OBJECTIVES: To determine whether high level of comorbidity, measured using a standardized instrument, can predict impaired immunity in older adults. SETTING: Geriatric outpatient Clinic and Nursing Home Care Unit of Veterans Affairs Greater Los Angeles Healthcare System. PARTICIPANTS: Fifteen men aged 51 to 95 with varying levels of chronic illness. MEASUREMENTS: Disease burden was measured using the Cumulative Illness Rating Scale (CIRS) and immunity using proliferation of T cells induced by phytohemagglutinin (PHA) and production of interleukin (IL)-12, a proinflammatory cytokine that promotes T helper cell-dependent immune response, and IL-10, a cytokine that inhibits T helper cell-dependent immune response, in response to mitogenic stimulation of peripheral blood mononuclear cells. RESULTS: With increasing comorbidity (increase in CIRS score) in older adults, there is a proportional decrease in immune response (decrease in T cell proliferation and IL-12 production and increase in IL-10 production in response to PHA stimulation). Neither immune response nor CIRS score was significantly correlated with chronological age in this sample of older adults with varying degrees of chronic illness. CONCLUSION: This study demonstrates that the level of comorbidity correlates with the magnitude of immune response in older adults and suggests that the CIRS could be used to determine the magnitude of impaired immunity in older adults with different specific illnesses and different levels of severity.
OBJECTIVES: To determine whether high level of comorbidity, measured using a standardized instrument, can predict impaired immunity in older adults. SETTING: Geriatric outpatient Clinic and Nursing Home Care Unit of Veterans Affairs Greater Los Angeles Healthcare System. PARTICIPANTS: Fifteen men aged 51 to 95 with varying levels of chronic illness. MEASUREMENTS: Disease burden was measured using the Cumulative Illness Rating Scale (CIRS) and immunity using proliferation of T cells induced by phytohemagglutinin (PHA) and production of interleukin (IL)-12, a proinflammatory cytokine that promotes T helper cell-dependent immune response, and IL-10, a cytokine that inhibits T helper cell-dependent immune response, in response to mitogenic stimulation of peripheral blood mononuclear cells. RESULTS: With increasing comorbidity (increase in CIRS score) in older adults, there is a proportional decrease in immune response (decrease in T cell proliferation and IL-12 production and increase in IL-10 production in response to PHA stimulation). Neither immune response nor CIRS score was significantly correlated with chronological age in this sample of older adults with varying degrees of chronic illness. CONCLUSION: This study demonstrates that the level of comorbidity correlates with the magnitude of immune response in older adults and suggests that the CIRS could be used to determine the magnitude of impaired immunity in older adults with different specific illnesses and different levels of severity.