Thermoregulatory responses, heart rate, and the susceptibility to anxiety in obese animals subjected to stress.

Obesity and stress are related to cardiovascular diseases. Rats fed a high-fat diet (HFD) show increased cardiovascular reactivity to emotional stress and altered defensive behavioral responses. Indeed, changes in thermoregulatory responses in an aversive environment are observed in these animals. However, studies aimed at clarifying the physiological mechanisms linking obesity, stress hyperreactivity and behavioral changes are needed. The aim of this study was to evaluate the changes in thermoregulatory responses, heart rate, and the susceptibility to anxiety in obese animals subjected to stress. Nine-week high-fat diet protocol was effective in inducing obesity by increasing weight gain, fat mass, adiposity index, white epididymal, retroperitoneal, inguinal and brown adipose tissue. Animals induced to obesity and subjected to stress (HFDS group) by the intruder animal method showed increases in heart rate (HR), core body temperature and tail temperature. HFDS showed an increase in the first exposure to the closed arm (anxiety-like behavior) in elevated T-Maze (ETM). The groups did not differ with respect to panic behavior assessed in the ETM and locomotor activity in the open field test. Our study shows that HFDS animals presented increased reactivity to stress with higher stress hyperthermia and anxious behavior. Thus, our results present relevant information regarding stress responsiveness and behavioral changes in obese animals.

Evaluation of the interaction between polymyxin B and Pseudomonas aeruginosa biofilm and planktonic cells: reactive oxygen species induction and zeta potential.

BACKGROUND: Although the most widely accepted mechanism of action for polymyxins is related to bacterial lysis via disruption, we hypothesized that this antimicrobial drug class could have other effects on Pseudomonas aeruginosa planktonic and sessile cells. Little is known regarding oxidative burst and zeta potential (ZP) data associated with the interaction between polymyxin B and P. aeruginosa cells. The present study evaluated endogenous reactive oxygen species (ROS) production and changes in the net charges of biofilm and planktonic cells in response to polymyxin B. RESULTS: Polymyxin B induced concentration-dependent killing at all concentrations tested in planktonic and sessile cells from P. aeruginosa strains. Sublethal concentrations of polymyxin B induced oxidative burst. ROS production was higher in resistant planktonic cells than in biofilm cells but this was not observed for susceptible cells. Moreover, no net surface charge alterations were observed in planktonic cells from a susceptible strain treated with polymyxin B, but a significant increase of ZP was noted in planktonic cells from a resistant strain. CONCLUSION: Oxidative burst generated by planktonic and sessile cells from P. aeruginosa strains against polymyxin B indicates that ROS may have an important role in the mechanism of action of this drug. ZP data revealed that electrostatic interactions of the cationic peptide with the anionic surface of the cells are strain-dependent. Therefore, we suggested that the intracellular effects of polymyxin B should be further investigated to understand polymyxin B-induced stress in P. aeruginosa.

Biophysical Effects of a Polymeric Biosurfactant in Candida krusei and Candida albicans Cells.

This study evaluated the effects of a polymeric biosurfactant produced by Trichosporon montevideense CLOA72 in the adhesion of Candida albicans and Candida krusei cells to human buccal epithelial cells and its interference in biofilm formation by these strains. The biofilm inhibition by biosurfactant (25 mg/mL) in C. krusei and C. albicans in polystyrene was reduced up to 79.5 and 85 %, respectively. In addition, the zeta potential and hydrodynamic diameter of the yeasts altered as a function of the biosurfactant concentration added to the cell suspension. The changes in the cell surface characteristics and the interface modification can contribute to the inhibition of the initial adherence of yeasts cells to the surface. In addition, the analyses of the biofilm matrix and planktonic cell surfaces demonstrated differences in carbohydrate and protein concentrations for the two studied strains, which may contribute to the modulation of cell adhesion or consolidation of biofilms, especially in C. krusei. This study suggests a possible application of the of CLOA72 biosurfactant in inhibiting the adhesion and formation of biofilms on biological surfaces by yeasts of the Candida genus.

Heteroresistance to Itraconazole Alters the Morphology and Increases the Virulence of Cryptococcus gattii.

Cryptococcus gattii is the main etiological agent of cryptococcosis in immunocompetent individuals. The triazole drug itraconazole is one of the antifungals used to treat patients with cryptococcosis. Heteroresistance is an adaptive mechanism to counteract the stress of increasing drug concentrations, and it can enhance the ability of a microorganism to survive under antifungal pressure. In this study, we evaluated the ability of 11 C. gattii strains to develop itraconazole heteroresistance. Heteroresistant clones were analyzed for drug susceptibility, alterations in cell diameter, capsule properties, and virulence in a murine model. Heteroresistance to itraconazole was intrinsic in all of the strains analyzed, reduced both the capsule size and the cell diameter, induced molecular heterogeneity at the chromosomal level, changed the negatively charged cells, reduced ergosterol content, and improved the antioxidant system. A positive correlation between surface/volume ratio of original cells and the level of heteroresistance to itraconazole (LHI) was observed in addition to a negative correlation between capsule size of heteroresistant clones and LHI. Moreover, heteroresistance to itraconazole increased the engulfment of C. gattii by macrophages and augmented fungal proliferation inside these cells, which probably accounted for the reduced survival of the mice infected with the heteroresistant clones and the higher fungal burden in lungs and brain. Our results indicate that heteroresistance to itraconazole is intrinsic and increases the virulence of C. gattii. This phenomenon may represent an additional mechanism that contributes to relapses of cryptococcosis in patients during itraconazole therapy.