Neutrophil functions in morbidly obese subjects

Abstract

SummaryThe present study aimed to determine different peripheral blood neutrophil functions in 18 morbidly obese subjects with body mass index (BMI) ranging between 35 and 69 kg/m 2 in parallel with age-and gender-matched lean controls. Peripheral blood neutrophil functions of obese subjects and matched lean controls were determined. Neutrophils of obese subjects showed significant elevation of the release of basal superoxides (P < 0Á0001), formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated superoxides (P < 0Á0001) and opsonized zymosan (OZ)-stimulated superoxides (P < 0Á045) compared with lean controls. Interestingly, there were no differences in phorbol myristate acetate (PMA)-stimulated superoxide production by neutrophils of the obese subjects and controls. There was also a significant elevation of chemotactic (P < 0Á0003) and random (P < 0Á0001) migration of neutrophils from obese subjects compared with lean controls. Phagocytosis, CD11b surface expression and adherence of neutrophils from obese subjects were not significantly different from those of the lean controls. The elevated superoxide production and chemotactic activity, together with the normal phagocytosis and adherence, suggest that neutrophils from obese subjects are primed and have the capability to combat infections. However, neutrophils in the priming state may participate in the pathogenesis of obesity-related diseases.

Obesity and type 2 diabetes mellitus drive immune dysfunction, infection development, and sepsis mortality

“…The elevated basal superoxide production from unstimulated neutrophils indicates a low grade of inflammation, which coincides with obesity being a pro‐inflammatory condition. The elevated basal superoxide production may be the result of neutrophils being activated by high levels of triglycerides …”

“…Correcting the dysfunction of neutrophils in obesity and T2D has the potential to improve outcomes following infections and sepsis; however, the mechanistic pathways necessary to target are unknown. After bariatric surgery with marked weight loss, part of the inflammatory cascade (calprotectin levels) decreases, whereas other products (myeloperoxidase) do not, indicating a partial reduction in neutrophil activation . Additionally, weight loss through bariatric surgery has been shown to result in sustained improvements in T2D, whereas weight loss through diet and exercise has not shown similar improvements .…”

An update on immune dysregulation in obesity‐related insulin resistance

“…NE and MPO have important roles in the inflammation‐induced IR, and their deletion in HFD‐fed mice leads to less tissue inflammation and subsequent lower AT neutrophil and macrophage content . In addition, AT neutrophils of obese individuals release higher levels of superoxide ion () that can damage surrounding tissues . Moreover, neutrophils in AT produce cytokines and chemokines to facilitate macrophage infiltration (Table ).…”

Mast cells participate in chronic low‐grade inflammation within adipose tissue

“…In obese humans, accumulation of neutrophils in adipose tissue and, furthermore, expression of neutrophil elastase and superoxide production are elevated . Plasma levels of myeloperoxidase, an enzyme stored in granules of neutrophils and calprotectin, as well as a level of neutrophil activation marker cluster of differentiation (CD) 66b, are increased in patients with obesity, suggesting that obesity influences systemic activation of neutrophils .…”