The survival of Alloiococcus otitidis (NCFB2890) with different nutritional supplements, including brain-heart infusion broth (BHI), phosphate-buffered saline (PBS), distilled water (DW), and middle ear effusion (MEE), as well as various atmospheres (aerobic, microaerobic, anaerobic), was compared using cultures, LIVE/DEAD staining, and transmission electron microscopy. The bacterial morphological traits and viability were maintained in BHI and MEE under aerobic conditions but were rapidly lost in PBS and DW. In contrast, anaerobic conditions did not support viability at all.
View Article and Find Full Text PDFEpithelial-derived thymic stromal lymphopoietin (TSLP) triggers dendritic cell (DC)-mediated Th2-type inflammatory responses and is a master switch for allergic inflammatory diseases. In the present study, the expression and induction of TSLP and the effects of TSLP on the tight-junctional barrier of human nasal epithelial cells (HNECs) have been investigated in order to elucidate the role of TSLP in allergic rhinitis. We have found high expression of TSLP in the epithelium from patients with allergic rhinitis with recruitment and infiltration of DCs.
View Article and Find Full Text PDFAlloiococcus otitidis is a newly discovered organism frequently detected in otitis media. However, the association of the organism with the development of otitis media has not been disclosed in detail yet. In the middle ear, proinflammatory cytokines and chemokines are released in association with infection by pathogens, and these cytokines contribute to the induction of an inflammatory reaction.
View Article and Find Full Text PDFRecently, the frequency of isolation of beta-lactamase-negative ampicillin resistant (BLNAR) strains of Haemophilus influenzae in Japanese children has been increasing rapidly. Drug resistance in BLNAR strains is associated with mutations of the fts I gene, which encodes penicillin-binding protein 3. In the otolaryngological field, only a few reports have been available concerning fts I gene mutations in BLNAR.
View Article and Find Full Text PDFThe epithelium of upper respiratory tissues such as human nasal mucosa forms a continuous barrier via tight junctions, which is thought to be regulated in part through a protein kinase C (PKC) signaling pathway. To investigate the mechanisms of the regulation of PKC-mediated tight junction barrier function of human nasal epithelium in detail, primary human nasal epithelial cells were treated with the PKC activator 12-O-tetradecanoylophorbol-13-acetate (TPA). In primary human nasal epithelial cells, treatment with TPA led not only to activation of phosphorylation of PKC, myristoylated alanine-rich C kinase substrate, and mitogen-activated protein kinase but also expression of novel PKC-delta, PKC-theta, and PKC-epsilon.
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