Modulation of Immune Function by Morphine: Implications for Susceptibility to Infection

Abstract

The outcome of microbial infection in an organism is a dynamic process that depends on factors derived from both the microorganism and the host. In chronic human infections, the kind of immune response made in response to pathogens may be of vital importance to host defense. An inappropriate immune response may not only result in lack of protection, but even contribute to disease severity. Chronic morphine use and abuse has been documented to result in severe immune consequence (Roy and Loh 1996; Dinda et al. 2005; Friedman and Eisenstein 2004) and thus may pose a significant risk factor to opportunistic infection. It is therefore not surprising that epidemiological studies show increased prevalence of opportunistic infections such as tuberculosis, HIV infection, and pneumonia in opioid abusers (Quaglio et al. 2002; Nath et al. 2002; Georges et al. 1999). Besides the sharing of unsterilized, contaminated needles, the occurrence of infections in these patients has been attributed to the immune modulatory effect of morphine. In animal studies where confounding variables such as nutritional status, environmental influences, history of drug use, and genetic variability can be controlled, morphine treatment resulted in significant immune deficits. Defense against microbes is mediated by the early reactions of innate immunity and the later response of adaptive immunity. Chronic morphine has been shown to affect both these arms of immune defense (Vallejo et al. 2004). This review on the immunological effects of morphine summarizes the effects of this drug on innate and adaptive immunity, identifies the role of the mu opioid receptor in these functions, and finally discusses how changes in these parameters increase the risk for opportunistic infection.