Leptin Levels Are Associated with Immune Response in Malnourished Infants

Abstract

Circulating leptin levels, proinflammatory and T helper cells type 1 (Th1), Th2 cytokine production, and lymphoproliferative response were measured in 15 infants with primary moderate protein calorie malnutrition on admission and after recovery of 10% of weight. Sixteen healthy, well nourished infants of comparable age served as controls. A significant deficit in the z-score of weight for age, weight for height, body mass index, and circulating leptin and growth factors were detected in malnourished infants on admission compared with controls (P < 0.05). These deficits were associated with a significant suppression of the lymphoproliferative response, Th1, and proinflammatory cytokine production (P < 0.05). After a 10% weight gain, a significant increase in circulating leptin levels was produced in parallel with a significant increase in Th1 activity, as revealed by an enhancement in interferon-gamma and a suppression in IL-4 production. Concomitantly, the lymphoproliferative response became similar to that detected in control infants. Furthermore, a significant increase in IL-1 and TNFalpha production compared with that at admission was shown. These findings suggest an association between the increase in leptin and the immunological recovery observed following refeeding of malnourished infants.

A mutation in the leptin receptor is associated with Entamoeba histolytica infection in children

“…Leptin is a product of the LEP gene on chromosome 7 that functions to signal satiety and is implicated in regulation of the immune system and the gastrointestinal tract (3,4). Circulating leptin concentrations are low in malnourished infants and are associated with a suppression of proinflammatory cytokine production (5). Leptin promotes differentiation, proliferation, survival, and function of both innate and adaptive immune cells (6)(7)(8)(9)(10) and acts as a proinflammatory cytokine that orchestrates the inflammatory response toward a Th1 phenotype while suppressing Th2 and regulatory T cell functions (5,11,12).…”

“…Circulating leptin concentrations are low in malnourished infants and are associated with a suppression of proinflammatory cytokine production (5). Leptin promotes differentiation, proliferation, survival, and function of both innate and adaptive immune cells (6)(7)(8)(9)(10) and acts as a proinflammatory cytokine that orchestrates the inflammatory response toward a Th1 phenotype while suppressing Th2 and regulatory T cell functions (5,11,12). In addition to the proinflammatory effects on the immune system, leptin may also modulate intestinal barrier function by promoting regeneration and inhibiting apoptosis of intestinal epithelium (13,14) as well as stimulating mucin secretion (15) and maintaining intestinal morphology (16).…”

Increased activity of interleukin-23/interleukin-17 proinflammatory axis in obese women

“…8 Moreover, some recent findings suggest that inflammation-related tissue damage in organ-specific autoimmunity could be associated with the IL-23/IL-17-dependent T-helper cell response (that is, Th17 response), rather than with the activity of IL-12/IFN-g cytokine axis as the main driving power behind the so-called Th1 response. 9 Although there are some data indicating that Th1 response might be reduced in malnourished and increased in obese children, [10][11][12] IL-23…”

Leptin Modulates Neutrophil Phagocytosis ofKlebsiella pneumoniae

“…Circulating leptin levels correlate with total body fat mass and signal the central nervous system regarding energy storage (1). Declining serum leptin, which occurs in both humans and mice during starvation or in malnutrition, may serve as a signal to the host to conserve energy by shutting down energy-expensive functions (such as immune function) when energy intake is lacking (2,16). In the leptin-deficient mouse, spontaneous mutation of the ob gene results in the formation of a nonfunctional leptin protein and leptin deficiency (19).…”