Analysis of cytokine production in a newly developed canine tracheal epithelial cell line infected with H3N2 canine influenza virus

2015 ◽  
Vol 160 (6) ◽  
pp. 1397-1405 ◽  
Author(s):  
Woo-Jung Park ◽  
Byung-Joo Park ◽  
Young-Jo Song ◽  
Dong-Hun Lee ◽  
Seong-Su Yuk ◽  
...  
1996 ◽  
Vol 14 (2) ◽  
pp. 146-154 ◽  
Author(s):  
S H Randell ◽  
J Y Liu ◽  
P C Ferriola ◽  
L Kaartinen ◽  
M M Doherty ◽  
...  

1982 ◽  
Vol 3 (11) ◽  
pp. 1283-1287 ◽  
Author(s):  
Alan Eastman ◽  
Brooke T. Mossman ◽  
Edward Bresnick

1993 ◽  
Vol 8 (5) ◽  
pp. 522-529 ◽  
Author(s):  
K. Kunzelmann ◽  
E. M. Schwiebert ◽  
P. L. Zeitlin ◽  
W.-L. Kuo ◽  
B. A. Stanton ◽  
...  

1993 ◽  
Vol 265 (3) ◽  
pp. C781-C791 ◽  
Author(s):  
R. A. Harris ◽  
J. W. Hanrahan

We have studied the cytosolic free Ca2+ concentration ([Ca2+]i) response to histamine and other inflammatory mediators in a cystic fibrosis tracheal epithelial cell line (CF/T43) using digital fluorescence imaging. Brief pulses of histamine increased [Ca2+]i in a concentration-dependent manner with threshold, half-maximal, and maximal responses at approximately 5 microM, 120 microM, and 10 mM, respectively. The calcium response to sustained histamine exposure was markedly biphasic, consisting of an early peak (to approximately 2.4 microM [Ca2+]i) followed by a smaller second peak that lasted 45-60 s. Neither peak was directly dependent on Ca2+ influx. In contrast, stimulation with bradykinin gave a single peak followed by a smooth decay back to baseline levels. Sustained perfusion with histamine did not affect the bradykinin response, which is known to be mediated by inositol 1,4,5-trisphosphate (IP3). The H1-type histamine receptor blockers mepyramine, diphenhydramine, and (+)-chlorpheniramine were potent antagonists of the histamine response. Diphenhydramine was also a weak agonist at high concentrations (> or = 1 mM) and gave a biphasic response similar to that with histamine. The H2-type receptor blocker cimetidine and the H3-type receptor blocker thioperamide had no effect. Indomethacin failed to inhibit the second phase of the histamine-stimulated [Ca2+]i response, suggesting that the second [Ca2+]i peak is not due to secondary production of prostaglandins. Neomycin, which inhibits IP3 production, completely abolished the [Ca2+]i response to bradykinin stimulation but did not affect the second phase of the histamine response. The biphasic nature of the histamine response, the insensitivity of the second [Ca2+]i peak to neomycin, and the independence of bradykinin and histamine responses suggest that histamine may modulate [Ca2+]i through multiple IP3 and non-IP3 pathways.


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