Testing a Model: Effects of Pain on Immunity in HIV+ and HIV-Participants

Article excerpt

In this study, the cold pressor test (CPT) was used to test a model of the effects of acute pain on 10 HIV+ and 10 HIV- adults. Participants were exposed to the CPT for a maximum of 5 minutes. Blood samples were collected immediately before, immediately after, and 1 hour after the CPT. Variables included immune measures (CD4+, CD8+, and CD 16+56+ lymphocyte number, CD4+CD8+ lymphocyte ratio and NK cell cytotoxicity), cardiovascular reactivity (heart rate, systolic and diastolic blood pressure), anxiety, perceived pain intensity and perceived self-efficacy. Effects of pain were generally consistent across HIV+ and HIV- groups, with no between-group differences across time in immune responses, state anxiety and diastolic blood pressure. Within-subjects differences across time averaged over both groups were significant for NK cell cytotoxicity, CD8+ and CD 16+56+ lymphocyte numbers, anxiety and heart rate. Significant nonlinear trends were observed for CD 16+56+ lymphocyte numbers, NK cell cytotoxicity and state anxiety in both groups and for heart rate in the HIV+ group only. Perceived pain intensity was significantly associated with state anxiety (r = .65), systolic (r = -.56) and diastolic (-.52) blood pressure and CD4+ lymphocyte number (r = .48). Heart rate and trait anxiety were significantly associated with all immune variables. Associations were positive for CD4+ lymphocyte number and inverse for all other immune measures. Associations between perceived self-efficacy and both perceived pain intensity and anxiety were inverse, as predicted, but not significant. Overall, the direction and strength of observed relationships provided some support for the theoretical model on which the study was based. Generally, responses to acute pain were consistent and did not differ by HIV status.

There is compelling evidence from laboratory studies in animal models that pain has an effect on immune responses. In these studies, pain resulted in consistent down regulation of the immune system, increased metastases of experimental tumors and reduced survival (Ben-Eliyahu, Yirmiya, Liebeskind, Taylor, & Gale, 1991; Keller, Weiss, Schleifer, Miller, & Stein, 1981; Lewis et al., 1983; Page, Ben-Eliyahu, Yirmaya, & Liebeskind, 1993; Shavit et al., 1986; 1987). The majority of human laboratory studies have examined the effects of psychological rather than physiological stressors and support their immunological effects (Schultz & Schultz, 1992). The few human laboratory studies of the effects of painful stressors have provided preliminary evidence that immune responses to pain do occur (see below). In addition, they demonstrate that these immune responses may be mediated by a number of psychological and physiological variables.

The immunomodulatory effects of pain may have as yet unrecognized consequences in clinical populations in terms of disease severity and survival. In addition, acute pain may increase susceptibility to viral infection in otherwise healthy individuals (Cohen & Williamson, 1991). Before potential longterm effects of pain-related immune responses can be addressed, however, the specific immunological effects and their mediators must be characterized. Therefore, the main objectives of this study, using a psychoneuroimmunology model, were: (a) to examine the effects of a cold pressor test (CPT) pain model on immunity in healthy and HIV positive men and women, and (b) to identify mediators of immune responses to acute pain. Immune measures included CD4+ and CD8+ and CD 16+56+ (natural killer) lymphocyte numbers, CD4+CD8+ ratio and natural killer cell cytotoxicity (NKCC). Mediators included sympathetic nervous system activation, perceived self-efficacy to withstand CPT pain, and perceived pain intensity.


Increasingly, human studies have documented immune responses to naturally occurring or laboratory induced physiological and psychological stressors. Immune markers most consistently influenced by pain and other stressors include natural killer cell activity (NKCC), lymphocyte proliferation in response to the plant mitogens phytohemagglutinin (PHA) and concanavalin A (ConA), and alterations in the number of lymphocyte subsets, including CD4+, CD8+ and CD16+CD56+ lymphocytes (Bachen et al. …