Publications by authors named "Aki Kaneko"

Background: From animal studies, it is known that mastitic inflammation of the mammary lobes can produce proinflammatory cytokines and can damage the milk fat globule (MFG).

Objective: To investigate, in women, whether MFG and interleukin (IL)-6 differences are observed between mastitic milk (MM) and healthy milk (HM) of a mother.

Methods: MM was obtained from the specific nipple pore leading to the mastitic lobe of 17 women; HM was obtained from the other breast.

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The deletion of MCD4 leads to an increase in beta-1,6-glucan level and a decrease in glycosylphosphatidylinositol-anchored protein and mannan levels in the cell wall of Saccharomyces cerevisiae, suggesting that mcd4 deletion mutant (mcd4Delta) displays beta-glucans on the cell surface without a mannan cover. An observation of the cell surface of mcd4Delta cells and an examination of the effect of contact between mcd4Delta cells and mouse macrophages indicated that macrophages were activated by contact with mcd4Delta cells displaying beta-glucans on the cell surface. We further examined the effect of intraperitoneal ethanol-fixed mcd4Delta cells on the survival period of mice infected with Candida albicans.

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The transcriptional factor CaTup1p represses many genes involved in intracellular processes, including the yeast-hypha transition, in the human fungal pathogen Candida albicans. Using tandem affinity purification technology, we identified a novel protein that interacts with CaTup1p, named Tcc1p (Tup1p complex component). Tcc1p is a C.

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Elevated expression of the plasma membrane drug efflux pump proteins Cdr1p and Cdr2p was shown to accompany decreased azole susceptibility in Candida albicans clinical isolates. DNA sequence analysis revealed extensive allelic heterozygosity, particularly of CDR2. Cdr2p alleles showed different abilities to transport azoles when individually expressed in Saccharomyces cerevisiae.

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The ability of the human fungal pathogen Candida albicans to transit its cell shape is important for its pathogenicity. To obtain additional evidence that the cell cycle of C. albicans is associated with its morphology, we generated and characterized a conditional mutant of C.

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Polyunsaturated fatty acids (PUFAs), including linoleic acid (C18 : 2) and alpha-linolenic acid (C18 : 3), are major components of membranes. PUFAs are produced from monounsaturated fatty acids by several fatty acid desaturases (FADs) in many fungi, but Saccharomyces cerevisiae, Schizosaccharomyces pombe and humans do not have these enzymes. Although the fungal pathogen Candida albicans produces C18 : 2 and C18 : 3, the enzymes that synthesize them have not yet been investigated.

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The human fungal pathogen Candida albicans is able to change its shape in response to various environmental signals. We analyzed the C. albicans BIG1 homolog, which might be involved in beta-1,6-glucan biosynthesis in Saccharomyces cerevisiae.

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Clinically important resistance of fungal pathogens to azole antifungal drugs is most frequently caused by the over-expression of energy-dependent drug efflux pumps. These pumps usually belong to either the ATP-binding cassette (ABC) family or the Major Facilitator Superfamily (MFS) class of membrane transporter. Little is known about how these pumps work and there is an urgent need to develop pump antagonists that circumvent azole resistance.

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Saccharomyces cerevisiae Hsl1p is a Ser/Thr protein kinase that regulates cell morphology. We identified Candida albicans CaHSL1 and analysed its function in C. albicans.

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A novel vector was constructed to enable the integrative marking of individual genes and the affinity purification of interacting molecules within protein complexes from Candida albicans using a tandem 6 x histidine and FLAG epitope tag. The system was verified by purifying the C. albicans septin complex (a self-associating complex of cytoskeletal proteins) from both yeast and hyphal cells.

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Thirty-one urease-positive thermophilic Campylobacter (UPTC) isolates, including three reference strains (NCTC12892, NCTC12895 and NCTC12896), and three Campylobacter lari isolates, which were isolated from several countries and sources, were compared genotypically by using multilocus enzyme electrophoresis (MLEE). We examined allelic variation around seven enzyme loci, including the adenylate kinase, alkaline phosphatase, catalase, fumarase, malic enzyme, malate dehydrogenase, and L-phenylalanyl-L-leucine peptidase loci. MLEE typing revealed the presence of 23 different electrophoretic types (ETs) among the 31 UPTC isolates, and 14 isolates shared six electrophoretic profiles.

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Shiga toxin 1 (Stx1) of enterohemorrhagic Escherichia coli O157:H7 was cloned, and four mutant Stx1s were constructed by site-directed mutagenesis with PCR. The wild-type and mutant Stx1s with amino acid replacements at positions 167 and 170 of the A subunit were purified by one-step affinity chromatography with commercially available Globotriose Fractogel, and the mutant Stxs were used for the immunization of mice. The mutant toxins were nontoxic to Vero cells in vitro and to mice in vivo and induced the immunoglobulin G antibody against the wild-type Stx1, which neutralized the cytotoxicity of Stx1.

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An investigation was carried out into the prevalence of thermophilic Campylobacter subspecies (spp.) and Cryptosporidium spp. in fresh fecal specimens collected from members of the gull family (Larus spp.

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Serum antibody titers against the lipopolysaccharides (LPSs) of Porphyromonas gingivalis and Fusobacterium nucleatum were compared between 9 periodontitis patients and 24 healthy persons. The IgG titers against the LPSs of P. gingivalis ATCC 33277(T) and W50 were clearly higher in the patients than in the healthy persons.

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The influence of slyA gene, originally found in Salmonella serovar Typhimurium as a regulatory gene for the expression of virulence genes, on a mouse virulence of S. serovar Choleraesuis was investigated by using an slyA-defective mutant. The defective mutant was constructed by the insertion of a kanamycin-resistance gene (aph) into the cloned slyA gene, and the homologous recombination with the intact slyA gene on the chromosome.

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