The Emerging Role of Interleukin 1β (IL-1β) in Cancer Cachexia

Treatment of cancer cachexia remains an unmet need. The host-tumour interface and the resulting sequestration of the pro-inflammatory cytokine Il-1 beta is critical in cachexia development. Neuroinflammation mediated via IL-1 beta through the hypothalamic pituitary axis results in increased muscle proteolysis and adipose lipolysis, thus creating a prolonged stress-like environment with loss of appetite and increased resting energy expenditure. Recent trials using a monoclonal antibody targeting IL-1 beta, canakinumab, have shown a potential role in lung cancer; however, a potential role of targeting IL-1 beta to treat cachexia in patients with lung cancer is unclear, yet the underlying pathophysiology provides a sound rationale that this may be a viable therapeutic approach.

Automated summary

Treatment of cancer cachexia is still an unmet need, with recent trials showing a potential role for targeting IL-1 beta using monoclonal antibody canakinumab in lung cancer. The neuroinflammation mediated by IL-1 beta plays a critical role in cachexia development, leading to muscle proteolysis and adipose lipolysis, but the precise mechanism of targeting IL-1 beta in treating cachexia remains unclear.