Obesity and the innate immune response
The benefits of a healthy lifestyle are extolled in the previous article to help maintain a healthy immune system. In fact, many scientific studies support the article’s contention that the first line of defence is a healthy lifestyle. One public health issue that has become extremely problematic in the developed world is that of obesity. Various recent studies suggest that, for example, obesity has a direct effect on elements of the innate immune system. For example a recent Journal of Immunology paper from the University Of Louisville School Of Medicine in the USA looked at alterations in inflammation resolution in obesity and type 2 diabetes. There is much evidence that the excess of nutrients in obesity result in chronic low-grade inflammation, although the mechanism remains unclear. Obese people also experience defective wound healing and are more susceptible to infections. This study looked specifically at a potential role for prostaglandins in inflammation resolution defects in obesity. The study on a mouse model of obesity/diabetes found that saturated free fatty acids that are elevated in obesity promote neutrophil survival and decrease macrophage phagocytosis, thus altering inflammation resolution. Furthermore, in isolated macrophages it was observed that the free fatty acid palmitic acid induced cyclooxygenase-2 and increased prostanoid production. These palmitic acid-induced macrophage phagocytosis effects could be mimicked by the prostaglandins PGE2 and PGD2 and reversed by cyclooxygenase inhibition or prostanoid receptor antagonism. Macrophages from the mouse model of obesity/diabetes expressed the prostanoid receptors EP2 (PGE2 receptor) and DP1 (PGD2 receptor) and had higher levels of the prostanoid receptor downstream signalling molecule cAMP than wild type mice. Importantly, the EP2/DP1 dual antagonist AH6809 reduced effects of impaired inflammation resolution including peritoneal neutrophil accumulation and thymic apoptotic cell accumulation. Thus, the study identified prostanoid receptors as a potential novel therapeutic target in resolution of inflammation in obesity and diabetes. However, as the original article recommends, prevention is better than cure and a healthy diet combined with adequate exercise is the best method to avoid obesity and its associated immune response problems.
Source
HELLMANN, J. et al., 2013. Increased saturated fatty acids in obesity alter resolution of inflammation in part by stimulating prostaglandin production. Journal Of Immunology (Baltimore, Md.: 1950), 191(3), pp. 1383-1392
The benefits of a healthy lifestyle are extolled in the previous article to help maintain a healthy immune system. In fact, many scientific studies support the article’s contention that the first line of defence is a healthy lifestyle. One public health issue that has become extremely problematic in the developed world is that of obesity. Various recent studies suggest that, for example, obesity has a direct effect on elements of the innate immune system. For example a recent Journal of Immunology paper from the University Of Louisville School Of Medicine in the USA looked at alterations in inflammation resolution in obesity and type 2 diabetes. There is much evidence that the excess of nutrients in obesity result in chronic low-grade inflammation, although the mechanism remains unclear. Obese people also experience defective wound healing and are more susceptible to infections. This study looked specifically at a potential role for prostaglandins in inflammation resolution defects in obesity. The study on a mouse model of obesity/diabetes found that saturated free fatty acids that are elevated in obesity promote neutrophil survival and decrease macrophage phagocytosis, thus altering inflammation resolution. Furthermore, in isolated macrophages it was observed that the free fatty acid palmitic acid induced cyclooxygenase-2 and increased prostanoid production. These palmitic acid-induced macrophage phagocytosis effects could be mimicked by the prostaglandins PGE2 and PGD2 and reversed by cyclooxygenase inhibition or prostanoid receptor antagonism. Macrophages from the mouse model of obesity/diabetes expressed the prostanoid receptors EP2 (PGE2 receptor) and DP1 (PGD2 receptor) and had higher levels of the prostanoid receptor downstream signalling molecule cAMP than wild type mice. Importantly, the EP2/DP1 dual antagonist AH6809 reduced effects of impaired inflammation resolution including peritoneal neutrophil accumulation and thymic apoptotic cell accumulation. Thus, the study identified prostanoid receptors as a potential novel therapeutic target in resolution of inflammation in obesity and diabetes. However, as the original article recommends, prevention is better than cure and a healthy diet combined with adequate exercise is the best method to avoid obesity and its associated immune response problems.
Source
HELLMANN, J. et al., 2013. Increased saturated fatty acids in obesity alter resolution of inflammation in part by stimulating prostaglandin production. Journal Of Immunology (Baltimore, Md.: 1950), 191(3), pp. 1383-1392
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