Published online Sep 19, 2022. doi: 10.5498/wjp.v12.i9.1183
Peer-review started: April 20, 2022
First decision: May 30, 2022
Revised: June 14, 2022
Accepted: August 10, 2022
Article in press: August 10, 2022
Published online: September 19, 2022
Processing time: 152 Days and 14.8 Hours
Galectin-3 (Gal-3), a multifaceted molecule of the glycan family, modulates T lymphocytes’ signalling pathway and effector functions. We have previously reported elevated serum Gal-3 levels in stable schizophrenia (SC) patients, but Gal-3 as a link between cognitive functioning and inflammation has not yet been investigated in SC.
Elevated serum Gal-3 levels in SC have not been studied in relation to other peripheral biomarkers and subsequent neuroinflammation. All of this may be an underlying indirect immunometabolic mechanism for cognitive performance in patients with SC.
Investigating the relationship between serum Gal-3 levels and cognitive performance, serum cytokines, and white blood cell count in three-month stably treated SC patients could contribute to a better understanding of the specific immune profile in patients with SC.
Twenty-seven patients with SC in remission and 18 healthy volunteers participated in this case-control and correlational study. Clinical assessment was performed using the Positive and Negative Syndrome Scale and the Montreal-Cognitive Assessment. The results of previously measured serum levels of Gal-3, interleukin (IL)-33, soluble suppression of tumorigenicity 2 (sST2), tumor necrosis factor-alpha (TNF-α), IL-6 and IL-17 were used for further statistical analyses, and IL-4, IL-23, IL-1β and transforming growth factor-beta (TGF-β) were now additionally measured with a sensitive enzyme-linked immunosorbent assay. The number of leukocytes in the blood and the percentage of neutrophils, lymphocytes, and monocytes were determined with a standardized routine measurement procedure. Statistical analyses were performed using SPSS 20.0 software.
Serum Gal-3 correlated positively with TNF-α, IL-23, and soluble sST2 in SC in remission and was associated with downregulation of the counterregulatory cytokine TGF-β and appears to play a role in disrupting leukocyte migration. The increase in Gal-3 might be influenced by risperidone dosing.
The combined activity of Gal-3 and proinflammatory cytokines, TGF-β downregulation and lower counts of leukocytes influence the SC duration. Gal-3 likely manifests indirect immunometabolic regulation of cognition in SC.
We observed that Gal-3 contributes to ongoing peripheral systemic inflammation and disease duration in patients with SC. Moreover, its influence on blood-brain barrier permeability and consequent neuroinflammation should be explored. Inflammation also appears to be the potential pathway by which Gal-3 may affect cognitive functioning in SC.