Abstract

Inflammation is a local response of tissue to microbial invasion or injury, which is usually a protective phenomenon. This inflammatory response, also called as inflammatory reflex, should be regulated precisely as deficiency or excess of the inflammatory response can cause morbidity and reduce lifespan.[1] If inflammation spreads into the bloodstream, as occurs in septic shock syndrome, systemic sepsis, meningitis and severe trauma, the inflammatory responses can be more harmful. Homeostasis is restored when inflammation is limited by antiinflammatory responses that are adaptive to changes in input and integration by autonomic nervous system (ANS). The recent discovery that cholinergic neurons inhibit acute inflammation has facilitated our understanding of how the ANS moderates immune responses. Recent studies have identified a basic neural pathway that reflexively monitors and inhibits inflammatory response. Therefore, the activation of anti-inflammatory responses has collectively been termed as anti-inflammatory reflex. Inflammatory stimuli activate sensory pathways that relay information to the hypothalamus, which integrates and mobilizes defences to eliminate the inflammation. The inflammation-sensing and inflammationmediating functions are the principal components of the inflammatory reflex. Though, the inflammation is mediated by many chemicals, important among them are tumor necrosis factor (TNF), IL-1 and high-mobility group B1 (HMGB1).[2] Read more. . .

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