The production of H2S by pure culture wine yeasts

Production of H2S by 12 pure culture wine yeasts on different substrates including grape juice has been studied. Under these conditions low- and high-sulphite forming yeasts showed different patterns of H2S formation : When grown with sulphate or sulphite as the only sulphur source the strains could be divided not only into low- or high-sulphite (S02) formers but also into low- or high-sulphide (H2S) forming yeasts. Growth on the ABY solid medium also separated high- from lowsulphide formers. A deficiency of pantothenate produced a similar pattern though with increased levels of H2S. The addition of L-cysteine with or without pantothenate caused a substantial increase in H 2S production with only some strains. Addition of colloidal sulphur produced high concentrations of H2S with all strains, such that they could not be differentiated. Neither did the fermentation of grape juice nor the addition of grape juice slurry to the synthetic substrate allow any differentiation of the yeasts. lt is concluded that H2S formation in grape juice comes mostly from residual colloidal sulphur from fungal sprays. It is also shown that more suitable yeast strains can be selected.Die Bildung von H2S durch ReinzuchthefenDie Bildung von H2S durch 12 Reinzuchthefen wurde mit verschiedenen Gärsubstratzusammensetzungen untersucht. Wenig- und viel-Sulfitbildende Hefen zeigten unterschiedliches H2S-Bildungsvermögen: Waren Sulfat oder Sulfit die einzigen Schwefelquellen, dann konnten die Hefen nicht nur in Wenig- und Viel-Sulfit-Bildner, sondern auch in wenig- und viel-Sulfid-bildende Stämme eingeteilt werden. Letzteres zeigte sich auch, wenn die Hefen auf ABY-Agar ausgestrichen wurden. Auch ein Pantothenat-Mangelsubstrat bewirkte im wesentlichen die gleichen Ergebnisse. Wurde Cystein zugegeben, mit oder ohne Pantothenat, so reagierten nur einige Stämme mit verstärkter H2S-Bildung. Alle Hefestämme produzierten gleich viel H2S, wenn dem Gärsubstrat kolloidaler Schwefel zugegeben worden war. Die Vergärung von Traubenmost oder von synthetischem Substrat, dem Zentrifugentrub zugesetzt worden war, ermöglichte ebenfalls keine Gruppierung der Stämme. Es wird vermutet, daß die H2S-Bildung bei der Vergärung von Traubensaft meistens durch kolloidalen Schwefel aus Spritzmittelrückständen verursacht wird. Es wird außerdem gezeigt, daß geeignetere Reinzuchthefen selektioniert werden können

Expression of the chemokine receptor CCR5 in psoriasis and results of a randomized placebo controlled trial with a CCR5 inhibitor

Several reports have indicated that the chemokine receptor CCR5 and its ligands, especially CCL5 (formerly known as RANTES), may play a role in the pathogenesis of psoriasis. The purpose of this investigation was to examine the expression of CCR5 and its ligands in chronic plaque psoriasis and to evaluate the clinical and immunohistochemical effect of a CCR5 receptor inhibitor. Immunohistochemical analysis showed low but significant increased total numbers of CCR5 positive cells in epidermis and dermis of lesional skin in comparison to non-lesional skin. However, relative expression of CCR5 proportional to the cells observed revealed that the difference between lesional and non-lesional skin was only statistically significant in the epidermis for CD3 positive cells and in the dermis for CD68 positive cells. Quantification of mRNA by reverse transcriptase-polymerase chain reaction only showed an increased expression of CCL5 (RANTES) in lesional skin. A randomized placebo-controlled clinical trial in 32 psoriasis patients revealed no significant clinical effect and no changes at the immunohistochemical level comparing patients treated with placebo or a CCR5 inhibitor SCH351125. We conclude that although CCR5 expression is increased in psoriatic lesions, this receptor does not play a crucial role in the pathogenesis of psoriasis

Glucagon-like peptide-1 (GLP-1) and the regulation of human invariant natural killer T cells: lessons from obesity, diabetes and psoriasis

