Differential TLR2- and TLR4-Associated Oxidative Responses After Bariatric Surgery: A Cross-Sectional Study in Women

Background/Objectives: Obesity is characterized by chronic low-grade inflammation and oxidative stress, mediated in part by Toll-like receptor (TLR)-associated pathways. Bariatric surgery improves clinical and metabolic parameters, but its effects on TLR-associated reactive oxygen species (ROS) responses in immune cells remain unclear. This study aimed to investigate ROS production following TLR2- and TLR4-associated stimulation in granulocytes from women with obesity before and after bariatric surgery, compared with age-matched non-obese controls. Methods: ROS production was evaluated using a luminol-dependent chemiluminescence assay in granulocytes isolated from women with obesity before (PRE, n = 12) and after (POST, n = 12) bariatric surgery, as well as from age-matched non-obese controls (n = 12). ROS production was assessed under basal conditions and following stimulation with lipopolysaccharide (LPS, a TLR4 agonist) or zymosan (ZY, a TLR2-associated stimulus). Clinical, anthropometric, and biochemical parameters were assessed, and their associations with ROS production were analyzed. Results: Bariatric surgery was associated with significant improvements in clinical and metabolic parameters, although mean BMI in the POST group remained within the obesity range. Granulocytes from the PRE group exhibited increased basal ROS production and enhanced responses following both LPS and ZY stimulation. In the POST group, basal ROS production and the response following ZY stimulation were comparable to those observed in controls, whereas LPS-associated ROS production remained elevated. Correlation analyses showed positive associations between anthropometric and biochemical parameters and ROS production in both PRE and POST groups, with body weight and BMI remaining positively associated with basal and LPS-associated ROS production after surgery. Conclusions: Bariatric surgery was associated with substantial clinical and metabolic improvement but did not completely restore innate immune redox homeostasis. The persistence of TLR4-driven ROS production suggests that some alterations in innate immune redox balance may persist after surgery despite metabolic improvement.