scholarly journals Infection of Human Tracheal Epithelial Cells by H5 Avian Influenza Virus Is Regulated by the Acid Stability of Hemagglutinin and the pH of Target Cell Endosomes

Viruses ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 82 ◽  
Author(s):  
Tomo Daidoji ◽  
Junichi Kajikawa ◽  
Yasuha Arai ◽  
Yohei Watanabe ◽  
Ryohei Hirose ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Avian Influenza ◽  
Respiratory Tract ◽  
Membrane Fusion ◽  
Lower Respiratory Tract ◽  
Influenza Viruses ◽  
Tracheal Epithelial Cells ◽  
Susceptibility To Infection ◽  
Tracheal Epithelial ◽  
Conducting Airways

Despite the possible relationships between tracheal infection and concomitant infection of the terminal part of the lower respiratory tract (bronchioles/alveoli), the behavior of avian influenza viruses (AIVs), such as H5N1, in the conducting airways is unclear. To examine the tropism of AIVs for cells lining the conducting airways of humans, we established human tracheal epithelial cell clones (HTEpC-Ts) and examined their susceptibility to infection by AIVs. The HTEpC-Ts showed differing susceptibility to H5N1 and non-zoonotic AIVs. Viral receptors expressed by HTEpC-Ts bound all viruses; however, the endosomal pH was associated with the overall susceptibility to infection by AIVs. Moreover, H5N1 hemagglutinin broadened viral tropism to include HTEpC-Ts, because it had a higher pH threshold for viral–cell membrane fusion. Thus, H5N1 viruses infect human tracheal epithelial cells as a result of their higher pH threshold for membrane fusion which may be one mechanism underlying H5N1 pathogenesis in human airway epithelia. Efficient replication of H5N1 in the conducting airways of humans may facilitate infection of the lower respiratory tract.

scholarly journals Human and Avian Influenza Viruses Target Different Cells in the Lower Respiratory Tract of Humans and Other Mammals

2007 ◽  
Vol 171 (4) ◽  
pp. 1215-1223 ◽  
Author(s):  
Debby van Riel ◽  
Vincent J. Munster ◽  
Emmie de Wit ◽  
Guus F. Rimmelzwaan ◽  
Ron A.M. Fouchier ◽  
...  
Keyword(s):  
Avian Influenza ◽  
Respiratory Tract ◽  
Lower Respiratory Tract ◽  
Influenza Viruses ◽  
Avian Influenza Viruses

scholarly journals Capsular Sialic Acid of Streptococcus suis Serotype 2 Binds to Swine Influenza Virus and Enhances Bacterial Interactions with Virus-Infected Tracheal Epithelial Cells

2013 ◽  
Vol 81 (12) ◽  
pp. 4498-4508 ◽  
Author(s):  
Yingchao Wang ◽  
Carl A. Gagnon ◽  
Christian Savard ◽  
Nedzad Music ◽  
Mariela Srednik ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Sialic Acid ◽  
Epithelial Cells ◽  
Respiratory Tract ◽  
Bacterial Adhesion ◽  
Swine Influenza ◽  
Streptococcus Suis ◽  
Content Type ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

ABSTRACTStreptococcus suisserotype 2 is an important swine bacterial pathogen, and it is also an emerging zoonotic agent. It is unknown howS. suisvirulent strains, which are usually found in low quantities in pig tonsils, manage to cross the first host defense lines to initiate systemic disease. Influenza virus produces a contagious infection in pigs which is frequently complicated by bacterial coinfections, leading to significant economic impacts. In this study, the effect of a preceding swine influenza H1N1 virus (swH1N1) infection of swine tracheal epithelial cells (NTPr) on the ability ofS. suisserotype 2 to adhere to, invade, and activate these cells was evaluated. Cells preinfected with swH1N1 showed bacterial adhesion and invasion levels that were increased more than 100-fold compared to those of normal cells. Inhibition studies confirmed that the capsular sialic acid moiety is responsible for the binding to virus-infected cell surfaces. Also, preincubation ofS. suiswith swH1N1 significantly increased bacterial adhesion to/invasion of epithelial cells, suggesting thatS. suisalso uses swH1N1 as a vehicle to invade epithelial cells when the two infections occur simultaneously. Influenza virus infection may facilitate the transient passage ofS. suisat the respiratory tract to reach the bloodstream and cause bacteremia and septicemia.S. suismay also increase the local inflammation at the respiratory tract during influenza infection, as suggested by an exacerbated expression of proinflammatory mediators in coinfected cells. These results give new insight into the complex interactions between influenza virus andS. suisin a coinfection model.

scholarly journals The Infection of Chicken Tracheal Epithelial Cells with a H6N1 Avian Influenza Virus

