These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Differential production of chemokines and their role in neutrophil infiltration in rat allergic inflammation. Author: Nakagawa H, Ando Y, Takano K, Sunada Y. Journal: Int Arch Allergy Immunol; 1998 Feb; 115(2):137-43. PubMed ID: 9482702. Abstract: BACKGROUND: Recently we demonstrated that activated rat macrophages produced neutrophil chemotactic factors (chemokines) including cytokine-induced neutrophil chemoattractant (CINC)-1, CINC-2alpha, CINC-2beta, CINC-3/rat macrophage inflammatory protein (MIP)-2 and rat MIP-1alpha (rMIP-1alpha). METHODS: In the present study, by using an enzyme-linked immunosorbent assay specific for each chemokine, we determined the levels of the chemokines in the pouch fluid (inflammatory site) of the fluorescein isothiocyanate-labeled ovalbumin (FITC-OVA)-induced allergic inflammation in rats. Effects of anti-chemokine antibodies on neutrophil chemotaxis were determined in vivo and in vitro. RESULTS: CINC-1 was the major chemokine which rapidly increased after challenge with FITC-OVA, whereas CINC-3 was a minor one, and CINC-2, CINC-3 and rMIP-1alpha increased slowly with a lag time of about 2 h. Anti-CINC-1/CINC-2 antibodies, which inhibited all the CINCs, suppressed both neutrophil infiltration in vivo and neutrophil chemotactic activity of the 8-hour pouch fluid in vitro, whereas anti-rMIP-1alpha antibody slightly suppressed the chemotaxis in vivo and in vitro. CONCLUSION: Our results suggest that CINCs, especially CINC-1 and CINC-2, play an important role in the infiltration of neutrophils into the inflammatory site of FITC-OVA-induced allergic inflammation in rats.[Abstract] [Full Text] [Related] [New Search]