scholarly journals Utilization of Ruminal Epithelial Cells by Ruminococcus albus, with or without Rumen Protozoa, and Its Effect on Bacterial Growth

2003 ◽  
Vol 16 (1) ◽  
pp. 44-49
Author(s):  
M. Goto ◽  
S. Karita ◽  
M. S. Yahaya ◽  
W. Kim ◽  
E. Nakayama ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bacterial Growth ◽  
Ruminococcus Albus ◽  
Rumen Protozoa

scholarly journals Thioredoxin Reductase Is Essential for Protection ofNeisseria gonorrhoeaeagainst Killing by Nitric Oxide and for Bacterial Growth during Interaction with Cervical Epithelial Cells

2009 ◽  
Vol 199 (2) ◽  
pp. 227-235 ◽  
Author(s):  
Adam J. Potter ◽  
Stephen P. Kidd ◽  
Jennifer L. Edwards ◽  
Megan L. Falsetta ◽  
Michael A. Apicella ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Bacterial Growth ◽  
Thioredoxin Reductase ◽  
Cervical Epithelial Cells

scholarly journals Chlamydia pneumoniae Resists Antibiotics in Lymphocytes

2003 ◽  
Vol 47 (6) ◽  
pp. 1972-1975 ◽  
Author(s):  
Hiroyuki Yamaguchi ◽  
Herman Friedman ◽  
Mayumi Yamamoto ◽  
Keigo Yasuda ◽  
Yoshimasa Yamamoto
Keyword(s):  
Epithelial Cells ◽  
Bacterial Growth ◽  
Chlamydia Pneumoniae ◽  
Inflammatory Diseases ◽  
Lymphoid Cells ◽  
Infection Model ◽  
Chronic Inflammatory Diseases

ABSTRACT Chlamydia pneumoniae infection of lymphocytes in blood has been well documented, and it is apparent that control of this pathogen in these cells may be critical in the development of chronic inflammatory diseases associated with infection by this bacterium. The activity of antibiotics against C. pneumoniae in lymphocytes was assessed in this study by utilizing an in vitro infection model with lymphoid cells. The results obtained indicated that although all of the antibiotics tested showed remarkable activity against bacterial growth in epithelial cells, C. pneumoniae in lymphocytes was less susceptible to antibiotics than was bacterial growth in epithelial cells, which are widely used for the evaluation of anti-C. pneumoniae antibiotics.

scholarly journals Insufficient Acidification of Autophagosomes Facilitates Group A Streptococcus Survival and Growth in Endothelial Cells

mBio ◽  
2015 ◽  
Vol 6 (5) ◽  
Author(s):  
Shiou-Ling Lu ◽  
Chih-Feng Kuo ◽  
Hao-Wen Chen ◽  
Yi-Shuan Yang ◽  
Ching-Chuan Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Epithelial Cells ◽  
Bacterial Growth ◽  
Group A Streptococcus ◽  
Multiorgan Failure ◽  
Specific Inhibitor ◽  
Low Ph ◽  
Bafilomycin A1 ◽  
Group A

ABSTRACTGroup A streptococcus (GAS) is an important human pathogen, and its invasion via blood vessels is critically important in serious events such as bacteremia or multiorgan failure. Although GAS was identified as an extracellular bacterium, the internalization of GAS into nonphagocytic cells may provide a strategy to escape from immune surveillance and antibiotic killing. However, GAS has also been reported to induce autophagy and is efficiently killed within lysosome-fused autophagosomes in epithelial cells. In this study, we show that GAS can replicate in endothelial cells and that streptolysin O is required for GAS growth. Bacterial replication can be suppressed by altering GAS gene expression in an acidic medium before internalization into endothelial cells. The inhibitory effect on GAS replication can be reversed by treatment with bafilomycin A1, a specific inhibitor of vacuolar-type H+-ATPase. Compared with epithelial cells in which acidification causes autophagy-mediated clearance of GAS, there was a defect in acidification of GAS-containing vesicles in endothelial cells. Consequently, endothelial cells fail to maintain low pH in GAS-containing autophagosomes, thereby permitting GAS replication inside LAMP-1- and LC3-positive vesicles. Furthermore, treatment of epithelial cells with bafilomycin A1 resulted in defective GAS clearance by autophagy, with subsequent bacterial growth intracellularly. Therefore, low pH is a key factor for autophagy-mediated suppression of GAS growth inside epithelial cells, while defective acidification of GAS-containing vesicles results in bacterial growth in endothelial cells.IMPORTANCEPrevious reports showed that GAS can induce autophagy and is efficiently killed within lysosome-fused autophagosomes in epithelial cells. In endothelial cells, in contrast, induction of autophagy is not sufficient for GAS killing. In this study, we provide the first evidence that low pH is required to prevent intracellular growth of GAS in epithelial cells and that this mechanism is defective in endothelial cells. Treatment of GAS with low pH altered GAS growth rate and gene expression of virulence factors and resulted in enhanced susceptibility of GAS to intracellular lysosomal killing. Our findings reveal the existence of different mechanisms of host defense against GAS invasion between epithelial and endothelial cells.

