Nocardiopsis yanglingensis sp. nov., a thermophilic strain isolated from a compost of button mushrooms.

A strain named A18 was recovered from a compost of button mushrooms. It was characterized using a polyphasic approach. On the basis of 16S rRNA gene sequence comparison, it belonged to the genus Nocardiopsis and was most closely related to the type strains of Nocardiopsis flavescens (sequence similarity 98.0%), Nocardiopsis prasina (97.5%), Nocardiopsis metallicus (97.4%), Nocardiopsis alba (97.3%). The combination of phylogenetic analysis, DNA-DNA hybridization, phenotypic characteristics and chemotaxonomic data supported the proposal that strain A18 represents a new species of the genus Nocardiopsis, for which the name Nocardiopsis yanglingensis sp. nov. was proposed (type strain A18(T) = KCTC 19723(T) = CCTCC 209063(T)).

G protein-coupled receptor160 regulates mycobacteria entry into macrophages by activating ERK.

Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis, invades and replicates within susceptible hosts by disturbing host antimicrobial mechanisms. Although G protein-coupled receptors (GPCRs) are involved in most physiological and pathological activities of mammalian cells, the roles of GPCRs in Mtb invasion into host cell remain elusive. Here, we report that GPR160 expression is elevated at both mRNA and protein level in macrophages in response to BCG infection. Both the PiggyBac (PB) transposon-mediated mutation of gpr160 gene in mouse primary macrophages and siRNA-mediated knockdown of GPR160 in the human macrophage cell line THP-1 markedly reduced the entry of green fluorescent protein (GFP) expressing BCG (BCG-GFP), also operative in vivo. BCG infection-induced phosphorylation of ERK1/2 was significantly reduced in gpr160 mutated (gpr160(-/-)) macrophages relative to levels observed in wild type macrophages, while inhibition of ERK by specific inhibitor or knockdown ERK1/2 by specific siRNA markedly reduced entry of BCG. Finally, lower bacteria burdens and attenuated pathological impairments were observed in the lungs of BCG-infected gpr160(-/-) mice. Furthermore, gpr160(-/-) macrophages also exhibits reduced uptake of Escherichia coli and Francisella tularensis. Taken together, these findings suggest an important role of GPR160 in regulating the entry of BCG into macrophages by targeting the ERK signaling pathway. As GPCRs have proven to be successful drug targets in pharmaceutical industry, it's tempting to speculate that compounds targeting GPR160, a G protein-coupled receptor, could intervene in Mtb infection.