Effect of glucocorticoids on the response of airway smooth muscle to catecholamine and resorcinol β-agonists

1989 ◽  
Vol 67 (11) ◽  
pp. 1442-1447
Author(s):  
Ralph C. Kolbeck ◽  
Bashir A. Chaudhary ◽  
William A. Speir

The influence of hydrocortisone (11β,17α,21-trihydroxy-pregn-4-ene-3,20-dione) or of methylprednisolone (6α-methyl-11β,17α-21-trihydroxy-1,4-pregnadiene-3,20-dione) on the response of airway smooth muscle to a variety of β-adrenergic bronchodilators was evaluated using incubated guinea pig tracheal rings, preconstricted with histamine. The adrenergic agonists chosen for this study included the nonselective β1- and β2-catecholamine, isoproterenol, the selective β2-catecholamine, rimiterol, and the selective β2-resorcinols, fenoterol and terbutaline. When the incubated rings were pretreated with 10–50 μg/mL of the steroids, there was a significant enhancement in smooth muscle sensitivity and reactivity to rimiterol and isoproterenol. Tracheal response to fenoterol or terbutaline, on the other hand, was not altered by the glucocorticoids. When used alone, neither steroid exerted an inotropic influence on the tracheal smooth muscle. The results of our study indicate that glucocorticoid enhancement of adrenergic bronchodilators is selective for catecholamines, and not for resorcinols.Key words: tracheal smooth muscle, glucocorticoids, β-adrenergic agonists, catecholamines, resorcinols.

1940 ◽  
Vol 72 (4) ◽  
pp. 389-405 ◽  
Author(s):  
J. E. Smadel ◽  
M. J. Wall

Anti-soluble substance antibodies and neutralizing substances, which develop following infection with the virus of lymphocytic choriomeningitis, appear to be separate entities. The times of appearance and regression of the two antibodies are different in both man and the guinea pig; the antisoluble substance antibodies appear earlier and remain a shorter time. Moreover, mice develop them but no demonstrable neutralizing substances. Injection of formalin-treated, virus-free extracts containing considerable amounts of soluble antigen fails to elicit anti-soluble substance antibodies and to induce immunity in normal guinea pigs; administration of such preparations to immune pigs, however, is followed by a marked increase in the titer of anti-soluble substance antibodies in their serum. On the other hand, suspensions of formolized washed virus are effective in normal guinea pigs in stimulating both anti-soluble substance antibodies and protective substances, and in inducing immunity to infection.


1990 ◽  
Vol 100 (4) ◽  
pp. 663-664 ◽  
Author(s):  
John F. Tucker ◽  
Sandra R. Brave ◽  
Litsa Charalambous ◽  
Adrian J. Hobbs ◽  
Alan Gibson

1995 ◽  
Vol 78 (4) ◽  
pp. 1555-1563 ◽  
Author(s):  
S. De ◽  
E. T. Zelazny ◽  
J. F. Souhrada ◽  
M. Souhrada

Guinea pig airway smooth muscle (ASM) cells were maintained in a primary tissue culture (passages 1–3). Cells were exposed to human recombinant interleukin-1 beta (IL-1 beta; 20–100 pg/ml) or interleukin-6 (IL-6; 1–4 ng/ml) in the presence of indomethacin (1 microgram/ml) for up to 5 days. Proliferation of ASM cells was assessed with two techniques, direct counting of cells with a hemacytometer and [3H]thymidine incorporation corrected for total protein content. Hypertrophy of ASM cells was assessed by [3H]leucine incorporation (evaluation of protein synthesis), determination of total DNA content, DNA content per cell, and protein content per cell. We observed that the exposure of ASM cells to human recombinant IL-1 beta or IL-6, in all studied concentrations, significantly increased the number of cells as well as [3H]thymidine incorporation into ASM cells. We also found that exposure of ASM to these two cytokines increased [3H]leucine incorporation into the ASM cells and increased protein content and DNA content per single cell. These changes were also concentration dependent. We conclude that the two proinflammatory cytokines, IL-1 beta and IL-6, which are present in asthmatic lungs, increased the proliferation of ASM cells (hyperplasia) as well as their overall size and size of their nuclei, as measured by biochemical markers. These findings are compatible with the presence of ASM hypertrophy.


1998 ◽  
Vol 12 (1) ◽  
pp. 45-49 ◽  
Author(s):  
H-J. Pennings ◽  
K. Kramer ◽  
A. Bast ◽  
W.A. Buurman ◽  
E.F.M. Wouters

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