Fig. 1

Preeclampsia etiology or exacerbation may be mediated by an upregulated sterile inflammation, it may be initiated by molecules in the host organism known as damage associated molecular patterns (DAMPs). In addition to DAMPs, the upregulation of this sterile inflammation is produced by an altered immune response in conjunction with autonomic dysfunctions. Particularly, immune alterations are characterized by the release of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) and decrease of anti-inflammatory cytokines such as interleukin-4 (IL-4) and interleukin-10 (IL-10). Finally, autonomic dysfunctions may involve diminished acetylcholine (ACh) synthesis, lower vagal tone, downregulation of both alpha 7 nicotinic acetylcholine receptor (α7nAChR) and cholinergic anti-inflammatory pathway (CAP)