Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 45, Issue 2, Pages 525-530Publisher
WILEY
DOI: 10.1002/eji.201444748
Keywords
innate immunity; interleukin-1 (IL-1); neuroinflammation; neutrophil
Categories
Funding
- British Heart Foundation
- Medical Research Council
- Biotechnology and Biological Sciences Research Council
- BBSRC [BBS/E/D/20251969] Funding Source: UKRI
- MRC [MR/K001744/1, MR/L003384/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/D/20251969] Funding Source: researchfish
- British Heart Foundation [PG/13/8/29989, FS/10/73/28464] Funding Source: researchfish
- Medical Research Council [MR/K001744/1, MR/L003384/1] Funding Source: researchfish
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The immune system is implicated in a wide range of disorders affecting the brain and is, therefore, an attractive target for therapy. Interleukin-1 (IL-1) is a potent regulator of the innate immune system important for host defense but is also associated with injury and disease in the brain. Here, we show that IL-1 is a key mediator driving an innate immune response to inflammatory challenge in the mouse brain but is dispensable in extracerebral tissues including the lung and peritoneum. We also demonstrate that IL-1 alpha is an important ligand contributing to the CNS dependence on IL-1 and that IL-1 derived from the CNS compartment (most likely microglia) is the major source driving this effect. These data reveal previously unknown tissue-specific requirements for IL-1 in driving innate immunity and suggest that IL-1-mediated inflammation in the brain could be selectively targeted without compromising systemic innate immune responses that are important for resistance to infection. This property could be exploited to mitigate injury- and disease-associated inflammation in the brain without increasing susceptibility to systemic infection, an important complication in several neurological disorders.
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