Regulation of interleukin-1 in acute brain injury
2011; Elsevier BV; Volume: 32; Issue: 10 Linguagem: Inglês
10.1016/j.tips.2011.06.002
ISSN1873-3735
AutoresDavid Brough, Pippa Tyrrell, Stuart M. Allan,
Tópico(s)S100 Proteins and Annexins
ResumoInflammation is a complex vascular response that has evolved to eliminate infection and to repair injured tissue. It is subject to tight regulatory control of its initiation and resolution. Failure of an inflammatory response to resolve has become recognised as a major contributor to the pathology of diverse diseases (including acute brain injuries). Interleukin-1 (IL-1) is a pro-inflammatory cytokine and key contributor to damage after acute brain injury. Understanding the regulation of IL-1 production is vital for the development of new drug targets and therapies. In recent years, there have been major advances in how we understand the resolution of inflammatory responses, and in how IL-1 is regulated after injury. Advances are summarised here in the context of addressing how dampening the inflammatory response and actions of IL-1 provides a strategy for reducing damage after acute brain injury such as stroke. Inflammation is a complex vascular response that has evolved to eliminate infection and to repair injured tissue. It is subject to tight regulatory control of its initiation and resolution. Failure of an inflammatory response to resolve has become recognised as a major contributor to the pathology of diverse diseases (including acute brain injuries). Interleukin-1 (IL-1) is a pro-inflammatory cytokine and key contributor to damage after acute brain injury. Understanding the regulation of IL-1 production is vital for the development of new drug targets and therapies. In recent years, there have been major advances in how we understand the resolution of inflammatory responses, and in how IL-1 is regulated after injury. Advances are summarised here in the context of addressing how dampening the inflammatory response and actions of IL-1 provides a strategy for reducing damage after acute brain injury such as stroke.
Referência(s)