Marijuana and Bacterial Infections

  • Thomas W. Klein
  • Catherine Newton
  • Raymond Widen
  • Herman Friedman
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 335)


Many studies in rodent models have demonstrated that Δ9 tetrahydrocannabinol (THC) can modulate the function of the immune system (1). Either injecting the drug into rodents or adding the drug to cultures of rodent T lymphocytes, B lymphocytes, natural killer cells or macrophages (1,2,3,4,5) has been consistently reported to be associated with suppressing cellular functions. However, as compelling as these reports are, the question still remains whether these drug-induced immune alterations lead to a heightened state of susceptibility of the animals to bacterial infections. A few reports have attempted to address this question and have examined the influence of cannabi- noids on in vitro infection models and on resistance to challenge infections with various bacteria. Huber et al., (6) reported that the addition of marijuana smoke to pulmonary alveolar macrophage cultures resulted in the suppression of the bactericidal capacity for Staphylococcus albus and recently we reported (7) a similar finding in THC treated peritoneal macrophage cultures infected with Legionella pneumophila. Regarding drug effects on challenge infections, Bradley et al., (8) reported an enhanced susceptibility of mice to combination injections of THC and living or killed gram-negative bacteria and Morahan et al., (9) reported similar findings in a murine infection model with Listeria monocytogenes. In both of these studies, however, drug doses in excess of 100 mg/kg were found to be most effective therefore frustrating attempts to extrapolate these findings to the human drug abuse situation. Also, although these studies showed that drug treatment suppressed host resistance, little is known concerning the immune cellular and humoral defects involved.


Listeria Monocytogenes Primary Infection Challenge Infection Marijuana Smoke Secondary Immune Response 
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Copyright information

© Springer Science+Business Media New York 1993

Authors and Affiliations

  • Thomas W. Klein
    • 1
  • Catherine Newton
    • 1
  • Raymond Widen
    • 1
  • Herman Friedman
    • 1
  1. 1.Department of Medical Microbiology and ImmunologyUniversity of South Florida College of MedicineTampaUSA

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