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Recent evidence suggests that there is a link between the gut microbial community and immune-mediated disorders. Systemic sclerosis (SSc) is an autoimmune disease characterized by immunonological abnormalities, vascular lesions, and extensive fibrosis. Since the gastrointestinal tract is one of the organs most involved, the goal of this study was to explore the composition of the intestinal microbiota in SSc patients with (SSc/GI+) and without gastrointestinal involvement (SSc/GI-) in comparison to healthy controls (HC). The fecal bacterial composition was investigated by Illumina sequencing of 16 S rRNA gene amplicons. The fecal microbiota of SSc/GI+ subjects was characterized by higher levels of Lactobacillus, Eubacterium and Acinetobacter compared with healthy controls, and lower proportions of Roseburia, Clostridium, and Ruminococcus. The gut microbiota of SSc/GI- subjects was more similar to the microbiota of HC than to that of SSc/GI+ subjects albeit Streptococcus salivarius was over-represented in SSc/GI- fecal samples compared with both SSc/GI+ subjects and controls. Our study reveals microbial signatures of dysbiosis in the gut microbiota of SSc patients that are associated with clinical evidence of gastrointestinal disease. Further studies are needed to elucidate the potential role of these perturbations in the onset and progression of systemic sclerosis, and gastrointestinal involvement in particular.

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The present work aimed to determine whether GnRH potentiates the effect of growth hormone (GH) on insulin-like growth factors (IGF-I and IGF-II) hepatic gene expression in Sparus aurata liver. Since several hepatic genes were shown to underlie direct regulation via the hepatic estrogen receptor, another aim was to extend our understanding of direct estrogen effects on liver IGFs gene expression. Pre-reproductive sea bream females were treated with GH, GnRH, estradiol-17beta, GH plus GnRH, and estradiol-17beta plus GH. After 72 hr, all treatment induced an increase of plasma estradiol well correlated with the increase of plasma vitellogenin (VTG) levels. IGF-I and IGF-II expression in the liver of treated females was determined by semi-quantitative RT-PCR, using beta-actin as internal standard. The results reported here show that GH significantly stimulates hepatic transcription of IGF-I and IGF-II genes. Surprisingly, E2 and GnRH treatments decreased both IGF-I and IGF-II mRNA levels. In fishes treated with GH plus GnRH, the GnRH contrasted the GH effect: the IGF-I mRNA levels were still significantly higher than in controls, while the effect of GH on IGF-II gene expression was totally abolished. At the same time, in the combined treatment with GH plus E2, the E2 counteracted the stimulatory effect of GH on both IGF-I and IGF-II genes expression.

No abstract