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Figure 3: The cholinergic pathways in allergic lung. During allergic reactions, the inflammatory mediators released in the tissue activate the sensory afferent fibers, which convey information to the CNS. The CNS sends information back to the inflammatory site by increasing ACh release from efferent vagus nerve. The neurotransmission in the parasympathetic ganglia is mediated by acetylcholine (ACh) via nicotinic (nAChR) or type 1 muscarinic (m1AChR) receptors. The stimulus generated induces ACh release in the pos ganglionic nerve fiber endings. Type 2 muscarinic receptors (m2AChRs) are autoinhibitory, and the dysfunction of this receptor, observed in allergic asthma, induces increased release of ACh. Increased ACh results in augmented mucus secretion via m3AchR expressed in the glandular epithelium, increased airway smooth muscle contraction (bronchoconstriction) via m3AchR expressed in muscle cells, and decreased inflammatory mediators production via a7nAChR receptor expressed on immune cells.