Staphylococcus aureus nasal carriage is associated with serum 25-hydroxyvitamin D levels, gender and smoking status. The Tromsø Staph and Skin Study.

Vitamin D induces the expression of antimicrobial peptides with activity against Staphylococcus aureus. Thus, we studied the association between serum 25-hydroxyvitamin D (25(OH)D) and S. aureus nasal colonization and carriage. Nasal swabs, blood samples and clinical data from 2,115 women and 1,674 men, aged 30-87 years, were collected in the Tromsø Staph and Skin Study 2007-08, as part of the population-based sixth Tromsø Study. Multivariate logistic regression analyses were stratified by recognized risk factors for S. aureus carriage: sex, age and smoking. In non-smoking men, we observed a 6.6% and 6.7% decrease in the probability of S. aureus colonization and carriage, respectively, by each 5 nmol/l increase in serum 25(OH)D concentration (P < 0.001 and P = 0.001), and serum 25(OH)D > 59 nmol/l and ≥75 nmol/l as thresholds for ~30% and ~50% reduction in S. aureus colonization and carriage. In non-smoking men aged 44-60 years, the odds ratio for S. aureus colonization was 0.44 (95% confidence interval, 0.28-0.69) in the top tertile of serum 25(OH)D versus the bottom tertile. In women and smokers there were no such associations. Our study supports that serum vitamin D is a determinant of S. aureus colonization and carriage.

Expression of melanoma-associated antigen of thermotolerant human cells.

The expression of the melanoma-associated antigen p250 on thermotolerant cells and the effect of a second heat dose on the antigen expression have been measured by flow cytometry. The human melanoma cell line FME was heated at 43.5 degrees C for 120 min after a priming heat dose at 43.5 degrees C for 20, 40 or 60 min. Cells preheated at 43.5 degrees C for 40 and 60 min followed the same kinetics of development and decay of thermotolerance, with maximum thermotolerance 16 h after the priming heating, and the thermotolerance had decayed by 48 h. Cells preheated at 43.5 degrees C for 20 min showed maximum thermotolerance after 7 h and decay by 24 h. Heat reduced the expression of the melanoma-associated antigen in a dose-dependent manner. Thermotolerant cells were given a second heat dose (43.5 degrees C for 120 min) and the antigen expression measured immediately after heating. Fractionated hyperthermia using the lower predose (43.5 degrees C for 20 min) might have an additive effect on the reduction of antigen expression, while the highest predose (43.5 degrees C for 60 min) protected against reduction in antigen expression. The development and decay of resistance against heat-induced reduction in expression of melanoma-associated antigen followed a similar time course as thermotolerance in terms of cell survival. Maximum resistance was observed 12 h after the priming heat treatment, and the resistance had decayed by 48 h.