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Modulation of rat granulocyte traffic by a surface active agent in vitro and bleomycin injury

J H Williams1, M Chen, J Drew

  • 1Division of Pulmonary and Critical Care Medicine, University of California Irvine Medical Center, Orange 92668.

Insights

Pluronic F68 (F68) reduces inflammatory cell accumulation in the lungs following bleomycin injury in rats. This surfactant impacts polymorphonuclear leukocyte (PMN) behavior, decreasing lung inflammation and weight gain.

Area of Science:

  • Biomedical Engineering
  • Pulmonary Medicine
  • Pharmacology

Background:

  • Pluronic F68 (F68), a nonionic surfactant, is known to inhibit polymorphonuclear leukocyte (PMN) adherence and migration in vitro.
  • The role of F68 in modulating inflammatory responses in vivo, particularly in lung injury models, requires further investigation.

Purpose of the Study:

  • To investigate the in vivo effects of Pluronic F68 (F68) on lung injury induced by intratracheal bleomycin instillation (ITB) in rats.
  • To assess the impact of F68 on PMN traffic and associated inflammatory markers in this acute lung injury model.

Main Methods:

  • Rats received a 12-hour infusion of F68 prior to intratracheal bleomycin instillation.
  • Lung lavage cellularity, lung weights, and spleen weights were measured 24 hours post-injury.
  • Circulating leukocyte counts, osmolality, and total complement levels were also analyzed.

Main Results:

  • F68 administration significantly decreased lavage leukocyte counts and lung weight gain in ITB-injured rats.
  • A strong correlation was observed between lung weight gain and logarithmic values of lavage PMN.
  • F68 also influenced circulating neutrophilia and reduced spleen weight gain in injured animals.

Conclusions:

  • Pluronic F68 (F68) demonstrates efficacy in modulating PMN traffic both in vitro and in vivo.
  • F68 treatment mitigates the inflammatory response in an acute rat lung injury model.
  • The findings highlight the critical role of PMN influx in early ITB-induced lung injury and suggest F68 as a potential therapeutic agent.

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