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Homeostasis is a complex process that is achieved by both ‘classic’ functions including the immune system and the central nervous system (CNS). Cross-talk between the immune system and the CNS has been established in several diseases, including pulmonary disease where the CNS plays a role in the pathogenesis of the disease based on interplay between the CNS and the immune system. Potential for a neuro-immune axis was investigated by Jonsson et al. [39] where the effect of FIX and FIXa on the activity of the NLRP3 inflammasome was assessed. According to this model, activation of the inflammasome requires the autoactivation of the NLRP3 protein and activation of the inflammasome in turn involves the activation of caspase‐1. Activation of caspase‐1, then, leads to activation of IL‐1β and IL‐18, the latter of which can be measured in the serum and is considered a biomarker of inflammasome activation [107]. Jonsson et al. [39] showed that autologous FIXa activate the NLRP3 inflammasome, and that the cleavage of FIX and FIXa is involved in this activation. To this end, activation of the inflammasome was inhibited by TRF through inhibition of FXII, as TRF is known to bind and inactivate FIXa [46],[69]. This mechanism was further investigated, and was shown to be NLRP3 dependent, as introduction of a mutation into NLRP3 that specifically abolished inflammasome activity markedly impeded the cleavage of FIXa by FIX. This mechanism was shown to be independent of the FXII/FIXa pathway, as TRF still mediated the suppression of inflammasome activity. The authors conclude that TRF-mediated suppression of the FXII/FIXa pathway prevents the subsequent activation of the inflammasome, which suggests that a TRF-mediated decrease in the activity of FXII/FIXa could be a potential treatment for pulmonary disease that could regulate the activity of the inflammasome.
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