Inflammation is a vital process that assists the body in fighting infections, including viral respiratory diseases. However, to prevent tissue damage and maintain internal organ functions, it is essential to regulate the inflammatory response carefully.
When the body encounters respiratory viruses, it initiates a complex set of reactions to combat the infection. This process begins with virus detection by pattern recognition receptors, leading to the production of inflammatory molecules, including type I interferons (IFN-I), which play a key role in antiviral defense.
Excessive inflammation can cause cell death and tissue damage. Therefore, strict control over IFN-I production is crucial. Macrophages, cells of the innate immune system, are at the center of this process, not only activating inflammation to combat infection but also regulating its resolution and maintaining IFN-I balance in tissues.
Scientists at Harvard Medical School have uncovered the mechanism by which macrophages regulate the inflammatory response by suppressing IFN-I production:
- Virus detection triggers the production of oncostatin M (OSM) in macrophages.
- OSM limits excessive IFN-I production by epithelial cells.
Macrophages play a crucial role in regulating the immune response to viral infections. By producing OSM, macrophages control reactions induced by type I interferons. The absence of OSM leads to enhanced IFN-I production in lung epithelial cells and may increase mortality from viral infections, including influenza. Macrophages restrain inflammation and promote survival during respiratory viral infections.
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Reference
Macrophages control pathological interferon responses during viral respiratory infection
