Approximately a quarter of patients with major depressive disorder have low-grade systemic inflammation, with higherrates in difficult-to-treat subgroups; service-level prevalence within European public mental health services for difficultto-treat depression (DTD) remains undetermined. Emerging data suggest that inflammation does not operate as a simplelinear cause of major depressive disorder, but rather as a modulator of corticostriatal circuits, altering reward processing,effort–cost estimation, feedback-based learning and decision-making. This can give rise to a depressive phenotypecharacterized by motivational anergia, effort avoidance, attenuated responsiveness to conventional treatments, frequentrelapse, and a substantial burden for patients, clinicians and services. In this viewpoint we propose an operational modelfor community mental health services based on: (1) a pragmatic and accessible inflammatory stratification pathway usinga focused biomarker panel (high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α)and interleukin-1β (IL-1β); (2) the integration of a circuit-based perspective into the functional formulation of DTD; and(3) the reorganization of community and outpatient mental health provision around point-of-care biomarker testing,standardized protocols, and explicit attention to equity of access. Unlike existing frameworks that require specialistbiomarker infrastructure, this model articulates a tiered pathway in which point-of-care hs-CRP is feasible at communitylevel, within routine publicly funded provision, while IL-6, TNF-α and IL-1β phenotyping is reserved for district specialist hubs.