Effects of Opioids, Cannabinoids, and Cocaine on NK Cells

The cannabinoids represent another class of abused drags affecting immune cell function. Although fewer studies have explored the effects of cannabinoids on NK cells, the literature to date shows that the activity of splenic NK cells is suppressed following in vivo injection of A -THC into rats and mice (Patel et al., 1985 Klein et al., 1987), and also after in vitro treatment of human peripheral blood NK cells (Specter et al., 1986). A -THC has also been shown to block proliferation of NK cells in response to the cytokine, IL-2, by down-regulating the IL-2 receptor (Zhu et al., 1993). 

There are a limited number of reports of immunomodulation by cocaine. In vivo administration of cocaine i.v. to humans elevated NK cell activity in peripheral blood, but exposure of leukocytes to the drug in vitro had no effect (Van Dyke et al., 1986). It was hypothesized that the in vivo effects occurred via release of epinephrine from the SNS (Van Dyke et al., 1986). Contradictory results have been reported for the effect of cocaine on NK activity in rats, with no effect in vivo (Bayer et al., 1996) or suppression of activity after acute or chronic in vivo administration (Pacifici et al., 2003). 

Drugs of Abuse Alter Functions of PMN Leukocytes and Monocytes/Macrophages 

Cocaine, like A -THC and morphine, has been reported to decrease the antimicrobial activity of alveolar macrophages obtained from chronic crack cocaine smokers (Roth et al., 2004) and to decrease parameters of mouse macrophage activation (Ou et al., 1989 Pacifici et al., 1993). However, in contrast to the effects of opioids, cocaine has been shown to increase the activation of PMNs in human subjects, as evidenced by increased kilhng of Staphylococcus aureus (Baldwin et al., 1997). 

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