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How does diet influence the response to particulate air pollution?

Source: GMC



Obesity and its common sequelae such as type II diabetes and cardio vascular diseases are a worldwide increasing health risk factor. The underlying physiological pathways and their genetic causes interacting with environmental factors still require substantial research efforts. Importantly, not only direct effects of increased adiposity e.g. on the sceleto-muscular system or insulin function need to be considered but also the sensitivity of obese patients to noxious substances resulting from air pollution or the adverse effects of very small airborne particles that are inhaled.
The adipose tissue is the largest endocrine organ in the body. Its products act secretory, endocrine and regulatory on physiologic and pathologic metabolic and cardio-vascular events and can thus be responsible for deregulation and disruption of these processes. In the adipose tissue adipocyte-derived pro-inflammatory molecules like leptin, visfatin and resistin are increased, while anti-inflammatory molecules like adiponectin are reduced. Since macrophages contribute to about 10% to the adipose tissues cell types, it is largely contributing to a pro-inflammatory situation.
Systemic pro-inflammatory conditions such as overweight and obesity are discussed to increase the susceptibility to adverse health effects of air pollution. In this context it is believed that pulmonary oxidative stress, resulting from inhaled particulate matter (PM) can lead to pulmonary and systemic inflammation, and subsequently to an increased cardiovascular risk.


Six weeks of diet is not enough

In this study C57BL/6J mice were used as a model for human obesity, induced by feeding either Cafeteria (CF) diet, high fat (HF) diet or low fat (LF) diet for a short period of six weeks. Following this period mice were challenged by exposure to carbon-nanoparticles (CNP), a surrogate for ambient combustion derived PM. This protocol allowed to test the following hypotheses: Do early diet-induced pre-obese like changes on body parameters result in a basal pro-inflammatory state in the lung alveolar compartment and blood systemic level? Will diet-induced changes affect/exaggerate the particle-triggered inflammatory response in the alveolar compartment on a cellular and molecular level?
After six weeks of diet results pointed to a pre-obese state in CF diet fed mice. HF diet fed mice showed increased body fat but were intermediate between CF and LF diets. In contrast white blood cell numbers were increased in HF but not CF and LF animals, pointing towards elevated systemic inflammatory conditions. In bonchoalveolar lavage (BAL) however diet related differences in inflammatory cell numbers did not differ, but pro-inflammatory leptin was present in higher concentrations in BAL of CF and HF mice.
The instillation with carbon-nanoparticles resulted in an substantial influx of inflammatory neutrophils into the alveolar compartment. However, it did not differ in the magnitude between the three diets.
All together the results provide insight into the changes of pro- and anti-inflammatory marker proteins caused by feeding diets of different caloric content and composition. The data suggest, that although the diet-challenge already was efficient in driving pro-inflammatory systemic events, extended feeding periods are necessary to generate an increased susceptibility to particle-induced lung inflammation.

„Comparison of particle-exposure triggered pulmonary and systemic inflammation in mice fed with three different diets “, Götz et al., Particle and Fibre Toxicology 2011, 8:30