Type 2 rhinovirus infection of cultured human tracheal epithelial cells: role of LDL receptor

2001 ◽  
Vol 280 (3) ◽  
pp. L409-L420 ◽  
Author(s):  
Tomoko Suzuki ◽  
Mutsuo Yamaya ◽  
Masahito Kamanaka ◽  
Yu X. Jia ◽  
Katsutoshi Nakayama ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Epithelial Cells ◽  
Cytokine Production ◽  
Primary Cultures ◽  
Ldl Receptor ◽  
Receptor Expression ◽  
Tracheal Epithelial Cells ◽  
Activation Of Transcription ◽  
Tracheal Epithelial

To examine the role of the low-density lipoprotein (LDL) receptor on minor group human rhinovirus (RV) infection, primary cultures of human tracheal epithelial cells were infected with a minor group (RV2) or a major group (RV14) RV. Viral infection was confirmed by showing with PCR that viral titers in supernatants and lysates from infected cells increased with time. RV2 and RV14 increased expression of mRNA and protein of the LDL receptor on the cells and the cytokine production. RV2 induced activation of transcription factors SP1 and nuclear factor-κB (NF-κB). An antibody to the LDL receptor inhibited RV2 infection and RV2-induced cytokine production without an effect on RV14 infection and RV14-induced cytokine production. These findings imply that RV2 upregulates LDL receptor expression on airway epithelial cells, thereby increasing susceptibility to minor group RV infection. LDL receptor expression and cytokine production may be mediated, in part, via activation of transcription factors by RV2. These events may be important in airway inflammation after minor group RV infection in asthma.

Effects of dexamethasone on rhinovirus infection in cultured human tracheal epithelial cells

2000 ◽  
Vol 278 (3) ◽  
pp. L560-L571 ◽  
Author(s):  
Tomoko Suzuki ◽  
Mutsuo Yamaya ◽  
Kiyohisa Sekizawa ◽  
Norihiro Yamada ◽  
Katsutoshi Nakayama ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Primary Cultures ◽  
Viral Rna ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Tracheal Epithelial Cells ◽  
Rhinovirus Infection ◽  
Infected Cells ◽  
Tracheal Epithelial ◽  
Viral Titers

To examine the effects of glucocorticoid on rhinovirus (RV) infection, primary cultures of human tracheal epithelial cells were infected with either RV2 or RV14. Viral infection was confirmed by demonstrating that viral RNA in infected cells and viral titers of supernatants and lysates from infected cells increased with time. RV14 infection upregulated the expression of mRNA and protein of intercellular adhesion molecule-1 (ICAM-1), the major RV receptor, on epithelial cells, and it increased the production of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α in supernatants. Dexamethasone reduced the viral titers of supernatants and cell lysates, viral RNA of infected cells, and susceptibility of RV14 infection in association with inhibition of cytokine production and ICAM-1 induction. In contrast to RV14 infection, dexamethasone did not alter RV2 infection, a minor group of RVs. These results suggest that dexamethasone may inhibit RV14 infection by reducing the surface expression of ICAM-1 in cultured human tracheal epithelial cells. Glucocorticoid may modulate airway inflammation via reducing the production of proinflammatory cytokines and ICAM-1 induced by rhinovirus infection.

Molecular responses of rat tracheal epithelial cells to transmembrane pressure

2000 ◽  
Vol 278 (6) ◽  
pp. L1264-L1272 ◽  
Author(s):  
Barbara Ressler ◽  
Richard T. Lee ◽  
Scott H. Randell ◽  
Jeffrey M. Drazen ◽  
Roger D. Kamm
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Muscle Activation ◽  
Primary Cultures ◽  
Transmembrane Pressure ◽  
Apical Surface ◽  
Dependent Manner ◽  
Tracheal Epithelial Cells ◽  
Compressive Stresses ◽  
Tracheal Epithelial

Smooth muscle constriction in asthma causes the airway to buckle into a rosette pattern, folding the epithelium into deep crevasses. The epithelial cells in these folds are pushed up against each other and thereby experience compressive stresses. To study the epithelial cell response to compressive stress, we subjected primary cultures of rat tracheal epithelial cells to constant elevated pressures on their apical surface (i.e., a transmembrane pressure) and examined changes in the expression of genes that are important for extracellular matrix production and maintenance of smooth muscle activation. Northern blot analysis of RNA extracted from cells subjected to transmembrane pressure showed induction of early growth response-1 (Egr-1), endothelin-1, and transforming growth factor-β1 in a pressure-dependent and time-dependent manner. Increases in Egr-1 protein were detected by immunohistochemistry. Our results demonstrate that airway epithelial cells respond rapidly to compressive stresses. Potential transduction mechanisms of transmembrane pressure were also investigated.

scholarly journals Bordetella pertussis Adenylate Cyclase-Hemolysin Induces Interleukin-6 Secretion by Human Tracheal Epithelial Cells

2004 ◽  
Vol 72 (9) ◽  
pp. 5530-5533 ◽  
Author(s):  
Laurence Bassinet ◽  
Catherine Fitting ◽  
Bruno Housset ◽  
Jean-Marc Cavaillon ◽  
Nicole Guiso
Keyword(s):  
Epithelial Cells ◽  
Adenylate Cyclase ◽  
Bordetella Pertussis ◽  
Interleukin 6 ◽  
Bacterial Toxins ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

