[Mechanisms of quorum sensing regulating antimicrobial resistance].

Antimicrobial resistance is a major threat to human health, so new strategies are urgently needed to impede antimicrobial resistance. Quorum sensing is an intracellular communication system that is activated to regulate downstream gene transcription when the population density reaches a threshold. Quorum sensing regulates drug resistance by altering biofilm formation and dispersion, efflux pump expression, and bacterial secretion systems, making it a promising target of overcoming antimicrobial resistance. To date, various quorum sensing inhibitors have been found to block quorum sensing by degrading signal molecules, interfering with the recognition and binding of signal molecules and receptors, and interrupting the synthesis of quorum sensing signals. Hence, quorum sensing inhibitors are expected to become a new way to control antimicrobial resistance.

Efficient images storage via modulating the atomic spin coherence in a N-type system.

A four-level N-type cold atomic system is proposed for optimizing images storage based on the electromagnetically induced transparency (EIT). Both analytical analysis and numerical simulation clearly show that the application, during the storage time, of an additional intensity-modulated signal field and an additional microwave field can impose an intensity and a phase-dependent factors on the atomic spin coherence in a controlled manner, then the amplitude of the retrieved images can be increased or decreased with an enhancement in the visibility. Our results are very promising for the realization of all-optical information processing of images coherently stored in EIT media in the future.

Long-term effects: Galectin-1 and specific immunotherapy for allergic responses in the intestine.

BACKGROUND AND AIMS: Mast cell activation interferes with the effects of allergen-specific immunotherapy (SIT). Galectin-1 (Gal-1) is capable of regulating immune cells' functions. This study tests the hypothesis that administration of Gal-1 promotes and prolongs the efficacy of SIT via suppressing mast cell activation. METHODS: An intestinal allergy mouse model was developed. The coadministration of SIT and Gal-1 on suppression of the allergic responses, prevention of mast cell activation, and generation of antigen-specific regulatory T cells (Treg) in the intestine was observed in sensitized mice. RESULTS: The coadministration of Gal-1 and SIT markedly suppressed the allergic responses in the mouse intestine vs the use of either SIT alone or Gal-1 alone. The Gal-1 binds to the IgE/FcɛRI complexes on the surface of mast cells to prevent mast cell activation during SIT. Gal-1 promoted the SIT-generated allergen-specific Tregs in the intestine of sensitized mice. Coadministration of Gal-1 and SIT significantly enhanced the efficacy of immunotherapy in suppressing allergic responses in the intestine, which lasted for at least for 12 months. CONCLUSIONS: Long-term effects of specific immunotherapy on intestinal allergy can be achieved with Gal-1/SIT therapy by inhibiting mast cell activation and facilitating Treg development.

[Homology analysis and historical tracing for inter-continental Burkholderia pseudomallei strains of sequence type 562].

Objective: To understand the homology of sequence type 562 (ST562) strains of Burkholderia pseudomallei which circulated in two separate continents (Asia and Australia) at different times. Methods:SpeⅠrestriction fragments and 4-locus multiple locus variable number tandem repeat analysis (MLVA-4) profiles were extracted from MSHR5858 (ST562 Australia strain) and 350105 (ST562 historical strain of Hainan) genomes respectively by in silico analysis and then compared with the PFGE and MLVA-4 results of five ST562 clinical isolates from Hainan to test their homology. Synteny and homology between MSHR5858 and 350105 genomes were evaluated with bioinformatics methods. Results: Five ST562 clinical strains from Hainan shared same PFGE pattern (similarity>97%) and this pattern coincided to the map of SpeⅠrestriction fragments of Australian strain MSHR5858. The amounts of genomic restriction fragments (SpeⅠ) for MSHR5858 and 350105 were 31 and 34 respectively, with 31 of them matched by each other. Five ST562 clinical strains of Hainan were distinct by MLVA-4 profiles, among which HPPH43 (MLVA-4 profile: 10, 8, 10, 8) was close to Australia strain MSHR5858 (10, 8, 8, 6), containing identical repeat numbers at VNTR loci 2341k and 1788k; while HK003 (11, 8, 15, 7) and HK061 (11, 8, 17, 7) similar to Hainan historical strain 350105 (11, 8, 11, 8), with same repeat numbers at loci 2341k and 1788k also. High-degree synteny and consistency on genomic contents were observed between 350105 and MSHR5858, indicating a similar origin for the 2 strains. Conclusion: All inter-continental and historical ST562 strains of B. pseudomallei had similar genomic characteristics, supporting the assumption that they had a common origin. Also, it is possible that Hainan historical strain 350105 is the ancestor of all circulating ST562 strains.

Eosinophil differentiation in the bone marrow is promoted by protein tyrosine phosphatase SHP2.

SHP2 participates in multiple signaling events by mediating T-cell development and function, and regulates cytokine-dependent granulopoiesis. To explore whether and how SHP2 can regulate bone-marrow eosinophil differentiation, we investigate the contribution of SHP2 in the bone-marrow eosinophil development in allergic mice. Blockade of SHP2 function by SHP2 inhibitor PHPS-1 or conditional shp2 knockdown by adenovirus-inhibited bone-marrow-derived eosinophil differentiation in vitro, with no detectable effects on the apoptosis of eosinophils. Furthermore, SHP2 induced eosinophil differentiation via regulation of the extracellular signal-regulated kinase pathway. Myeloid shp2 conditional knockout mice (LysM(cre)shp2(flox/flox)) failed to induce eosinophilia as well as airway hyper-responsiveness. The SHP2 inhibitor PHPS-1 also alleviated eosinophilic airway inflammation and airway hyper-responsiveness, accompanied by significantly reduced levels of systemic eosinophils and eosinophil lineage-committed progenitors in allergic mice. We demonstrate that inhibition of eosinophil development is SHP2-dependent and SHP2 is sufficient to promote eosinophil formation in vivo. Our data reveal SHP2 as a critical regulator of eosinophil differentiation, and inhibition of SHP2 specifically in myeloid cells alleviates allergic airway inflammation.

Proteins with antifungal properties and other medicinal applications from plants and mushrooms.

Living organisms produce a myriad of molecules to protect themselves from fungal pathogens. This review focuses on antifungal proteins from plants and mushrooms, many of which are components of the human diet or have medicinal value. Plant antifungal proteins can be classified into different groups comprising chitinases and chitinase-like proteins, chitin-binding proteins, cyclophilin-like proteins, defensins and defensin-like proteins, deoxyribonucleases, embryo-abundant protein-like proteins, glucanases, lectins, lipid transfer proteins, peroxidases, protease inhibitors, ribonucleases, ribosome-inactivating proteins, storage 2S albumins, and thaumatin-like proteins. Some of the aforementioned antifungal proteins also exhibit mitogenic activity towards spleen cells, nitric oxide inducing activity toward macrophages, antiproliferative activity toward tumor cells, antibacterial activity, and inhibitory activity toward HIV-1 reverse transcriptase. In contrast to the large diversity of plant antifungal proteins, only a small number of mushroom antifungal proteins have been reported. Mushroom antifungal proteins are distinct from their plant counterparts in N-terminal sequence. Nevertheless, some of the mushroom antifungal proteins have been shown to inhibit HIV-1 reverse transcriptase activity and tumor cell proliferation.