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Eosinophil leukocyte degranulation in response to serum-opsonized beads: C5a and platelet-activating factor enhance ECP release, with roles for protein kinases A and C

Egesten, Arne LU and Malm, Johan LU (1998) In Allergy 53(11). p.1066-1073
Abstract
BACKGROUND: Eosinophils have a typical content of granule-bound, cytotoxic, cationic proteins which may, when released to the external milieu, play roles in diseases such as asthma and parasitic infestation. Therefore, we have investigated possible mechanisms by which their release is regulated in eosinophils. METHODS: The enzyme-linked immunosorbent assay (ELISA) was used to detect released eosinophil cationic protein (ECP). Release of ECP was induced by serum-opsonized, nonphagocytosable Sephadex beads (SOS). RESULTS: The complement fragment C5a and platelet-activating factor (PAF) were found to enhance ECP release in response to SOS in a dose-dependent fashion, and, contrary to previous reports, they were not found to act as... (More)
BACKGROUND: Eosinophils have a typical content of granule-bound, cytotoxic, cationic proteins which may, when released to the external milieu, play roles in diseases such as asthma and parasitic infestation. Therefore, we have investigated possible mechanisms by which their release is regulated in eosinophils. METHODS: The enzyme-linked immunosorbent assay (ELISA) was used to detect released eosinophil cationic protein (ECP). Release of ECP was induced by serum-opsonized, nonphagocytosable Sephadex beads (SOS). RESULTS: The complement fragment C5a and platelet-activating factor (PAF) were found to enhance ECP release in response to SOS in a dose-dependent fashion, and, contrary to previous reports, they were not found to act as secretagogues themselves on eosinophils in suspension. The role of protein kinase C (PKC) in eosinophil degranulation has been controversial. We found that ECP release induced by SOS was inhibited by the PKC inhibitors staurosporine and calphostin C. Activation of protein kinase A (PKA), by raising cAMP, also inhibited ECP release. Furthermore, pertussis toxin decreased ECP release on opsonized beads, indicating the involvement of pertussis-toxin-sensitive G proteins. CONCLUSIONS: C5a, and PAF enhance granule release, rather than acting as secretagogues themselves. PKC and PKA have opposing roles in the regulation of ECP release in response to SOS. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Allergy
volume
53
issue
11
pages
1066 - 1073
publisher
Wiley-Blackwell
external identifiers
  • scopus:0031736641
ISSN
1398-9995
DOI
10.1111/j.1398-9995.1998.tb03816.x
language
English
LU publication?
yes
id
70837beb-233e-41f1-8d9d-53806db0e524 (old id 1296516)
date added to LUP
2009-07-31 11:16:24
date last changed
2017-01-01 06:59:46
@article{70837beb-233e-41f1-8d9d-53806db0e524,
  abstract     = {BACKGROUND: Eosinophils have a typical content of granule-bound, cytotoxic, cationic proteins which may, when released to the external milieu, play roles in diseases such as asthma and parasitic infestation. Therefore, we have investigated possible mechanisms by which their release is regulated in eosinophils. METHODS: The enzyme-linked immunosorbent assay (ELISA) was used to detect released eosinophil cationic protein (ECP). Release of ECP was induced by serum-opsonized, nonphagocytosable Sephadex beads (SOS). RESULTS: The complement fragment C5a and platelet-activating factor (PAF) were found to enhance ECP release in response to SOS in a dose-dependent fashion, and, contrary to previous reports, they were not found to act as secretagogues themselves on eosinophils in suspension. The role of protein kinase C (PKC) in eosinophil degranulation has been controversial. We found that ECP release induced by SOS was inhibited by the PKC inhibitors staurosporine and calphostin C. Activation of protein kinase A (PKA), by raising cAMP, also inhibited ECP release. Furthermore, pertussis toxin decreased ECP release on opsonized beads, indicating the involvement of pertussis-toxin-sensitive G proteins. CONCLUSIONS: C5a, and PAF enhance granule release, rather than acting as secretagogues themselves. PKC and PKA have opposing roles in the regulation of ECP release in response to SOS.},
  author       = {Egesten, Arne and Malm, Johan},
  issn         = {1398-9995},
  language     = {eng},
  number       = {11},
  pages        = {1066--1073},
  publisher    = {Wiley-Blackwell},
  series       = {Allergy},
  title        = {Eosinophil leukocyte degranulation in response to serum-opsonized beads: C5a and platelet-activating factor enhance ECP release, with roles for protein kinases A and C},
  url          = {http://dx.doi.org/10.1111/j.1398-9995.1998.tb03816.x},
  volume       = {53},
  year         = {1998},
}