ABSTRACT After interaction with tracheal epithelial cells, Bordetella pertussis induces the secretion of interleukin-6. This secretion is dependent on the expression of adenylate cyclase-hemolysin by the bacterium but not on the expression of other characterized bacterial toxins or adhesins. This finding confirms the important role of adenylate cyclase-hemolysin in the pathogenicity of the bacterium.

scholarly journals Levofloxacin Inhibits Rhinovirus Infection in Primary Cultures of Human Tracheal Epithelial Cells

2012 ◽  
Vol 56 (8) ◽  
pp. 4052-4061 ◽  
Author(s):  
Mutsuo Yamaya ◽  
Hidekazu Nishimura ◽  
Yukimasa Hatachi ◽  
Hiroyasu Yasuda ◽  
Xue Deng ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
Bacterial Infections ◽  
Mrna Level ◽  
Primary Cultures ◽  
Intercellular Adhesion Molecule ◽  
Soluble Form ◽  
Chronic Obstructive ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

ABSTRACTRespiratory virus infections, including infections with rhinoviruses (RVs), are related to exacerbations of chronic obstructive pulmonary disease (COPD). A new quinolone antibiotic, levofloxacin (LVFX), has been used to treat bacterial infections that cause COPD exacerbations as well as bacterial infections that are secondary to viral infection in COPD patients. However, the inhibitory effects of LVFX on RV infection and RV infection-induced airway inflammation have not been studied. We examined the effects of LVFX on type 14 rhinovirus (RV14) (a major human RV) infection of human tracheal epithelial cells pretreated with LVFX. LVFX pretreatment reduced the RV14 titer, the level of cytokines in the supernatant, the amount of RV14 RNA in the cells after RV14 infection, and the cells' susceptibility to RV14 infection. LVFX pretreatment decreased the mRNA level of intercellular adhesion molecule 1 (ICAM-1), a receptor for RV14, in the cells and the concentration of the soluble form of ICAM-1 in the supernatant before RV14 infection. LVFX pretreatment also decreased the number and the fluorescence intensity of the acidic endosomes from which RV14 RNA enters the cytoplasm. LVFX pretreatment inhibited the activation of nuclear factor κB proteins, including p50 and p65, in nuclear extracts. LVFX pretreatment did not reduce the titers of RV2 (a minor human RV) but reduced the titers of RV15 (a major human RV). These results suggest that LVFX inhibits major-group rhinovirus infections in part by reducing ICAM-1 expression levels and the number of acidic endosomes. LVFX may also modulate airway inflammation in rhinoviral infections.

Prostaglandin secretion by guinea pig tracheal epithelial cells caused by eosinophil major basic protein

1993 ◽  
Vol 265 (3) ◽  
pp. L234-L242 ◽  
Author(s):  
S. R. White ◽  
K. S. Sigrist ◽  
S. M. Spaethe
Keyword(s):  
Epithelial Cells ◽  
Guinea Pig ◽  
Basic Protein ◽  
Primary Cultures ◽  
Thromboxane B2 ◽  
Major Basic Protein ◽  
Tracheal Epithelial Cells ◽  
Subsequent Response ◽  
Tracheal Epithelial ◽  
Eosinophil Major Basic Protein

We examined the effect of eosinophil major basic protein (MBP) on prostaglandin (PG) secretion from guinea pig tracheal epithelial (GPTE) cells. Primary cultures of GPTE cells were incubated with 10(-6) M MBP for up to 6 h and then stimulated with 10(-6) M bradykinin (BK). PGE2, 6-ketoprostaglandin F1 alpha (PGF1 alpha), PGF2 alpha, and thromboxane B2 (TxB2) concentrations in media were determined by enzyme-linked immunoabsorbent assay (EIA). Incubation with MBP for 6 h caused secretion of both PGE2 (17,614 +/- 4,416 vs. 1,426 +/- 555 pg/10(6) cells at baseline, P < 0.001, n = 7) and PGF2 alpha (20,303 +/- 5,724 vs. 3,790 +/- 1.075 pg/10(6) cells at baseline, P < 0.002, n = 7). Secretion of PGE2 and PGF2 alpha stimulated by MBP required at least 2 h. Incubation with MBP for 6 h also augmented the subsequent response to BK: PGE2 secretion was 29,215 +/- 6,853 vs. 3,445 +/- 1,041 pg/10(6) cells for BK alone (P < 0.0001), and PGF2 alpha secretion was 25,407 +/- 6,237 vs. 5,213 +/- 1,535 pg/10(6) cells for BK alone (P < 0.0001). MBP did not change 6-keto-PGF1 alpha and TxB2 secretion. Incubation of GPTE cells from seven animals with polylysine, a protein with mass and ion charge similar to MBP, for 2 h, both caused secretion of PGE2 (8,579 +/- 3,244 vs. 788 +/- 419 pg/10(6) cells at baseline, P < 0.01) and augmented the response to BK (12,732 +/- 4,788 vs. 1,653 +/- 680 pg/10(6) cells after BK alone, P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document