Sulfidopeptide leukotrienes contribute to human alveolar macrophage activation in asthma

Prostaglandins Leukot Essent Fatty Acids. 1991 Feb;42(2):95-100. doi: 10.1016/0952-3278(91)90074-f.


The mechanism involved in amplification of the local inflammatory process, characteristic of asthma, was investigated through the role of human alveolar macrophages. During asthma attacks, mast cells and eosinophils are known to be activated in order to release arachidonic acid derived inflammation mediators such as sulfidopeptide leukotrienes. It is now known that these metabolites, particularly leukotriene C4, are present in bronchoalveolar lavage from asthmatic patients. Alveolar macrophages, recovered by bronchoalveolar lavage and purified by adherence, are able to transform LTC4 into LTE4. In four asthmatic patients with severe local inflammation as determined by fibrobronchoscopy, these phagocytes, incubated in the presence of LTC4, also generated LTB4 and 5-HETE, which remained within the cells. These preliminary results are discussed relative to amplification of the local process, involving cooperation between the different cells involved in airway responsiveness.

MeSH terms

  • Adult
  • Asthma / metabolism*
  • Asthma / physiopathology
  • Humans
  • Hydroxyeicosatetraenoic Acids / metabolism
  • In Vitro Techniques
  • Leukotriene B4 / metabolism
  • Leukotrienes / metabolism*
  • Macrophage Activation
  • Macrophages / metabolism*
  • Pulmonary Alveoli / metabolism*
  • SRS-A / metabolism


  • Hydroxyeicosatetraenoic Acids
  • Leukotrienes
  • SRS-A
  • Leukotriene B4
  • 5-hydroxy-6,8,11,14-eicosatetraenoic acid