The inflammatory reflex is a neurophysiological mechanism that represents the body’s rapid, neural-mediated system for controlling systemic inflammation. It involves the efferent arm of the vagus nerve, which acts as a “brake” on the immune system, modulating the release of pro-inflammatory cytokines. This reflex is a crucial, fast-acting component of the neuro-immune axis, ensuring that the inflammatory response remains localized and proportionate to the threat. A compromised reflex can lead to chronic, low-grade systemic inflammation.
Origin
This concept emerged from the pioneering work in neuroimmunology, identifying the vagus nerve’s role as a direct modulator of the immune system, not just a passive observer. The term “reflex” is used to emphasize the rapid, involuntary, and integrated nature of this neural-immune circuit. This discovery fundamentally changed the understanding of the mind-body connection in disease.
Mechanism
The reflex is activated when peripheral inflammatory signals, such as cytokines, are sensed by afferent vagal fibers. This signal is relayed to the brainstem, which then sends an efferent signal back down the vagus nerve to the spleen and other immune organs. At the immune cell level, the neurotransmitter acetylcholine, released from vagal nerve endings, interacts with alpha-7 nicotinic acetylcholine receptors on macrophages, suppressing the release of inflammatory mediators like TNF-alpha.
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