"Take away the greed of the private landlord housing market … because that is killing people": Examining the political economy of housing and health inequalities in four English coastal towns.

People with persistent pain typically report more psychological distress than their pain-free peers. Although there is some reciprocal influence between distress and pain, distress seems to influence pain more strongly than pain influences distress in both population and clinical samples; distress is a recognised risk factor for developing persistent pain [; ; ; ; ; ; ]. However, despite the compelling evidence that distress influences pain, the mechanisms that support this influence are poorly elucidated. From a psychological perspective, distress may promote pain through a bias that favours threat perception [; ; ; ; ; ; ]. However, distress also alters both peripheral and spinal immunology. Sustained distress is associated with a subtle increase in tonic pro-inflammatory signalling that is thought to confer a propensity for a heightened inflammatory response —an elevated “inflammatory reactivity”—in response to a phasic challenge, such as psychosocial or physical trauma [; ; ]. Experimental immune provocation, with agents such as endotoxin, models the expression of inflammatory cytokines and chemokines in response to a standardised phasic challenge, allowing insight into this inflammatory reactivity. Inflammatory signalling has been linked to pain in both clinical samples and healthy controls. Elevated inflammatory reactivity (i.e. stronger inflammatory response to immune challenge) in peripheral blood is associated with clinical pain [; –] and other clinical conditions that feature pain [; ]. PET-detected markers of central nervous system astrocyte activation are associated with low back pain and fibromyalgia, as well as negative affect [; ; ]. The extensive neuroimmune interactions within the central nervous system may explain this. In healthy controls, intravenous endotoxin exposure potentiates capsaicin-induced hyperalgesia and allodynia, indicating a priming effect of inflammation on pain, likely through heterotopic spinal facilitation of nociception []. Together, these data connect inflammatory signalling, nociceptive processing, and pain, but two questions remain unanswered: what influences inflammatory reactivity, and what are the consequences of inflammatory reactivity?