Diet-Induced Pulmonary Inflammation and Incipient Fibrosis in Mice: a Possible Role of Neutrophilic Inflammation.
M C Della VedovaF M Soler GarciaM D MuñozM W FornesSandra E Gomez MejibaN N GómezDario C RamirezPublished in: Inflammation (2020)
Chicken fat and fructose are added into food-processing to reduce costs and enhance acceptability; however, these additives turn food into unhealthy and hypercaloric meals. Herein we have hypothesized that chronic feeding with chicken fat and fructose, together or by separate, can cause pulmonary redox and inflammatory changes. These changes are particularly related to neutrophils and myeloperoxidase, with consequent changes in the organ histophysiology. To test this hypothesis, we fed mice for 16 weeks with either control food (low-fat diet, LFD) or control food supplemented with 22% chicken fat and with or without 10% fructose in the drinking water. At the end of the feeding regimen, we measured redox and inflammatory changes in the lung with particular emphasis on neutrophil accumulation/activation and molecular-histological markers of fibrosis. Our results suggest that a diet supplemented with chicken fat and fructose causes additive effects on pulmonary oxidative stress, inflammation, and a pro-fibrotic status. Neutrophilic inflammation may play a critical role in pulmonary pathology associated with metabolic syndrome.
Keyphrases
- oxidative stress
- adipose tissue
- drinking water
- pulmonary hypertension
- metabolic syndrome
- fatty acid
- dna damage
- ischemia reperfusion injury
- human health
- diabetic rats
- physical activity
- high fat diet induced
- induced apoptosis
- weight loss
- risk assessment
- systemic sclerosis
- uric acid
- type diabetes
- cardiovascular disease
- skeletal muscle
- health risk
- health risk assessment
- drug induced
- idiopathic pulmonary fibrosis
- heavy metals
- sensitive detection
- liver fibrosis