Morphologic adaptation to persistent inflammation. Centrally controlled increase of sympathetic nervous system (SNS) activity is a basic response to inflammation. The constant increase in SNS activity supports inflammation in several ways; for example, increasing blood flow, lymph flow, antigen presentation, and liberation of energy-rich fuels like lipids and glucose from adipose tissue and liver. However, the specific interaction with immune cells in secondary lymphoid organs and at local sites of inflammation (for example, joints) shows a net anti-inflammatory effect. Therefore, to mount an effective immune response, non-specific support of inflammation on a systemic level is maintained, while the anti-inflammatory influence on a local level is decreased and uncoupled from central regulation through repulsion of sympathetic nerve fibers and the appearance of tyrosine hydroxylase (TH) + catecholamine-producing cells during the inflammatory process. In the end, a systemic proinflammatory configuration is established, which helps to optimally clear the antigen. However, if inflammation persists, like during chronic inflammation, this constant increase in SNS activity and resultant catabolic state is detrimental to the body and results in known disease sequelae of chronic inflammatory conditions, like cachexia, diabetes, hyperlipidemia, high blood pressure, increased cardiovascular risk, and so on.