Altered gut microbiome composition in nontreated plaque psoriasis patients.

Recent studies have demonstrated that dysbiosis of the gut microbiota is associated with psoriasis, but these studies showed some conflicting results. Our study examined differences in microbiome composition associated in people with psoriasis and those without. Comparing individuals with their healthy partners was a second strategy. We explored the fecal microbiota among 32 nontreated plaque psoriasis patients, 15 healthy controls and 17 healthy couples by metagenomic gene sequencing. The relative levels of intestinal microbiota of the psoriasis cohort differed from those in healthy controls and these patients' partners. However, there was no microbial diversity among these three cohorts. On the level of the phylum, Firmicutes and Bacteroidetes' relative abundances were reversed. Escherichia coli was significantly enriched in the psoriasis group compared with the healthy people and the healthy spouses. Gene functional analysis indicated that Ribosome (ko03010) was upregulated, Flagellar assembly (ko02040) and Bacterial chemotaxis (ko02030) were downregulated in the psoriasis cohort compared with the healthy individuals and the healthy spouses. The microbiota in severe psoriasis patients differed from those with milder conditions. These findings strongly support the association between intestinal flora and psoriasis. It is necessary to perform more meaningful experiments to identify whether the differences of gut microbiota are the cause or consequences of psoriasis in future.

[Expression of NLRP3 inflammasome in BALB/c mice with imiquimod-induced psoriasis-like inflammation and therapeutic effect of mustard seed (Sinapis Alba Linn)].

OBJECTIVE: To investigate the role of NLRP3 inflammasome in imiquimod-induced psoriasis-like inflammation in mice and the therapeutic effects of mustard seed (Sinapis Alba Linn). METHODS: Thirty BALB/c mice were randomized equally into blank control group (fed with normal forage and treated with vehicle), model group (fed with normal forage and treated with 5% imiquimod cream), and experimental group (fed with 5% mustard seed forage and treated with 5% imiquimod cream). RT-PCR was used to detect the mRNA expression of NLRP3, ASC, caspase-1, and caspase-11. Immunohistochemistry was performed to determine the expression and distribution of ASC and caspase-1. ELISA was used to test the serum levels of interleukin-1ß (IL-1ß) and IL-18. RESULTS: Compared with the blank control group, the mice with imiquimod-induced psoriasis-like inflammation showed significantly increased NLRP3, ASC, caspase-1, and caspase-11 mRNA expressions, ASC and caspase-1 protein expressions , and serum levels of IL-1ß and IL-18 (P<0.05). These changes were obviously attenuated by feeding the mice with mustard seed. CONCLUSION: NLRP3 inflammasome is involved in imiquimod-induced psoriasis-like inflammation in mice, and mustard seed may suppress the inflammation induced by IL-1ß and IL-18 through down-regulating the expression of NLRP3 inflammasome.

Mustard seed (Sinapis Alba Linn) attenuates imiquimod-induced psoriasiform inflammation of BALB/c mice.

Psoriasis is a chronic inflammatory autoimmune disease with undefined etiology. All present treatments are symptomatic. The unsatisfactory outcome in the treatment of psoriasis is partially due to the poor compliance to the present therapies with more or less side-effects. As is known, drug homologous food is a popular intervention of some chronic diseases in Chinese traditional medicine. Mustard seed, consumed largely as a spice and a medicine in China, has recently been found to possess the bioactivities of anti-oxidation, anti-inflammation and anticancer. Therefore, it was supposed that mustard seed may have effects on psoriasis, and it was preliminarily validated using a BALB/c mouse model of psoriasiform inflammation induced by the topical application of imiquimod cream (Aldara) for 6 days consecutively. It was found that the forage containing 5% mustard seed obviously attenuated imiquimod-induced psoriasiform inflammation, but did not clear it completely, accompanied by reduced infiltrations of T cells, plasmacytoid dendritic cells (pDC) and macrophages in lesional skin; reduced percentages of pDC and macrophages in the composition of immunocytes of spleens; reduced content of lesion nuclear factor-κB p65, plasma malondialdehyde, lesion inducible nitric oxide synthase, interferon-α, interleukin (IL)-17 and IL-22 at mRNA and protein levels; increased activities of superoxide dismutase, catalase and glutathione peroxidase; and increased percentage of CD4(+) T cells and increased ratio of CD4(+) /CD8(+) T cells in the composition of immunocytes of spleen. These results presented herein provide a basis for mustard seed to be used as a promising intervention for psoriasis in the future.

[Effects of mustard seed on 2, 4-dinitrofluorobenzene-induced allergic contact dermatitis in BALB/c mice].

OBJECTIVE: To investigate the therapeutic effect of mustard seed on allergic contact dermatitis (ACD) in mice and explore the mechanism. METHODS: Eighteen BALB/c mice were randomly divided into normal control group, model group and mustard seed group. The mice in the normal control group and model group were fed with normal chow, and those in mustard seed group were given 5% mustard seed mixed in the chow. Three weeks later, ACD was induced on the ear using 2, 4-dinitrofluorobenzene. After 24 h, the swelling of the ear was examined, and the rats were sacrificed to collect the ear tissue ears and blood for histopathological and immunohistochemical examinations, RT-PCR and enzyme-linked immunosorbent assay. RESULTS: In mice with ACD, feeding with mustard seeds significantly lessened the ear swelling, improved the tissue histopathology, lowered the number of infiltrating Langerhans cells, and reduced the expressions of IL-1ß, TNF-α and IL-6 mRNA in the ear, but did not cause significant changes in serum levels of IL-4, IFN-γ and IL-17. CONCLUSION: Mustard seed inhibits ACD in mice possibly by suppressing the expressions of IL-1ß, TNF-α and IL-6 mRNA and inhibiting Langerhans cell migration in the epidermis.

A novel approach obtaining intron-containing hairpin RNA constructs.

Recently, much research on constitutive expression of an intron-containing self-complementary hair-pin RNA (ihpRNA) have been reported to silence target genes efficiently in a variety of species. Here we designed a new recombinant-PCR mediated method called direct amplification of ihpRNA from genomic DNA. This approach has proved to be easy, stable, and efficient.