Cortisone acetate,
hydrocortisone, and
hydrocortisone acetate depress the resistance of mice to pneumococcal and
influenza viral infections, although
hydrocortisone acetate is somewhat less effective than the free alcohol, when given subcutaneously. Pituitary
adrenocorticotropin, even in highly purified form and in oil and
beeswax, does not significantly alter the resistance of mice to these experimental
infections, even when given in doses which may cause profound eosinopenia,
lymphopenia, and
weight loss, and which are at the limit of tolerance of the animals.
Corticosterone depresses resistance to
pneumococcal infections significantly, but fails to alter resistance to
influenza viral infections. The findings suggest that murine adrenals may produce one of the known adrenal
steroids such as
corticosterone along with another
steroid, or may produce a
steroid other than
cortisone,
hydrocortisone, or
corticosterone. When resistance is decreased by adrenal
steroids, survival time is invariably shortened, and the effect of the
steroid hormones is frequently demonstrable within the 1st day after
infection with pneumococci, making it unlikely that the depression of resistance that is seen is primarily due to depression of antibody formation. A single dose of 5 mg. of
cortisone may cause depression of resistance and may decrease the survival time for 3 to 6 days afterward.
Growth hormone (somatotropic
hormone) in highly purified form, and in the doses used, did not overcome the
weight loss induced by
cortisone, but the animals treated with
growth hormone and
cortisone regained their lost weight more rapidly than those receiving
cortisone alone.
Growth hormone alone caused a slight increase in the rate of gain in weight over controls.
Growth hormone alone did not increase resistance to
infection, and did not increase the survival time, in mice infected with either pneumococci or influenza virus.
Growth hormone in various dosages failed to overcome the effect of
cortisone in depressing resistance to these
infections.
Cortisone,
hydrocortisone,
corticosterone, and
corticotropin did not alter significantly the titers of influenza virus attained in the murine lungs during the first 2 days after
infection, but
cortisone and
hydrocortisone markedly delayed the rate at which virus titers declined during the subsequent 6 days.
Corticosterone and
corticotropin delayed the rate at which the titers declined but slightly, and
growth hormone had no apparent effect, as compared with controls.
Growth hormone did not overcome the effect of
cortisone and
hydrocortisone on viral titers. No detectable antibody was found as late
as 6 days after
infection, in controls or in
hormone-treated animals.