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Myroides odoratus is a low-virulence opportunistic human pathogen. Infections caused by M. odoratus are not common, but reports are increasing in recent years. The biggest challenge for treatment is its resistance to most antibiotics. In 2015, we isolated a pathogenic multidrug-resistant strain of M. odoratus from a urinary tract infection (UTI) patient's urine sample. To report the experience in managing M. odoratus-related UTI and investigate the genetic mechanism of this carbapenem-resistant strain, we conducted a series of microbiological and molecular studies. The bacterial strain was identified as M. odoratus by 16S rRNA gene sequencing. The minimum inhibitory concentrations (MICs) of 17 antimicrobial agents were determined against this strain. Whole-genome sequencing was performed and screened for possible β-lactamase genes. A β-lactamase gene, blaMOC, was identified by whole-genome sequencing, then cloned and expressed in Escherichia coli DH5α to characterize its function. Antimicrobial susceptibility testing showed that the strain had relatively low MIC to levofloxacin and sulfamethoxazole/trimethoprim (SMZ/TMP). After unsuccessful empirical therapy, the UTI was controlled by levofloxacin in combination with SMZ/TMP. Whole-genome sequencing identified a subclass B1 metallo-β-lactamase gene, blaMOC, which conferred resistance to most β-lactams except for aztreonam and cefepime. In conclusion, a new β-lactamase gene, blaMOC, was found in an isolate of M. odoratus. The broad antimicrobial resistance of this isolate is at least attributed partially to this gene. [ABSTRACT FROM AUTHOR]

Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta . This study was designed to evaluate the pharmacological effects of EsA on lipopolysaccharide (LPS)-stimulated BV2 microglia and primary microglia cells. Our results indicated that EsA pretreatment significantly decreased LPS-induced production of Nitric Oxide (NO) and Prostaglandin E2 (PGE2) and impeded LPS-mediated upregulation of pro-inflammatory mediators' expression such as nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-12 (IL-12) and tumor necrosis factor-a (TNF-α) in both BV2 microglia and primary microglia cells. Moreover, EsA markedly suppressed nuclear factor-κB p65 (NF-κB p65) translocation by blocking IκB-α phosphorylation and degradation in LPS-treated BV2 cells. EsA also decreased phosphorylation level of mitogen-activated protein kinases (MAPKs) and inhibited NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome mediated caspase-1 activation in LPS-stimulated BV2 cells. Additionally, EsA decreased β-amyloid 1–42 (Aβ 1–42 )-induced production of TNF-α, IL-1β and IL-6 in primary microglia. Thus, EsA might be a promising therapeutic agent for alleviating neuroinflammatory diseases. [ABSTRACT FROM AUTHOR]

The dilational rheological properties of hydrophobically modified polyacrylamide (HMPAM) or hydrolyzed polyacrylamide (HPAM) solutions without and with imidazolium surfactants ([C-4-Cim]Br and [Cmim]Br) at the air/water surface were investigated using oscillating bubble measurements. The results obtained suggest that imidazolium surfactants interact with the polymer on the surface, enhancing the dilational viscoelasticity of surface film. The dilational modulus value of [C-4-Cim]Br/HMPAM is higher than that of the [Cmim]Br/HMPAM system at low polymer concentration, confirming that [C-4-Cim]Br with two head groups and two hydrophobic chains can combine with a polymer to form a strong film on the surface. Moreover, imidazolium surfactants have stronger hydrophobic interaction with HMPAM chains than those of HPAM, thus enhancing the surface film strength for a surfactant/HMPAM system. The surface interaction mechanism between polyacrylamide and imidazolium surfactant is proposed to result from the electrostatic interactions and the hydrophobic effect. [ABSTRACT FROM AUTHOR]