Leukotrienes are involved in leukocyte recruitment induced by live Histoplasma capsulatum or by the beta-glucan present in their cell wall

Citation
Ai. Medeiros et al., Leukotrienes are involved in leukocyte recruitment induced by live Histoplasma capsulatum or by the beta-glucan present in their cell wall, BR J PHARM, 128(7), 1999, pp. 1529-1537
Citations number
46
Categorie Soggetti
Pharmacology & Toxicology
Journal title
BRITISH JOURNAL OF PHARMACOLOGY
ISSN journal
00071188 → ACNP
Volume
128
Issue
7
Year of publication
1999
Pages
1529 - 1537
Database
ISI
SICI code
0007-1188(199912)128:7<1529:LAIILR>2.0.ZU;2-5
Abstract
1 The inflammatory cell influx towards the peritoneal cavity in mice inocul ated i.p. with live or dead Histoplasma capsulatum or with its subcellular preparations was studied. We also evaluated the effects of dexamethasone (D exa) or MK886, an inhibitor of leukotriene (LT) biosynthesis, on the recrui tment of leukocytes. 2 Live yeast form of fungus (LYH) induced an increase in neutrophils (NE) w hich was highest 4 to 24 h after inoculation. Mononuclear cell (MN) migrati on beginning at 24 h with a gradual increase over -18 and 168 h, and an eos inophil (EO) recruitment occurs between 24 and 48 h. 3 NE and EO recruitment induced by dead mycelial form of fungus (DMH) was g reater than that observed for dead yeast form of fungus (DYH). A similar le ukocyte migration pattern was seen after i.p, injection of the alkali-insol uble fraction (F1) from DYH (F1Y) and F1 from DMH (FIM) this being more act ive than former. The difference in concentration of beta-glucan in DYH and DMH could explain the different inflammatory capacity exhibited by the two forms of H. capsulatum. 4 LT seems to be the principal mediator of leukocyte migration in response to LYH, DYH or DMH or to beta-glucan. However, other mediators appear to co ntribute to NE and EO migration since the treatment with Dexa was more effe ctive in inhibiting cell migration than MK886. Complement dependent leukocy te migration may participate in this recruitment. Treatment with MK886 comp letely abolished MN cell migration, indicating its dependence on the presen ce of LT.