. Treatment with surfactant at a concentration of 875 microg/mL did not alter neutrophil migration; however, treatment with 292 microg/mL significantly decreased neutrophil chemotaxis suggesting that at low concentrations, surfactant inhibits chemokine release and may reduce pulmonary neutrophil sequestration in vivo.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chemotaxis, Leukocyte / physiology
  • Escherichia coli*
  • Guinea Pigs
  • Lipopolysaccharides / pharmacology*
  • Macrophages, Alveolar / drug effects
  • Macrophages, Alveolar / physiology*
  • Male
  • N-Formylmethionine Leucyl-Phenylalanine / pharmacology
  • Neutrophils / physiology*
  • Surface-Active Agents / pharmacology*

Substances

  • Lipopolysaccharides
  • Surface-Active Agents
  • N-Formylmethionine Leucyl-Phenylalanine