No abstract

Objective: Growing evidence supports a link between obesity and inflammation. Current research is focused on the role of adipokines such as adiponectin and immune cells, especially macrophages, in adipose tissue. Our aim was to examine the role of inflammation not in tissue but in the peripheral blood of healthy overweight and obese subjects. We especially investigated the role of neutrophils and their possible regulation by adiponectin. Methods: In healthy normal-weight, overweight, and obese human subjects (n = 32) the peripheral blood concentrations of adipokines, satiety hormones, apoptosis markers, and cytokines as well as the blood count were related to inflammation and neutrophils, at 3 independent days of examination. The response of neutrophils to stimulation by adiponectin was also investigated in vitro. Results: In obese and by tendency already in overweight subjects, inflammation was increased showing a higher neutrophil-to-lymphocyte ratio, elevated high-sensitivity C-reactive protein, increased chemokines (CXCL8, CCL3, CCL5), increased apoptosis markers (M30 and M65), and changes in hormone levels in the peripheral blood. LPS- and fMLP-induced production of CXCL8 by neutrophils was elevated in overweight and obese subjects. High plasma levels of adiponectin were associated with reduced CXCL8 production in peripheral blood neutrophils. In vitro, production of CXCL8 by neutrophils was inhibited by adiponectin. Conclusion: Reduced adiponectin and enhanced apoptosis may occur already in the peripheral blood of healthy overweight subjects. This process seems to further enhance neutrophil activity in overweight and obese.

Brain and immune system are linked by bidirectional pathways so that changes of the central nervous system may influence various immune functions. The olfactory system may be involved in this interaction. In most odor studies subjects are aware of an odor exposure, using frequently high odor concentrations or long-term exposures without controls. In this pilot study, the potential immune effects of short-term odor exposure were examined in 32 blinded subjects (16 male, 16 female). Subjects were exposed without their knowledge either to a stimulant essential oil (grapefruit, fennel, pepper), a no-odor control or a relaxant essential oil (lavender, patchouli, rose) during a set of psychological questionnaires for 30 min at three separate visits. Activity of neutrophil granulocytes (CXCL8 release, CD16) and peripheral blood concentrations of mainly neutrophil-related immunological markers were measured. We tested the triple of stimulant odor, control and relaxant odor for every subject in a model which assumed opposite effects of the stimulant and the relaxant odor. This hypothesis was falsified by our experimental data, as no significant effect was observed for the parameters tested. The human immune functions tested in our study are not modulated by short-term odor exposure in blinded subjects. Further studies should directly dissect possible differences between long-term and short-term exposures of non-blinded subjects versus blinded subjects.