Bacteriophages targeting Enterococcus faecalis enhance the therapeutic efficacy of levodopa in an MPTP-induced Parkinson's disease mouse model with E. faecalis gut colonization.

Despite the intensive research on gut microbiome-associated diseases over the past 20 years, pharmacological methods for effectively eliminating pathobionts remain unsatisfactory. This study investigated the therapeutic potential of bacteriophages against Enterococcus faecalis, in which bacterial tyrosine decarboxylase (TDC) converts orally administered levodopa (L-DOPA) to dopamine, in an MPTP mouse model of Parkinson's disease (PD). E.

Supercritical CO Foaming of Poly(3-hydroxybutyrate--4-hydroxybutyrate).

The supercritical carbon dioxide foaming characteristics of the biodegradable polymer poly(3-hydroxybutyrate-co-4-hydroxybutyrate) (P(3HB--4HB)) are studied for environmentally friendly packaging materials. The effect of the 4HB composition of the P(3HB--4HB) copolymers on the foaming conditions such as pressure and temperature is studied and the density and the expansion ratio of the resulting P(3HB--4HB) foam are together evaluated. The increase in the 4HB content reduces the crystallinity and tan δ value of P(3HB--4HB) required for the growth of the foam cells.

The Modification of Poly(3-hydroxybutyrate--4-hydroxybutyrate) by Melt Blending.

Crystalline and noncrystalline poly(3-hyroxybutylate-co-4-hyroxybutylate) (P(3HB-co-4HB)) were melt blended to obtain mixtures of P(3HB-co-4HB) copolymers. The mixtures and P(3HB-co-4HB) copolymers of different 4HB contents were compared to study the effect of 4HB content on the properties of the copolymers and mixtures. P(3HB-co-4HB) copolymer mixtures, having various 4HB content, have been successfully made by melt blending instead of bacterial biosynthesis.

Identification of SpiA that interacts with Corynebacterium glutamicum WhcA using a two-hybrid system.

The Corynebacterium glutamicum whcA gene is known to play a negative role in the expression of genes responding to oxidative stress. The encoded protein contains conserved cysteines, which likely coordinate the redox-sensitive Fe-S cluster. To identify proteins which may interact with WhcA, we employed a two-hybrid system utilizing WhcA as 'bait'.

Human brain endothelial ATP synthase beta-subunit is mannose-insensitive binding target of FimH.

Binding of meningitis-causing Escherichia coli K1 to human brain microvascular endothelial cells (HBMEC) contributes to traversal of the blood-brain barrier, which occurs in part by the mannose-sensitive binding of FimH. In this study, we showed that FimH also binds to HBMEC, independent of mannose, and identified ATP synthase beta-subunit and actin proteins from the surface biotinylated HBMEC as the mannose-insensitive binding targets for FimH. Co-immunoprecipitation experiments in the presence of alpha-methyl mannose verified the binding of FimH to ATP synthase beta-subunit of HBMEC.

Acetate consumption activity directly determines the level of acetate accumulation during Escherichia coli W3110 growth.

Escherichia coli excretes acetate during aerobic growth on glycolytic carbon sources, which has been explained as an overflow metabolism when the carbon flux into the cell exceeds the capacity of central metabolic pathways. Nonacetogenic growth of E. coli on gluconeogenic carbon sources like succinate or in carbon-limited slow growth conditions is believed an evidence for the explanation.

FimH-mediated Escherichia coli K1 invasion of human brain microvascular endothelial cells.

Adhesion to brain microvascular endothelial cells, which constitute the blood-brain barrier is considered important in Escherichia coli K1 bacterial penetration into the central nervous system. Type 1 fimbriae are known to mediate bacterial interactions with human brain microvascular endothelial cells (HBMEC). Here, we demonstrate that type 1 fimbriae, specifically FimH adhesin is not only an adhesive organelle that provides bacteria with a foothold on brain endothelial cells but also triggers signalling events that promote E.

