| Leptospirosis, caused by pathogenic species of the genus Leptospira, has emerged as the most widespread zoonotic disease worldwide. The innate immune system plays an important role in killing the leptospires. However, except for the complement receptor of macrophages, there have been no other phagocytosis receptors were found. Scavenger receptor A(SR‐A), a pattern recognition receptor for macrophages, takes part in defending against microbial pathogens. Combining with the groundwork on SR‐A involving in the phagocytosis to leptospires, we address the hypothesis that macrophages can recognize and phagocytize the leptospires through SR‐A participating in the innate immune and regulating the inflammatory. In the present study, we showed that murine macrophages phagocytized leptospires efficiently in the absence of specific opsonization, which was blocked by either poly I, a general SR inhibitor, or the monoclonal SR‐A antibody through the flow cytometry or confocal methods. SR‐A transfected HEK293 T cells by lentivirus compaired to control cells significantly enhance the adherence to L. interrogans. Macrophages from SR‐A knockout(SR‐A‐/‐) mice also exhibited the significantly less phagocytosis to leptospires. 1μm beads were coated by purified LPS extracted from L. interrogans. Results showed that WT macrophages phagocytized significantly more LPS coated beads than control beads, and phagocytosis to LPS beads of macrophages from SR‐A‐/‐ mice were obviously less than that from WT mice. Similarly, transfected HEK293 T cell expressing SR‐A adhered significantly more LPS beads than the control cell. On the other hand, after leptospires stimulation, SR‐A can be co‐located with TLR4 as the coreceptor showing the immunoregulation effect. Therefore, the present study demonstrated that during the process of leptospiral infection, macrophages can phagocytize the leptospires through SR‐A which recognizes the LPS components of L. interrogans and shows the coreceptor effect with TLR4 participating in the body’s innate immune and regulating the inflammatory.Uropathogenic Escherichia coli(UPEC) is the major cause of urinary tract infections(UTIs). The epidemic data of it provides the guidance to clinical treatment. In the present study, 198 E. coli isolates from patients with UTIs in Shanghai in 2008 were examined by susceptibility testing for drug resistance phenotype, while drug resistance and virulence genes were molecularly detected based on PCR methods. Pulsed‐field gel electrophoresis(PFGE) and phylogenetic analysis were performed for genetic relation. Distribution and relationships of genes in respective groups were also consideration. We found an extremely high number(153/198) showing multidrug resistance(MDR). And the expression of extended‐spectrum β‐lactamases(ESBLs) reached 48.5%(96/198). The resistance rates to penicillins, fluoroquinolone, folate pathway inhibitors, and first‐ and second‐generation cephalosporins were high. Molecular analyses showed that the CTX‐M‐9 group(70/96) was the most common CTX‐M group among UPEC, followed by the CTX‐M‐1 group(27/96). Phylogenetic group D accounted for 42.4%(84/198) of the isolates, exhibiting the highest ESBLs(50/84) and MDR(75/84) rates. Virulence genes were present in a significantly high proportion in the phylogenetic group B2 isolates, except for the afa BC gene. The ESBL‐producing strains analysed by PFGE were clustered into six groups at a cutoff of 67%. Notably, the findings that afa BC was specific to phylogenetic group D and PFGE group I and was correlated with the CTX‐M‐9 group were different from a previous report. In conclusion, knowledge of antimicrobial resistance data and virulence factors may enable clinicians to tailor empirical antibiotic treatments for UTIs. |
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