Rabbits were injected intramuscularly with cortisone acetate (2 mg/kg) on alternate days. Six days after the first injection these rabbits and controls were injected intradermally in multiple sites with BCG (the vaccine strain of tubercle bacillus). Periodically, over the next 2 months, the resulting lesions were measured and surgically biopsied, and the animals were tuberculin-tested. Macrophage activation in the BCG lesions was evaluated histochemically by staining forβ-galactosidase activity. Both BCG lesions (and tuberculin reactions) in the cortisone-treated group were considerably smaller than those in the control group. Cortisone was highly effective in reducing the number of infiltrating mononuclear cells (MN), the amount of caseous necrosis and ulceration, and the percent of NM that wereβ-galactosidase-positive. The decreased activation and reduced number of macrophages readily explains the increased susceptibility to tuberculosis found among patients receiving glucocorticosteroids. In the BCG lesions, the local decrease in the number and function of leukocytes probably explains the decreased tissue necrosis. Such antiinflammatory effects of corticosteroids may offset, in selected antimicrobial-treated cases, the hormone's detrimental effect on host resistance to infectious agents.
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Supported by Grant HE-14153 from the National Heart, Lung and Blood Institute, U.S. Public Health Service, for the Johns Hopkins Specialized Center on Lung; Contract DAAK-11-77-C0091, Biomedical Laboratory, Chemical Systems Laboratory, Aberdeen Proving ground, Maryland 21010; and Grant ES-01879 from the National Institute of Environmental Health Sciences, U.S. Public Health Service.
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McCue, R.E., Dannenberg, A.M., Higuchi, S. et al. The effect of cortisone on the accumulation, activation, and necrosis of macrophages in tuberculous lesions. Inflammation 3, 159–176 (1978). https://doi.org/10.1007/BF00910737
- Mononuclear Cell
- Detrimental Effect