Changes in gut microbiota due to supplemented fatty acids in diet-induced obese mice.

Consumption of a high-fat diet (HFD), which is associated with chronic 'low-grade' systemic inflammation, alters the gut microbiota (GM). The aim of the present study was to investigate the ability of an oleic acid-derived compound (S1) and a combination of n-3 fatty acids (EPA and DHA, S2) to modulate both body weight and the GM in HFD-induced obese mice. A total of eighty mice were fed either a control diet or a HFD, non-supplemented or supplemented with S1 or S2. At week 19, faeces were collected in order to analyse the GM. Group-specific primers for accurate quantification of several major bacterial groups from faecal samples were assayed using quantitative PCR. The HFD induced an increase in body weight, which was reduced by supplementation with S1. Furthermore, S1 supplementation markedly increased total bacterial density and restored the proportions of bacteria that were increased (i.e. clostridial cluster XIVa and Enterobacteriales) or decreased (i.e. Bifidobacterium spp.) during HFD feeding. S2 supplementation significantly increased the quantities of Firmicutes (especially the Lactobacillus group). Correlation analysis revealed that body weight correlated positively with the phylum Firmicutes and clostridial cluster XIVa, and negatively with the phylum Bacteroidetes. In conclusion, the consumption of a HFD induced changes in the faecal microbiota, which were associated with the appearance of an obese phenotype. Supplementation of the HFD with S1 counteracted HFD-induced gut dysbiosis, together with an improvement in body weight. These data support a role for certain fatty acids as interesting nutrients related to obesity prevention.

Effects of cold stress, corticosterone and catecholamines on phagocytosis in mice: differences between resting and activated macrophages.

OBJECTIVE: We subjected mice to acute cold stress and studied the effect on phagocytosis by peritoneal macrophages mediated by 3 types of phagocytic receptors: Fcgamma, complement receptors 3 (CR3) and mannose and beta-glucan receptors. METHODS: Mice were subjected to a cold stress condition (4 degrees C for 4 h), and then peritoneal macrophages were harvested and phagocytosis assays performed in vitro. RESULTS: We found a striking difference between resting and lipopolysaccharide (LPS)-activated macrophages (by intraperitoneal injection of LPS 4 days before the stress experiment): for resting macrophages cold stress caused a decrease in phagocytosis mediated by Fcgamma or mannose receptors, while for activated macrophages we observed an increase in phagocytosis by the 3 types of receptors. These effects were associated with an increase in plasma concentrations of corticosterone and catecholamines following the cold stress. In order to verify whether these hormone changes could account for the observed effects on phagocytosis, we performed in vitro assays by incubating macrophages harvested from nonstressed animals with these hormones for 4 h at 37 degrees C and measuring their phagocytic capacity. The following experiments were done: (a) with resting (nonactivated) macrophages; (b) with macrophages previously activated in vitro by incubation with LPS; (c) with macrophages previously activated in vivo by intraperitoneal injection of mice with LPS, 4 days before harvesting the cells. We found that for resting macrophages, corticosterone decreased phagocytosis mediated by Fcgamma and mannose and beta-glucan receptors, but catecholamines had no effect. For macrophages activated either in vivo or in vitro, catecholamines caused an increase in phagocytosis (excluding mannose receptors) while corticosterone had no effect. CONCLUSION: The above findings suggest that stress can regulate phagocytosis in different ways, depending on the kind of phagocytic receptor involved, the level of stress hormones and the physiological state of the macrophages.

Stress and immunological phagocytosis: possible nongenomic action of corticosterone.

Some immunological responses triggered by stress can be mediated by corticosterone activity through cytosolic receptors regulating gene expression. There are, however some reports on the possibility of a nongenomic effect of this hormone to explain phenomena observed in a few minutes. We have found that macrophages from mice subjected to 10 min of cold stress (at -15 degrees C) showed a lower phagocytic capacity mediated by Fcgamma-receptors than cells from control animals. Treating mice with glucocorticoid antagonist RU 486 did not block the decrease in phagocytic capacity. This inhibitory effect on phagocytosis was also observed by experiments in vitro with corticosterone in the concentration found in serum after stress, and could not be prevented by RU 486, actinomicyn D or cycloheximide. These results indicate that corticosterone could affect phagocytosis by macrophages through a nongenomic mechanism, and may have physiological implications.