Author(s): James G McLarnon
Interleukin -8 (IL-8), a member of the CXC chemokine family, is well-documented as an important chemotactic signaling factor for recruitment of neutrophils to sites of infection and damage. However in neurodegenerative disease such as Alzheimer’s disease (AD), it is the resident macrophage cells, microglia, which are primary responding cells to brain insult such as deposition of amyloid β peptide. IL-8 exhibits an autocrine interaction with microglia by inducing a recruitment of the cells to specific sites of inflammation and subsequent increased production of the chemokine from activated cells. This positive feedback process thus has the capacity to amplify and sustain inflammatory response and brain neuroinflammation. The net result is that a localized and enhanced inflammatory response is induced by accumulating activated microglia at sites of inflammation serving to exacerbate inflammatory reactivity in AD brain. Importantly, under certain conditions the chemotaxis and subsequent activation of microglia may be deleterious to bystander cells including neurons. This review summarizes work from selected studies concerning the involvement and contributions of IL-8 mobilization from activated microglia to brain neuroinflammation as documented in the neurodegenerative diseases Alzheimer’s disease (AD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS) and Parkinson’s disease (PD).
