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T helper 17(Th17) cell is a new subset of CD4+ T cells that produce a proinflammatory cytokine interleukin‐17 (IL‐17). Th17 cells have recently been shown to play a critical role in many autoimmune diseases that had previously been thought to be Th1 dominant. Although Hashimoto’s thyroiditis (HT) was thought to be a Th1‐type disease, the contributions of Th17 cells to the pathogenesis remain unclear. In this study, we investigated the expression levels of Th1/Th17 cell‐associated factors in peripheral blood mononuclear cells (PBMC) and plasma from patients with HT by quantitative real‐time polymerase chain reaction (RT‐qPCR) and enzyme‐linked immunosorbent assay (ELISA). Our results showed that the expression levels of Th1 cells‐related T‐bet and interferon‐γ (IFN‐γ) mRNA in PBMC from HT significantly decreased. However, the mRNA of Th17 coherent retinoic acid‐related orphan nuclear receptor gamma t (RORγt) and IL‐17 in patients with HT increased. In addition, a negative correlation between T‐bet and RORγt mRNA expression was found in patients with HT, and the similar phenomena also appeared on the levels of mRNA and plasma concentration between IFN‐γ and IL‐17. It suggested that Th17 cells rather than Th1 cells predominated among patients suffering from HT, and Th17 cells might be involved in the pathogenesis of HT.

BackgroundThe osmotic regulator OmpR in Escherichia coli regulates differentially the expression of major porin proteins OmpF and OmpC. In Yersinia enterocolitica and Y. pseudotuberculosis, OmpR is required for both virulence and survival within macrophages. However, the phenotypic and regulatory roles of OmpR in Y. pestis are not yet fully understood.ResultsY. pestis OmpR is involved in building resistance against phagocytosis and controls the adaptation to various stressful conditions met in macrophages. The ompR mutation likely did not affect the virulence of Y. pestis strain 201 that was a human-avirulent enzootic strain. The microarray-based comparative transcriptome analysis disclosed a set of 224 genes whose expressions were affected by the ompR mutation, indicating the global regulatory role of OmpR in Y. pestis. Real-time RT-PCR or lacZ fusion reporter assay further validated 16 OmpR-dependent genes, for which OmpR consensus-like sequences were found within their upstream DNA regions. ompC, F, X, and R were up-regulated dramatically with the increase of medium osmolarity, which was mediated by OmpR occupying the target promoter regions in a tandem manner.ConclusionOmpR contributes to the resistance against phagocytosis or survival within macrophages, which is conserved in the pathogenic yersiniae. Y. pestis OmpR regulates ompC, F, X, and R directly through OmpR-promoter DNA association. There is an inducible expressions of the pore-forming proteins OmpF, C, and × at high osmolarity in Y. pestis, in contrast to the reciprocal regulation of them in E. coli. The main difference is that ompF expression is not repressed at high osmolarity in Y. pestis, which is likely due to the absence of a promoter-distal OmpR-binding site for ompF.

Summary Vibrio parahaemolyticus, the leading cause of seafood‐associated gastroenteritis worldwide, requires the two type‐III secretion systems (T3SS1 and T3SS2) and a thermostable direct hemolysin (encoded by tdh1 and tdh2) for full virulence. The tdh genes and the T3SS2 gene cluster constitute an 80 kb pathogenicity island known as Vp‐PAI located on the chromosome II. Expression of T3SS1 and Vp‐PAI is regulated in a quorum sensing (QS)‐dependent manner but its detailed mechanisms remain unknown. Herein, we show that three factors (QS regulators AphA and OpaR and an AraC‐type transcriptional regulator QsvR) form a complex regulatory network to control the expression of T3SS1 and Vp‐PAI genes. At low cell density (LCD), whereas Vp‐PAI expression is repressed, T3SS1 genes are induced by AphA, which directly binds (an operator region of) the exsBAD‐vscBCD operon. At high cell density (HCD), the bacterium turns off T3SS1 expression by replacing AphA with OpaR, triggering the induction of Vp‐PAI. Furthermore, QsvR binds to the regulatory regions of all the tested T3SS1 and Vp‐PAI genes to activate their transcription at HCD. Taken together, our data highlight how multiple QS regulators contribute to the pathogenicity of V. parahaemolyticus by precisely controlling the expression of major virulence determinants during different stages of growth.

Class 1 integrons were found to be widespread in P. aeruginosa isolated from clinical samples in the Zhenjiang area of China. The antibiotic resistance rates in class 1 integron-positive strains of P. aeruginosa were noticeably higher than those in class 1 integron-negative strains. PFGE showed that particular clones were circulating among patients.