Abstract

Differences in measures of inflammation (e.g., IL-6, TNF-α, and CRP), are reported in individuals with chronic pain compared to healthy controls. Additionally, elevations in immune measures have been observed in response to quantitative sensory testing and associated with pain-related catastrophizing. Importantly, inflammatory measures do not act in isolation but as part of a dynamic, comprehensive network. Increases in a single measure ideally need to be considered in concert with other positively and negatively associated measures. In order to better understand immune system functioning and the relationship with clinical and experimental pain, a comprehensive panel of measures warrants investigation. The intent of our study was to evaluate the inflammatory profiles in middle and older age individuals (56.6+7.4) with and without knee OA pain. A total of 108 individuals (72% Women and 28% Men), who took part in a larger study were included. A high sensitivity chemokine/cytokine kit measuring 13 cytokines was used to assay blood samples collected at the conclusion of the quantitative sensory testing protocol. Data reduction was performed separately by group using Principal Component Analysis with a Promax rotation. Results indicated factor profile differences between groups. Specifically, individuals with no knee OA pain had a clearly differentiated pro and anti-inflammatory profile. The individuals with knee OA had a less clearly differentiated profile. Additional analyses will be completed to explore relationships between immune patterns and clinical and experimental pain measures. In summary, although differences in individual inflammatory measures have been previously reported, our findings indicate immune system profile differences in middle age and older adults with knee OA pain compared to healthy controls. This is one of the first studies to investigate a comprehensive inflammatory panel to better understand immune system patterns in a chronic pain population. Differences in measures of inflammation (e.g., IL-6, TNF-α, and CRP), are reported in individuals with chronic pain compared to healthy controls. Additionally, elevations in immune measures have been observed in response to quantitative sensory testing and associated with pain-related catastrophizing. Importantly, inflammatory measures do not act in isolation but as part of a dynamic, comprehensive network. Increases in a single measure ideally need to be considered in concert with other positively and negatively associated measures. In order to better understand immune system functioning and the relationship with clinical and experimental pain, a comprehensive panel of measures warrants investigation. The intent of our study was to evaluate the inflammatory profiles in middle and older age individuals (56.6+7.4) with and without knee OA pain. A total of 108 individuals (72% Women and 28% Men), who took part in a larger study were included. A high sensitivity chemokine/cytokine kit measuring 13 cytokines was used to assay blood samples collected at the conclusion of the quantitative sensory testing protocol. Data reduction was performed separately by group using Principal Component Analysis with a Promax rotation. Results indicated factor profile differences between groups. Specifically, individuals with no knee OA pain had a clearly differentiated pro and anti-inflammatory profile. The individuals with knee OA had a less clearly differentiated profile. Additional analyses will be completed to explore relationships between immune patterns and clinical and experimental pain measures. In summary, although differences in individual inflammatory measures have been previously reported, our findings indicate immune system profile differences in middle age and older adults with knee OA pain compared to healthy controls. This is one of the first studies to investigate a comprehensive inflammatory panel to better understand immune system patterns in a chronic pain population.

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