No abstract

The microbiota of the gut–lung axis affects local and far-reaching immune responses and might also trigger chronic and inflammatory diseases. We hypothesized that gut dysbiosis induced by obesity, which coexists in countries with a high tuberculosis burden, aggravates the host susceptibility and the pulmonary damage tolerance. To assess our hypothesis, we used a model of high-fat diet (HFD)-induced obesity, followed by infection of C57BL/6 mice with Mycobacterium tuberculosis. We showed that obesity increased the susceptibility, the pulmonary inflammation and IFN-γ levels in M. tuberculosis-infected mice. During the comorbidity obesity and tuberculosis, there is an increase of Bacteroidetes and Firmicutes in the lungs, and an increase of Firmicutes and butyrate in the feces. Depletion of gut microbiota by antibiotic treatment in the obese infected mice reduced the frequencies of CD4+IFN-γ+IL-17− cells and IFN-γ levels in the lungs, associated with an increase of Lactobacillus. Our findings reinforce the role of the gut–lung axis in chronic infections and suggest that the gut microbiota modulation may be a potential host-directed therapy as an adjuvant to treat TB in the context of IFN-γ-mediated immunopathology.

Background & aims: Malnutrition is a common condition of difficult diagnosis in patients with hepatocellular carcinoma. The objective of this study was to evaluate the nutritional status of patients with hepatocellular carcinoma in palliative care through handgrip strength and adductor pollicis muscle thickness. Methods: Data on the severity of liver disease, and oncological and nutritional assessment data, including body mass index (BMI), hand grip strength (HGS), and adductor pollicis muscle thickness (APMT), were collected from the electronic medical records of patients in nutritional outpatient follow-up. Analyzes were performed with all patients in a single group or according to Child-Turcotte-Pugh classification. Associations were analyzed by the Pearson correlation coefficient, with a p value > 0.05 indicating significance.Results: Mean values of BMI and APMT increased while HGS decreased as disease severity increased according to the CHILD scale. According to the Performance Status evaluation by ECOG, the higher the severity of the disease assessed by the CHILD scale the worse the HGS and ECOG values. A correlation between HGS and CHILD B and C was found.

Background. Nonalcoholic fatty liver disease (NAFLD) is the most common hepatic disorder, affecting 22–28% of the adult population and more than 50% of obese people all over the world. Modulation of the fatty acids in diet as a means of prevention against nonalcoholic fatty liver disease in animal models (NAFLD) remains unclear. The treatment of NAFLD has not been described in specific guidelines so far. Thus, the justification for the study is to check modifications in macronutrients composition, fatty acids, in particular, play a significant role in the treatment of NAFLD regardless of weight loss. Aim. To investigate different vegetable oils in prevention and progression of NAFLD in animal models. Methods. For the experiment were used fifty C57BL/6J mice male fed with high fat and fructose diet (HFD) to induce the NAFLD status and they received different commercial vegetable oils for 16 weeks to prevent steatosis. Liver steatosis and oxidative stress parameters were analyzed using biochemical and histological methods. Fatty acids profile in the oils and in the liver samples was obtained. Results. The high fat and fructose diet led to obesity and the vegetable oils offered were effective in maintaining body weight similar to the control group. At the end of the experiment (16 weeks), the HFHFr group had a greater body weight compared to control and treated groups (HFHFr: 44.20 ± 2.34 g/animal vs. control: 34.80 ± 3.45 g/animal; p < 0.001 ; HFHFr/OL: 35.40 ± 4.19 g/animal; HFHFr/C: 36.10 ± 3.92 g/animal; HFHFr/S: 36.25 ± 5.70 g/animal; p < 0.01 ). Furthermore, the HFD diet has caused an increase in total liver fat compared to control ( p < 0.01 ). Among the treated groups, the animals receiving canola oil showed a reduction of hepatic and retroperitoneal fat ( p < 0.05 ). These biochemical levels were positively correlated with the hepatic histology findings. Hepatic levels of omega-3 decreased in the olive oil and high fat diet groups compared to the control group, whereas these levels increased in the groups receiving canola and soybean oil compared to control and the high fat groups. Conclusion. In conclusion, the commercial vegetable oils either contributed to the prevention or reduction of induced nonalcoholic fatty liver with high fat and fructose diet, especially canola oil.