The infectivity of Enterococcus faecalis was compared with that of Escherichia coli in the urinary tract in mice. The infectivity of E. faecalis in normal mice was found to be equal to that of E. coli. The mice previously treated with cyclophosphamide, carrageenin or alloxan as the immunosuppressive drug, and restricted water supply, were more susceptible to enterococcal infection than non-treated ones. These data were confirmed with histological examinations. E. faecalis is a pathogenic organism in the urinary tract and therefore cautions should be given to the treatment in clinical practice
The virulence of clinical isolates of Acinetobacter calcoaceticus, Pseudomonas cepacia, and Pseudomonas maltophilia in urinary tract in mice was studied.In general, the virulence of these organisms in urinary tract of normal mice was relatively mild.The effect of anti-inflammatory and immunosuppressive drugs on pathogenicity of these organisms was studied in mice.The mice previously treated with betamethasone or prednisolone as anti-inflammatory drug, and with cyclophosphamide or azathiopurine as immunosuppressive drug, were more susceptible to these bacterial infections than were the non-treated ones.As for the capacity of bacterial attachment to the epithelial cells of the bladder, these organisms were generally shown to have low adhesion.Furthermore, the hemagglutination patterns were mannose-sensitive in human and guinea pig erythrocytes.
In vitro and in vivo antibacterial activities of FK037, a new parenteral cephalosporin, were compared with those of cefpirome, ceftazidime and flomoxef. The advantages of in vitro activity of FK037 were as follows: (1) a broad-spectrum antibacterial activity, (2) the most potent activity (MIC90: 25 micrograms/ml) of the cephalosporins tested against highly methicillin-resistant Staphylococcus aureus (H-MRSA), (3) a strong activity against Enterobacter spp. and Citrobacter freundii resistant to the third-generation cephalosporins tested. The MICs of FK037 for 90% of the clinical isolates tested (MIC90s) were 0.012 microgram/ml for Streptococcus pyogenes, 0.05 microgram/ml for Escherichia coli, 0.1 microgram/ml for Streptococcus pneumoniae, 0.2 microgram/ml for Haemophilus influenzae and Proteus mirabilis, 0.39 microgram/ml for Klebsiella pneumoniae, 1.56 micrograms/ml for methicillin-sensitive S. aureus, Proteus vulgaris and Enterobacter aerogenes, 3.13 micrograms/ml for Staphylococcus epidermidis and Moraxella catarrhalis, 6.25 micrograms/ml for C. freundii, 12.5 micrograms/ml for low-level methicillin-resistant S. aureus (L-MRSA), Enterobacter cloacae and Pseudomonas aeruginosa, and 25 micrograms/ml for H-MRSA and Serratia marcescens. FK037 was similar in potency to cefpirome against strains except MRSA, and was superior to ceftazidime and flomoxef against strains except P. vulgaris and/or M. catarrhalis. The increase in MICs of FK037 against 2 L-MRSA strains (2- or 4-fold) was smaller than that of cefpirome and flomoxef (16- to 64-fold) after the third serial culture in the presence of each drug. FK037 was highly bactericidal against S. aureus, E. coli, K. pneumoniae and P. aeruginosa at the MIC or higher. FK037 had a potent protective activity against murine experimental systemic infections due to a wide variety of bacteria. Its protective activity was the strongest among the cephalosporins tested against H-MRSA and Acinetobacter calcoaceticus. Against the other strains, FK037 was as effective as cefpirome and similar or superior to flomoxef and ceftazidime though it was inferior to ceftazidime against P. aeruginosa. Transmission electron microscopic studies revealed that FK037 inhibited septum formation and induced thick cross walls and bacteriolysis at the division sites in MRSA after 4 h incubation.
Pseudomonas aeruginosa and Escherichia coli were exposed to nocardicin A, and were subsequently observed with transmission and scanning electron microscopes. Although the nocardicin A-induced morphological alterations such as bulges and spheroplast formations were observed both in P. aeruginosa and E. coli, their positions on the cell surface were different in the two species.
Abstract Background Bronchioalveolar stem cells (BASCs) located at the bronchioalveolar-duct junction (BADJ) are stem cells residing in alveoli and terminal bronchioles that can self-renew and differentiate into alveolar type (AT)-1 cells, AT-2 cells, club cells, and ciliated cells. Following terminal-bronchiole injury, BASCs increase in number and promote repair. However, whether BASCs can be differentiated from mouse-induced pluripotent stem cells (iPSCs) remains unreported, and the therapeutic potential of such cells is unclear. We therefore sought to differentiate BASCs from iPSCs and examine their potential for use in the treatment of epithelial injury in terminal bronchioles. Methods BASCs were induced using a modified protocol for differentiating mouse iPSCs into AT-2 cells. Differentiated iPSCs were intratracheally transplanted into naphthalene-treated mice. The engraftment of BASCs into the BADJ and their subsequent ability to promote repair of injury to the airway epithelium were evaluated. Results Flow cytometric analysis revealed that BASCs represented ~ 7% of the cells obtained. Additionally, ultrastructural analysis of these iPSC-derived BASCs via transmission electron microscopy showed that the cells containing secretory granules harboured microvilli, as well as small and immature lamellar body-like structures. When the differentiated iPSCs were intratracheally transplanted in naphthalene-induced airway epithelium injury, transplanted BASCs were found to be engrafted in the BADJ epithelium and alveolar spaces for 14 days after transplantation and to maintain the BASC phenotype. Notably, repair of the terminal-bronchiole epithelium was markedly promoted after transplantation of the differentiated iPSCs. Conclusions Mouse iPSCs could be differentiated in vitro into cells that display a similar phenotype to BASCs. Given that the differentiated iPSCs promoted epithelial repair in the mouse model of naphthalene-induced airway epithelium injury, this method may serve as a basis for the development of treatments for terminal-bronchiole/alveolar-region disorders.
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