PLoS ONE ◽  
2011 ◽  
Vol 6 (5) ◽  
pp. e18894 ◽  
Author(s):  
Ching-I Shen ◽  
Ching-Ho Wang ◽  
Shih-Cheng Shen ◽  
Hsiu-Chin Lee ◽  
Jiunn-Wang Liao ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Epithelial Cells ◽  
Avian Influenza ◽  
Avian Influenza Virus ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

Endothelin stimulates chloride secretion across canine tracheal epithelium

1991 ◽  
Vol 261 (2) ◽  
pp. L188-L194 ◽  
Author(s):  
P. I. Plews ◽  
Z. A. Abdel-Malek ◽  
C. A. Doupnik ◽  
G. D. Leikauf
Keyword(s):  
Epithelial Cells ◽  
Short Circuit ◽  
Second Messengers ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Tracheal Epithelium ◽  
Membrane Phospholipids ◽  
Cl Secretion ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

The endothelins (ET) are a group of isopeptides produced by a number of cells, including canine tracheal epithelial cells. Because these compounds are endogenous peptides that may activate eicosanoid metabolism, we investigated the effects of ET on Cl secretion in canine tracheal epithelium. Endothelin 1 (ET-1) was found to produce a dose-dependent change in short-circuit current (Isc) that increased slowly and reached a maximal value within 10-15 min. When isopeptides of ET were compared, 300 nM ET-1 and ET-2 produced comparable maximal increases in Isc, whereas ET-3 produced smaller changes in Isc (half-maximal concentrations of 2.2, 7.2, and 10.4 nM, respectively). Ionic substitution of Cl with nontransported anions, iodide and gluconate, reduced ET-1-induced changes in Isc. Furthermore, the response was inhibited by the NaCl cotransport inhibitor, furosemide. In paired tissues, ET-1 significantly increased mucosal net 36Cl flux without significant effect on 22Na flux. The increase in Isc induced by ET was diminished by pretreatment with indomethacin. The second messengers mediating the increase in Isc were investigated in cultured canine tracheal epithelial cells. ET-1 stimulated the release of [3H]arachidonate from membrane phospholipids, increased intracellular Ca2+ (occasionally producing oscillations), and increased adenosine 3',5'-cyclic monophosphate accumulation. The latter was diminished by indomethacin. Thus ET is a potent agonist of Cl secretion (with the isopeptides having the following potency: ET-1 greater than or equal to ET-2 greater than ET-3) and acts, in part, through a cyclooxygenase-dependent mechanism.

scholarly journals Fucoxanthin Ameliorates Oxidative Stress and Airway Inflammation in Tracheal Epithelial Cells and Asthmatic Mice

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1311
Author(s):  
Shu-Ju Wu ◽  
Chian-Jiun Liou ◽  
Ya-Ling Chen ◽  
Shu-Chen Cheng ◽  
Wen-Chung Huang
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Eosinophil Infiltration ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
And Oxidative Stress

Fucoxanthin is isolated from brown algae and was previously reported to have multiple pharmacological effects, including anti-tumor and anti-obesity effects in mice. Fucoxanthin also decreases the levels of inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. The purpose of the present study was to investigate the effects of fucoxanthin on the oxidative and inflammatory responses in inflammatory human tracheal epithelial BEAS-2B cells and attenuated airway hyperresponsiveness (AHR), airway inflammation, and oxidative stress in asthmatic mice. Fucoxanthin significantly decreased monocyte cell adherence to BEAS-2B cells. In addition, fucoxanthin inhibited the production of pro-inflammatory cytokines, eotaxin, and reactive oxygen species in BEAS-2B cells. Ovalbumin (OVA)-sensitized mice were treated by intraperitoneal injections of fucoxanthin (10 mg/kg or 30 mg/kg), which significantly alleviated AHR, goblet cell hyperplasia and eosinophil infiltration in the lungs, and decreased Th2 cytokine production in the BALF. Furthermore, fucoxanthin significantly increased glutathione and superoxide dismutase levels and reduced malondialdehyde (MDA) levels in the lungs of asthmatic mice. These data demonstrate that fucoxanthin attenuates inflammation and oxidative stress in inflammatory tracheal epithelial cells and improves the pathological changes related to asthma in mice. Thus, fucoxanthin has therapeutic potential for improving asthma.

scholarly journals In Vitro Radiation-induced Effects on Rat Tracheal Epithelial Cells

2002 ◽  
Vol 43 (1) ◽  
pp. 27-27 ◽  
Author(s):  
CAROLE KUGEL ◽  
ISABELLE BAILLY ◽  
FRANÇOISE TOURDES ◽  
JEAN-LUC PONCY
Keyword(s):  
Epithelial Cells ◽  
Tracheal Epithelial Cells ◽  
Radiation Induced ◽  
Tracheal Epithelial
Sign in / Sign up

Export Citation Format

Share Document