Study of The specificity of gut microbiota in adult patients with delayed-onset of atopic dermatitis

Background Atopic dermatitis (AD) is a common and recurrent skin disease. The first onset of AD in adults is known as adult-onset atopic dermatitis (AOAD). Gut microbiota is closely associated with AD, and the “gut–skin” axis is considered as a novel target for prevention of AD. However, only a few studies have analyzed AOAD, particularly the studies that compared differences in intestinal flora between AOAD and persistent AD patients. Objective To investigate main specificities of intestinal microbiota in AOAD patients, particularly comparing with persistent AD patients. Methods A comprehensive taxonomic and functional analysis of gut microbiota in 10 healthy, 12 AOAD, and 10 persistent AD patients was done by using bacterial 16S ribosomal RNA (rRNA) gene analysis. Chao1 and Shannon diversity indices were measured to analyze alpha diversity, and the linear discriminant analysis (LDA) effect size (LEfSe) algorithm was applied to identify differences in genus. Results The alpha diversity of gut microbiota in AOAD patients was decreased, with Escherichia-shigella (15.8%) being the predominant genus of AOAD group. Agathobacter and Dorea in AOAD patients were significantly reduced, whereas the relative level of Bacteroides pectinophilus group was remarkably elevated compared with healthy volunteers and persistent AD patients. Conclusion The present study revealed differences in intestinal flora between AOAD, healthy adults, and non-adult onset of AD, and explored differential dominant bacteria between AOAD and persistent AD patients (AU)

EBV-induced human CD8+ NKT cells suppress tumorigenesis by EBV-associated malignancies.

The underlying mechanism of the protective and suppressive role of NKT cells in human tumor immunosurveillance remains to be fully elucidated. We show that the frequencies of CD8(+) NKT cells in patients with EBV-associated Hodgkin's lymphoma or nasopharyngeal carcinoma are significantly lower than those in healthy EBV carriers. These CD8(+) NKT cells in tumor patients are also functionally impaired. In human-thymus-severe combined immunodeficient (hu-thym-SCID) chimeras, EBV challenge efficiently promotes the generation of IFN-gamma-biased CD8(+) NKT cells. These cells are strongly cytotoxic, drive syngeneic T cells into a Th1 bias, and enhance T-cell cytotoxicity to EBV-associated tumor cells. Interleukin-4-biased CD4(+) NKT cells are predominately generated in unchallenged chimeras. These cells are noncytotoxic, drive syngeneic T cells into a Th2 bias, and do not affect T-cell cytotoxicity. In humanized xenogeneic tumor-transplanted hu-thym-SCID chimeras, adoptive transfer with EBV-induced CD8(+) NKT cells significantly suppresses tumorigenesis by EBV-associated malignancies. EBV-induced CD8(+) NKT cells are necessary and sufficient to enhance the T-cell immunity to EBV-associated malignancies in the hu-thym-SCID chimeras. CD4(+) NKT cells are synergetic with CD8(+) NKT cells, leading to a more pronounced T-cell antitumor response in the chimeras cotransferred with CD4(+) and CD8(+) NKT cells. Thus, immune reconstitution with EBV-induced CD8(+) NKT cells could be a useful strategy in management of EBV-associated malignancies.