Eosinophil degranulation in the presence of lung fibroblasts.
BACKGROUND
Although eosinophils (Eos) and fibroblasts (Fb) are closely approximated in the bronchial submucosae of asthmatics, and are believed to play important roles in the pathogenesis of bronchial asthma, the interaction between Eos and Fb has not been thoroughly elucidated. In this study, we have examined eosinophil cationic protein (ECP) release from human Eos cultured in the presence of human lung Fb.


METHODS
Eos from healthy donors were cultured with or without C5a for 16 h in the presence of human fetal lung Fb which had previously been incubated with or without some cytokines for 4 h. ECP in supernatants was measured by RIA.


RESULTS
ECP release was potentiated only when both Eos and Fb were activated by C5a and TNF, respectively, while it was not significantly potentiated when either Eos or Fb were activated. ECP release from Eos activated by C5a was also potentiated when Fb were stimulated by IL-1beta. The enhancement of ECP release in cocultured Eos and Fb with stimulation was partly inhibited by monoclonal antibodies against GM-CSF and was accompanied by the enhancement of adhesion of Eos to Fb.


CONCLUSIONS
This study shows that the stimulation of both Eos and Fb increases ECP release. It is suggested that Fb may influence Eos degranulation and play a role in the pathogenesis of bronchial asthma.
Takafuji
S
S
Department of Medicine and Physical Therapy, Faculty of Medicine, University of Tokyo,Tokyo, Japan. takafu@po.iijnet.or.jp
Shoji
S
S
Ito
K
K
Yamamoto
K
K
Nakagawa
T
T
D001249:Asthma / Q000209:etiology; D001798:Blood Proteins / Q000378:metabolism; D002450:Cell Communication; D015550:Cell Degranulation / Q000187:drug effects; D002460:Cell Line; D018920:Coculture Techniques; D015936:Complement C5a / Q000494:pharmacology; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000187:drug effects / Q000276:immunology / Q000502:physiology*; D005347:Fibroblasts / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000209:etiology; D007375:Interleukin-1 / Q000494:pharmacology; D008168:Lung / Q000166:cytology* / Q000187:drug effects / Q000502:physiology*; D012260:Ribonucleases; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D015936:Complement C5a; D012260:Ribonucleases