Aims/hypothesis The innate immune cells, invariant natural killer T cells (iNKT cells), are implicated in the pathogenesis of psoriasis, an inflammatory condition associated with obesity and other metabolic diseases, such as diabetes and dyslipidaemia. We observed an improvement in psoriasis severity in a patient within days of starting treatment with an incretin-mimetic, glucagon-like peptide-1 (GLP-1) receptor agonist. This was independent of change in glycaemic control. We proposed that this unexpected clinical outcome resulted from a direct effect of GLP-1 on iNKTcells. Methods We measured circulating and psoriatic plaque iNKT cell numbers in two patients with type 2 diabetes and psoriasis before and after commencing GLP-1 analogue therapy. In addition, we investigated the in vitro effects of GLP-1 on iNKT cells and looked for a functional GLP-1 receptor on these cells. Results The Psoriasis Area and Severity Index improved in both patients following 6 weeks of GLP-1 analogue therapy. This was associated with an alteration in iNKT cell number, with an increased number in the circulation and a decreased number in psoriatic plaques. The GLP-1 receptor was expressed on iNKT cells, and GLP-1 induced a dose-dependent inhibition of iNKT cell cytokine secretion, but not cytolytic degranulation in vitro. Conclusions/interpretation The clinical effect observed and the direct interaction between GLP-1 and the immune system raise the possibility of therapeutic applications for GLP-1 in inflammatory conditions such as psoriasis

Memory effector (CD45RO+) and cytotoxic (CD8+) T cells appear early in the margin zone of spreading psoriatic lesions in contrast to cells expressing natural killer receptors, which appear late.

Contains fulltext : 57298.pdf (publisher's version ) (Closed access)BACKGROUND: An influx of immunocytes, increased epidermal proliferation and abnormal keratinization are hallmarks of the psoriatic lesion. T-lymphocyte subsets in particular activated effector memory T cells and natural killer (NK) T cells have been suggested to play an important role in the pathogenesis of psoriasis. OBJECTIVES: In the present study we investigated the number of T-cell subsets (CD4, CD8, CD45RO, CD45RA, CD2, CD25), cells expressing NK receptors (CD94 and CD161), the proliferation marker Ki67 and the keratinization marker keratin (K10) across the margin of the spreading psoriatic plaque: distant uninvolved skin, the outer margin (immediately outside the clinical edge), the inner margin (immediately inside the clinical edge) and the central area. PATIENTS AND METHODS: Eight patients with active psoriasis vulgaris participated in this study. Biopsies were taken from the spreading psoriatic lesion from the distant uninvolved skin, the outer margin, the inner margin and the central area. Biopsies were processed for immunohistochemical staining. RESULTS: In the outer margin CD8+ (cytotoxic T cells) and CD45RO+ (memory effector T cells) T lymphocytes invade the epidermis and in this early stage the activation markers CD2 and CD25 also show a substantial increase. The next phase, from the outer to the inner margin, shows a statistically significant increase of these markers, and especially, the cells expressing NK receptors (CD94 and CD161) show a massive increase together with a significant increase of epidermal proliferation (Ki67) and a decrease of the K10+ epidermal surface. CONCLUSIONS: CD8+, CD45RO+, CD2+ and CD25+ T cells have a role in the early phase of the psoriatic process, whereas CD94- and CD161-expressing cells together with epidermal proliferation and keratinization are involved in a later phase

Leukocyte extravasation as a target for anti-inflammatory therapy - Which molecule to choose?

In view of the central pathogenic importance of leukocyte extravasation in inflammatory skin diseases, therapeutic interference with this-surprisingly complex-process is clearly a promising new approach for treating these dermatoses. Despite some disappointments during the clinical use of these agents and despite their crippling price tag, the recent incorporation of biologicals that target defined molecular controls of leukocyte extravasation into dermatological and rheumatological practise, consequently, has greatly enriched our therapeutic options for battling major, chronic, inflammatory dermatoses such as psoriasis. However, the-as yet unresolved and still rather controversially discussed-critical question is: Which of the multiple steps that control leukocyte extravasation in the human system really offer the most promising, most pragmatic, and safest molecular targets for therapeutic intervention for which disease entity? The current debate intends to stimulate public and rational debate of this crucial issue, beyond the evident commercial interests that are touched by whatever stand one take