Abstract
Inflammation contributes to the pathogenesis of ischaemic stroke both as a long-term causal factor and through the inflammatory cascade in acute stroke. Interleukin-1 beta (IL-1β) is a potent pro-inflammatory molecule, while interleukin-1 receptor antagonist (IL-1Ra) acts as its antagonist. Free fatty acids (FFAs) play a role in atherosclerosis formation and serve as substrates for inflammatory molecules. This study aimed to determine the potential interplay between FFAs, IL-1β, and IL-1Ra in stroke patients. A prospective analysis was conducted on 73 ischaemic stroke patients. All participants had their FFA, IL-1β, and IL-1Ra levels assessed. Significant correlations between IL-1β and certain FFAs were detected: C15:0 pentadecanoic acid (rho = 0.488), C15:1 cis-10 pentadecanoic acid (rho = 0.473), C17:1 cis-10 heptadecanoic acid (rho = 0.411), C18:0 stearic acid (rho = 0.302), C24:0 lignoceric acid (rho = -0.280), C24:1 nervonic acid (rho = -0.276), C18:2n6t linoleic acid (rho = -0.272), C17:0 heptadecanoic acid (rho = 0.241), and C13:0 tridecanoic acid (rho = 0.238). After multivariate analysis C15:0 pentadecanoic acid remained statistically significant. The strongest correlation was found between IL-1Ra and fatty acids: C15:1 cis-10-pentadecanoid acid (rho = -0.357), C18:2n6t linoleic acid (rho 0.341) and C24:1 nervonic acid (rho 0.302), but after multivariate analysis significantly correlated remained: C22:1n9 13 erucic acid (rho = 0.299), C18:3n6 gamma-linoleic acid (rho = 0.277), with close to significant correlation with C22:4n6 docosatetraenoate (rho = -0.241, p = 0.055). Certain FFAs may play a role in enhancing both pro- and anti-inflammatory responses in the early subacute phase of stroke, where inflammatory and resolving processes are ongoing. Fatty acids such as C15:0 pentadecanoic acid, C15:1 cis-10 pentadecanoic acid and C22:4n6 docosatetraenoate might be involved in pro-inflammatory responses, while C22:1n9 13 erucic acid and C18:3n6 gamma-linoleic acid in the anti-inflammatory pathways with the overlay of IL-1β and IL-1Ra.