Moreover, SIBD patients with higher IFN-[gamma] levels displayed higher S100b levels (p<0.0001, R=0.737), whereas other cytokines and complement factors were not significantly correlated with S100b.
Serum levels of investigated parameters were also compared among SIBD patients with and without unfavorable clinical features such as bacteremia, requirement for steroid treatment, septic shock and death during the follow-up.
SIBD patients with and without cognitive impairment showed comparable age, gender, education level and cognitive assessment time values.
Increased serum pro-and anti-inflammatory cytokine levels have been well defined in patients with critically ill and sepsis patients and animal model of SIBD. Moreover, levels of cytokines have been reported to be associated with neurological outcome and sepsis-related complications such as bacteremia and septic shock (16, 17).
Thus, our results suggest that cytokines are not directly involved in cognitive dysfunction observed in SIBD patients and cognition is presumably afflicted by altered activation of intracellular pathways that regulate neuronal functions and cell survival by other inflammatory mediators, as demonstrated in animal models of sepsis (17, 18).
No significant changes were observed in serum levels of IL-17 and IFN-[gamma] in SIBD patients indicating that polarization to Th1-and Th17-type immunity does not play a critical role in SIBD.
SIBD patients showed reduced common pathway (C5a, iC3b levels) and increased classical pathway (C4 d levels) activity, while alternative pathway activity (Factor Bb levels) did not appear to be crucially involved in SIBD pathogenesis.
On the other hand, SIBD patients with septic shock and mortality displayed reduced C5a or iC3b levels in our study and higher C5a levels were associated with a better short and long-term neurological outcome (GOSE) score.
As exciting as they are, these amyloid [beta]-related mechanisms do not appear to play a major role in SIBD pathogenesis.
SIBD patients show increased baseline S100b and NSE levels indicating blood-brain barrier damage, gliosis and neuronal loss during early stages of the disease.