Alterations in sphingolipids (SLs), oxylipins (OLs) and cytokines (CKs) are central to neuroinflammation. However, the effects of low doses Fumonisins B (FBs) on these analytes in the avian brain remain unclear.This study investigated SLs, OLs, CKs, and the activities of phospholipase A2c (PLA2c) and cyclooxygenase 2 (COX2) in the brains of chickens exposed to FB at a nominally safe dose of 14.6 mg FB1 + FB2/kg for 14 and 21 days. Targeted LC-MS/MS analyses revealed that FB exposure increased brain concentrations of sphingosine, N-acetyl-sphingosine, sphingosine 1-phosphate (So1P), ceramides (Cers), and sphingomyelins (SM). The Cer:SM ratio was elevated at 14 days but normalized by 21 days, whereas the So1P:Cer ratio rose at 14 days and continued to increase at 21 days. These changes coincided with elevated PLA2c and COX2 activities. OL profiling indicated a modest rise in pro-inflammatory arachidonic acid-derived COX metabolites at 14 days, while anti-inflammatory OLs derived from COX and lipoxygenase (LOX) pathways, including PGE2, 15-HETE, and 17-HDHA, increased significantly at 21 days. In contrast, the levels of CKs changed only slightly. Brain concentrations of Fumonisin B1 (FB1) indicated increased blood–brain barrier permeability.These findings highlight a key role of Cers in modulating OL production in FB neurotoxicity.
Guerre et al. (Sat,) studied this question.