scholarly journals Esterase D Is Essential for Protection ofNeisseria gonorrhoeaeagainst Nitrosative Stress and for Bacterial Growth during Interaction with Cervical Epithelial Cells

2009 ◽  
Vol 200 (2) ◽  
pp. 273-278 ◽  
Author(s):  
Adam J. Potter ◽  
Stephen P. Kidd ◽  
Jennifer L. Edwards ◽  
Megan L. Falsetta ◽  
Michael A. Apicella ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bacterial Growth ◽  
Nitrosative Stress ◽  
Cervical Epithelial Cells

scholarly journals A lung-on-chip model of early Mycobacterium tuberculosis infection reveals an essential role for alveolar epithelial cells in controlling bacterial growth

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Vivek V Thacker ◽  
Neeraj Dhar ◽  
Kunal Sharma ◽  
Riccardo Barrile ◽  
Katia Karalis ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Epithelial Cells ◽  
Bacterial Growth ◽  
Alveolar Epithelial Cells ◽  
Host Cells ◽  
Elderly Persons ◽  
Spatiotemporal Resolution ◽  
Alveolar Epithelial ◽  
Increased Risk ◽  
On Chip

We establish a murine lung-on-chip infection model and use time-lapse imaging to reveal the dynamics of host-Mycobacterium tuberculosis interactions at an air-liquid interface with a spatiotemporal resolution unattainable in animal models and to probe the direct role of pulmonary surfactant in early infection. Surfactant deficiency results in rapid and uncontrolled bacterial growth in both macrophages and alveolar epithelial cells. In contrast, under normal surfactant levels, a significant fraction of intracellular bacteria are non-growing. The surfactant-deficient phenotype is rescued by exogenous addition of surfactant replacement formulations, which have no effect on bacterial viability in the absence of host cells. Surfactant partially removes virulence-associated lipids and proteins from the bacterial cell surface. Consistent with this mechanism, the attenuation of bacteria lacking the ESX-1 secretion system is independent of surfactant levels. These findings may partly explain why smokers and elderly persons with compromised surfactant function are at increased risk of developing active tuberculosis.

Some conditions influencing the association of Yersinia enterocolitica with epithelial cells in vitro

1985 ◽  
Vol 31 (10) ◽  
pp. 953-956
Author(s):  
Donald A. Schiemann ◽  
Pamela J. Swanz
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Stationary Phase ◽  
Yersinia Enterocolitica ◽  
Growth Medium ◽  
Bacterial Growth ◽  
Associated Bacteria ◽  
Cell Association

The association of Yersinia enterocolitica serotype 0:5,27 with Henle 407 epithelial cells in vitro was measured by using 35S-labelled bacteria with separation of unassociated bacteria by filtration (Nuclepore polycarbonate 5-μm membrane). The number of associated bacteria was related to the initial multiplicity. Changes in beginning pH, the presence of protein, availability of Ca2+ and Mg2+, and nature of carbohydrate in a defined bacterial growth medium did not change the degree of epithelial cell association. Bacteria recovered from the log phase of growth at 25 °C, or after growth to stationary phase at 35 °C, showed no association with epithelial cells. Optimal association occurred when the pH provided during interaction was between 7.6 and 8.6 and the temperature was either 25 or 35 °C. No association occurred within 30 min at 4 °C. The presence of Ca2+ and (or) Mg2+ during interaction had no effect, but the addition of peptone increased association. The results of this study demonstrate the importance of controlling both conditions provided for bacterial growth and those provided for interaction to achieve optimal association of Y. enterocolitica with epithelial cells in vitro.

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