Effects of ompA deletion on expression of type 1 fimbriae in Escherichia coli K1 strain RS218 and on the association of E. coli with human brain microvascular endothelial cells.

We have previously shown that outer membrane protein A (OmpA) and type 1 fimbriae are the bacterial determinants involved in Escherichia coli K1 binding to human brain microvascular endothelial cells (HBMEC), which constitute the blood-brain barrier. In investigating the role of OmpA in E. coli K1 binding to HBMEC, we showed for the first time that ompA deletion decreased the expression of type 1 fimbriae in E.

Focal adhesion kinase is involved in type III group B streptococcal invasion of human brain microvascular endothelial cells.

Group B streptococcus (GBS), the leading cause of neonatal meningitis, has been shown to invade human brain microvascular endothelial cells (HBMEC), which constitute the blood-brain barrier. GBS invasion of HBMEC has been shown to require the host cell actin cytoskeleton rearrangements. The present study examined the mechanisms underlying actin cytoskeleton rearrangements that are involved in type III GBS invasion of HBMEC.

RhoA and Rac1 contribute to type III group B streptococcal invasion of human brain microvascular endothelial cells.

Type III group B streptococcus (GBS) has been shown to invade human brain microvascular endothelial cells (HBMEC), which constitute the blood-brain barrier, but the underlying mechanisms remain incompletely understood. In the present study, we showed that the geranylgeranyl transferase I inhibitor, GGTI-298, not the farnesyltransferase inhibitor, FTI-277 inhibited type III GBS invasion of HBMEC. The substrates for GGTI-298 include Rho family GTPases, and we showed that RhoA and Rac1 are involved in type III GBS invasion of HBMEC.

FimH adhesin of Escherichia coli K1 type 1 fimbriae activates BV-2 microglia.

The generation of intense inflammation in the subarachnoid space in response to meningitis-causing bacteria contributes to brain dysfunction and neuronal injury in bacterial meningitis. Microglia, the major immune effector cells in the central nervous system (CNS), become activated by bacterial components to produce proinflammatory immune mediators. In this study, we showed that FimH adhesin, a tip component of type 1 fimbriae of meningitis-causing Escherichia coli K1, activated the murine microglial cell line, BV-2, which resulted in the production of nitric oxide and the release of tumor necrosis factor-alpha.

Escherichia coli K1 RS218 interacts with human brain microvascular endothelial cells via type 1 fimbria bacteria in the fimbriated state.

Escherichia coli K1 is a major gram-negative organism causing neonatal meningitis. E. coli K1 binding to and invasion of human brain microvascular endothelial cells (HBMEC) are a prerequisite for E.

Escherichia coli outer membrane protein A adheres to human brain microvascular endothelial cells.

Escherichia coli K1 is the most common gram-negative bacterium causing neonatal meningitis. The outer membrane protein A (OmpA) assembles a beta-barrel structure having four surface-exposed loops in E. coli outer membrane.

Outer membrane protein A and cytotoxic necrotizing factor-1 use diverse signaling mechanisms for Escherichia coli K1 invasion of human brain microvascular endothelial cells.

Escherichia coli K1 invasion of brain microvascular endothelial cells (BMEC) is a prerequisite for penetration into the central nervous system. We previously have shown that outer membrane protein A (OmpA) and cytotoxic necrotizing factor-1 (CNF1) contribute to E. coli K1 invasion of BMEC.

37-kDa laminin receptor precursor modulates cytotoxic necrotizing factor 1-mediated RhoA activation and bacterial uptake.

Cytotoxic necrotizing factor 1 (CNF1) is a bacterial toxin known to activate Rho GTPases and induce host cell cytoskeleton rearrangements. The constitutive activation of Rho GTPases by CNF1 is shown to enhance bacterial uptake in epithelial cells and human brain microvascular endothelial cells. However, it is unknown how exogenous CNF1 exhibits such phenotypes in eukaryotic cells.