According to Thomas Butler, the mechanism of JHR in spirochetal infections is due to the inefficient killing of the bacteria by antibiotics, enabling whole live bacteria to be engulfed by the body’s macrophages, causing the production of excessive amounts of proinflammatory cytokines, such as tumor necrosis factor (TNF), interleukin 6, and interleukin 8, within the macrophages [32]. This evidence concerns the gene CXCL8 and spirochaetales infections.