BCG, in Contrast to C. parvum, Does Not Induce Increased Sensitivity to the Toxic Effects of Indomethacin in Mice

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Abstract
Treatment of mice with killed Corynebacterium parvum (also designated Propionibacterium acnes, P. acnes) or Bacille Calmette Guerin (BCG) leads to modification of several of the same host systems. However, BCG, in contrast to C. parvum, did not induce increased sensitivity to the toxic effects of indomethacin in BALB/c or C57B1/6 mice. In addition, treatment of mice with BCG did not interfere with the induction of sensitivity by C. parvum. Therefore C. parvum must uniquely induce changes in host systems which alter the sensitivity to this anti-inflammatory drug. Additional experiments with splenectomized animals revealed that the presence of this organ, which undergoes hypertrophy following C. parvum treatment, was not necessary for the induction of indomethacin sensitivity. Presentation of C. parvum via the subcutaneous route versus the intraperitoneal route revealed that the two routes were equally efficient in inducing sensitivity in C57B1/6 mice but the former route was less effective (50% deaths) than the intraperitoneal route (95% deaths) in BALB/c mice. These results indicate that host related factors (genetic) may be important in the generation of enhanced sensitivity to the toxic effects of indomethacin.