RESUMEN
Bacterial non-coding RNAs (ncRNAs) are pivotal transcriptional regulators during bacterial proliferation and infection processes.Bacterial ncRNAs play important roles in responding to environmental changes and regulating bacterial gene expression to resist environmental stress.Transcriptome profiling of neonatal meningitis-causing Escherichia coli K1 RS218 (NMEC) reveals abundant ncRNAs.Bioinformatic analyses identified 45 potential ncRNAs.Comparative genome analyses of non-pathogenic E.coli K12 and NMEC identified 300 NMEC-specific sequences (above 100 bp), which contain 9 NMEC-specific ncRNAs (Nsr).Moreover, deletion of one ncRNA, Nsr21, enhanced NMEC survival and proliferation in mouse blood (P< 0.01) , compared to the wild-type RS218 control, in a mouse tail vein injection model.qRT-PCR analysis further revealed expression of Nsr21 decreased in NMEC collected from mouse blood compared to that in NMEC collected from in vitro medium (P<0.001) , indicating that NMEC downregulates Nsr21 expression to benefit its survival and proliferation in blood.This study suggests that the NMEC genome contains a number of ncRNAs, which may be involved in regulating NMEC pathogenicity.During infection process in the blood, NMEC enhances its proliferation ability in blood by downregulating the expression of Nsr21.
RESUMEN
Neonatal purulent meningitis is one of the severe infectious diseases of the central nervous system.Escherichia coli K1 (E.coli K1) strain is the most common Gram-negative bacteria which leads to neonatal purulent meningitis.The mechanism of E.coli K1 translocation of the blood-brain barrier(BBB) include the high degree of bacteremia,invasion of brain microvessel endothelia cell by E.coli K1,receptor-mediated pinocytosis transport for E.coli K1 and the living bacteria across the BBB.The current knowledge on the mechanisms underlying the successful E.coli K1 translocation of the BBB are summarized in this review.
RESUMEN
The existence of symbiotic relationships between Acanthamoeba and a variety of bacteria is well-documented. However, the ability of Acanthamoeba interacting with host bacterial pathogens has gained particular attention. Here, to understand the interactions of Escherichia coli K1 and E. coli K5 strains with Acanthamoeba castellanii trophozoites and cysts, association assay, invasion assay, survival assay, and the measurement of bacterial numbers from cysts were performed, and nonpathogenic E. coli K12 was also applied. The association ratio of E. coli K1 with A. castellanii was 4.3 cfu per amoeba for 1 hr but E. coli K5 with A. castellanii was 1 cfu per amoeba for 1 hr. By invasion and survival assays, E. coli K5 was recovered less than E. coli K1 but still alive inside A. castellanii. E. coli K1 and K5 survived and multiplied intracellularly in A. castellanii. The survival assay was performed under a favourable condition for 22 hr and 43 hr with the encystment of A. castellanii. Under the favourable condition for the transformation of trophozoites into cysts, E. coli K5 multiplied significantly. Moreover, the pathogenic potential of E. coli K1 from A. castellanii cysts exhibited no changes as compared with E. coli K1 from A. castellanii trophozoites. E. coli K5 was multiplied in A. castellanii trophozoites and survived in A. castellanii cysts. Therefore, this study suggests that E. coli K5 can use A. castellanii as a reservoir host or a vector for the bacterial transmission.