S100B as a new fecal biomarker of inflammatory bowel diseases.

OBJECTIVE: S100 proteins are demonstrated to exert a protective role in the gastrointestinal tract. In the present study, we investigated whether S100B protein, that is typically expressed by enteroglial cells, is detectable in feces and could be a useful noninvasive indicator of gut chronic inflammation. PATIENTS AND METHODS: This clinical prospective study included n=48 patients suffering Crohn's disease (CD) or ulcerative colitis (UC) and non IBD-controls. The clinical disease activity was evaluated using Harvey-Bradshaw or Mayo Score Index while the diagnosis of IBD was defined based on standard endoscopic and histological criteria. S100B and calprotectin were extracted and analyzed using commercial enzyme-linked immunosorbent assay (ELISA) kits. RESULTS: Unlike calprotectin, S100B was significantly decreased in both CD and UC compared to non IBD-patients. The strongest quantitative alterations of S100B were detected concomitantly with signs of active or quiescent disease, including high/normal expression of fecal calprotectin, mucosal damage/cryptitis, mucin depletion and inflammatory infiltrate, as defined by endoscopic evaluation and histological analysis. At the onset of disease and under no Infliximab-based therapy, the lowest was detected suggesting that S100B in feces could have a potential diagnostic value for IBD. CONCLUSIONS: Testing for S100B and calprotectin could be a useful screening tool to better predict IBD activity.

Inter- and intra-specific variability in isoprene production and photosynthesis of Central European oak species.

European deciduous oaks are closely related and are known for their strong emission of volatile isoprenoids. They are chemo-taxonomically diverse, but hybridise frequently. Four-year-old oak seedlings growing together in a model ecosystem facility under near-natural conditions were studied. The leaves were morphologically classified in the three oak species Quercus robur, Q. pubescens and Q. petraea (with four provenances each) and further investigated by a molecular-genetic approach. Q. robur was morphologically and genetically clearly different from Q. pubescens and Q. petraea, whereas Q. pubescens and Q. petraea individuals used in this study were morphologically and genetically more similar. There was a minor impact of among and within species variability on isoprene synthesis, isoprene emission and photosynthesis. Isoprene emission rates normalised to 25 °C leaf temperature ranged from 5.78 to 10.66 nmol m(-2)  s(-1) , whereas photosynthesis ranged from 12.8 to 17.6 µmol m(-2)  s(-1) . On cloudy days, among the provenances of each species, only net photosynthesis of the Q. robur provenance Hünenberg was reduced and isoprene synthase activity of the Q. pubescens provenance Promotogno increased. On sunny days, photosynthesis did not differ among the provenances. Over all provenances, gas exchange on cloudy days did not differ significantly from sunny days. In the combined data of cloudy and sunny days, no differences between the studied provenances and oak species were detected in isoprene emission and photosynthesis. Thus, isoprene emission and photosynthesis rates were remarkably stable among oak species and provenances. The results indicate that taxonomic differences in the studied oak species are not reflected in isoprene emission and photosynthesis, probably because of the high plasticity of gene expression resulting in high phenotypic flexibility.

Physiological and biochemical responses of Quercus pubescens to air warming and drought on acidic and calcareous soils.

The drought- and thermo-tolerant Quercus pubescens, a tree species growing on both acidic and calcareous soils in the sub-Mediterranean region, was exposed to soil drought (-60% to -80% soil water content) and air warming (+1.2 °C daytime temperature), singly and in combination. The experiment was conducted on two natural forest soils with similar texture but different pH (acidic and calcareous soils). The physiological (photosynthesis) and biochemical (antioxidant system) responses of Q. pubescens were investigated. On acidic soil, Q. pubescens had a higher reactive oxygen species (ROS) content than on calcareous soil, confirming that this species is better adapted to the latter soil type. A down-regulation of ascorbate-glutathione cycle enzymes suggests that ROS were used as signalling molecules. Air warming stimulated stomatal opening, while soil drought induced stomatal closure in the late afternoon and reduced Rubisco carboxylation efficiency. Photosynthetic performance in the combined treatment was higher than under single drought stress and similar to control and air warming. Q. pubescens biochemical responses depended on soil pH. On acidic soil, Q. pubescens trees exposed to air warming used ROS as signalling molecules. On calcareous soil, these trees were able to balance both soil drought and air warming stress, avoiding ROS toxic effects by increasing antioxidant enzyme activitiy and maintaining a high enzymatic antioxidant defence. When combined, drought and air warming induced either more severe (higher oxidative pressure and impairment of the light-harvesting complex) or different responses (decline of the thermal energy dissipation capacity) relative to the single stressors. Overall, however, Q. pubescens preserved the functionality of the photosynthetic apparatus and controlled the antioxidant system response, thus confirming its drought and thermo-tolerance and therefore its potential to adapt to the ongoing climate change.

Cyclosporin A inhibits programmed cell death and cytochrome c release induced by fusicoccin in sycamore cells.

Programmed cell death plays a vital role in normal plant development, response to environmental stresses, and defense against pathogen attack. Different types of programmed cell death occur in plants and the involvement of mitochondria is still under investigation. In sycamore (Acer pseudoplatanus L.) cultured cells, the phytotoxin fusicoccin induces cell death that shows apoptotic features, including chromatin condensation, DNA fragmentation, and release of cytochrome c from mitochondria. In this work, we show that cyclosporin A, an inhibitor of the permeability transition pore of animal mitochondria, inhibits the cell death, DNA fragmentation, and cytochrome c release induced by fusicoccin. In addition, we show that fusicoccin induces a change in the shape of mitochondria which is not prevented by cyclosporin A. These results suggest that the release of cytochrome c induced by fusicoccin occurs through a cyclosporin A-sensitive system that is similar to the permeability transition pore of animal mitochondria and they make it tempting to speculate that this release may be involved in the phytotoxin-induced programmed cell death of sycamore cells.