Modifying action of nicotine and acetylcholine at low concentrations on N-formyl-MLF-induced ROS production and adhesion of neutrophils from inflammatory site of mice was demonstrated.
Antagonists of nicotinic acetylcholine receptors (nAChRs) eliminated agonist effects. Nicotine induced Ca2+-spiking activity which was prevented by nAChR antagonist. RT-PCR analysis revealed the expression of mRNAs encoding α2, α3, α4, α5, α6, α7, α9, β2, β3, and β4 nAChR subunits.
The data suggest involvement of nAChRs of α7 and possibly α3β2 or α6* subtypes in regulation of specific neutrophil functions.