Author´s contributions DC did the bacterial cultures, harvested the supernatants, performed the EIA, established and performed the cytotoxicity assays. RW did the bacterial cultures, harvested the supernatants, and quantified the transcriptional response of bacteria. MW established conditions for the bacterial cultures, harvested the supernatants. GP genotyped the bacteria and quantified the transcriptional response of bacteria. OU coordinated the study, established the cytotoxicity

assay, analysed data and wrote the manuscript. MK designed the study, analysed data and wrote the manuscript. All authors read and approved the final manuscript.”
“Background learn more Enterovirus 71 (EV71), an RNA virus of the Picornaviridae family, is first recognized from the patients with neurological abnormalities SCH727965 in California in 1969 [1]. It is known to be a causative agent of hand-foot-and-mouth disease (HFMD), and occasionally its infection would

lead to severe complications including encephalitis, aseptic meningitis, pulmonary edema or hemorrhage, and acute flaccid paralysis [2]. Outbreaks of EV71 had been reported worldwide during the last decade [2–7]. In Taiwan, there was a large epidemic of HFMD in 1998. More than 120,000 cases were reported and the outbreak resulted in 78 deaths [2]. Two years later, there was another outbreak of HFMD with 80,677 reports and 41 deaths (data from

CDC, Taiwan). Tenofovir EV71 can induce the apoptosis of human glioblastoma cells [8], human microvascular endothelial cells [9], and Jurkat cells [10]. Although it has been demonstrated that the spinal cord and brain stem were the target of EV71 infections [6, 11], the infection mechanism, tissue tropism, and the neurovirulence of EV71 remain unclear. In 2009, two receptors for EV71 were discovered [12, 13]. Nishimura et al. found that human P-selectin glycoprotein ligand-1 (PSGL-1) was a functional receptor for EV71 [12]. Yamayoshi et al. reported that scavenger receptor class B2 (SCARB2) was cellular receptor for EV71 [13]. PSGL-1 is glycosylated with sialyl Lewisx epitope, and SCARB2 is also a highly glycosylated protein. According to these results, cell surface glycans should participate in the infection of EV71. Hence, the glycomic factors which contribute to the epidemics of EV71 infection have attracted our attention. Carbohydrates expressed on cell surface involve in many physiological and pathological communications by interacting with their corresponding proteins or receptors [14, 15]. Among these events, cell surface glycan receptors which mediate viral binding and infection were well documented. For instance, Jackson et al. indicated that the entry of food-and-mouse disease virus (FMDV) into cell was initiated by the contact with cell surface heparin sulfate [16].