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Article ; Online: Endoplasmic reticulum stress enhances the expression of TLR3-induced TSLP by airway epithelium.

Pathinayake, Prabuddha S / Hsu, Alan C-Y / Nichol, Kristy S / Horvat, Jay C / Hansbro, Philip M / Wark, Peter A

American journal of physiology. Lung cellular and molecular physiology

2024

Abstract: Thymic stromal lymphopoietin (TSLP) is an epithelial-derived pleiotropic cytokine that regulates T-helper 2 (Th2) immune responses in the lung and plays a major role in severe uncontrolled asthma. Emerging evidence suggests a role for endoplasmic ... ...

Abstract	Thymic stromal lymphopoietin (TSLP) is an epithelial-derived pleiotropic cytokine that regulates T-helper 2 (Th2) immune responses in the lung and plays a major role in severe uncontrolled asthma. Emerging evidence suggests a role for endoplasmic reticulum (ER) stress in the pathogenesis of asthma. In this study, we determined if ER stress and the unfolded protein response (UPR) signalling are involved in TSLP induction in the airway epithelium. For this, we treated human bronchial epithelial basal cells and differentiated primary bronchial epithelial cells with ER stress inducers and the TSLP mRNA and protein expression was determined. A series of siRNA gene knockdown experiments were conducted to determine the ER stress-induced TSLP signalling pathways. cDNA collected from asthmatic bronchial biopsies was used to determine the gene correlation between ER stress and TSLP. Our results show that ER stress signalling induces TSLP mRNA expression via the PERK-CHOP signalling pathway. AP-1 transcription factor is important in regulating this ER stress-induced TSLP mRNA induction, though ER stress alone cannot induce TSLP protein production. However, ER stress significantly enhances TLR3-induced TSLP protein secretion in the airway epithelium. TSLP and ER stress (PERK) mRNA expression positively correlates in bronchial biopsies from participants with asthma, particularly in neutrophilic asthma. In conclusion, these results suggest that ER stress primes TSLP which is then enhanced further upon TLR3 activation, which may induce severe asthma exacerbations. Targeting ER stress using pharmacological interventions may provide novel therapeutics for severe uncontrolled asthma.
Language	English
Publishing date	2024-03-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00378.2023
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Uc I Zs.89: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Mechanical forces suppress antiviral innate immune responses from asthmatic airway epithelial cells following rhinovirus infection.

Veerati, Punnam Chander / Reid, Andrew T / Nichol, Kristy S / Wark, Peter A B / Knight, Darryl A / Bartlett, Nathan W / Grainge, Christopher L

American journal of physiology. Lung cellular and molecular physiology

2023 Volume 325, Issue 2, Page(s) L206–L214

Abstract: Bronchoconstriction is the main physiological event in asthma, which leads to worsened clinical symptoms and generates mechanical stress within the airways. Virus infection is the primary cause of exacerbations in people with asthma, however, the impact ... ...

Abstract	Bronchoconstriction is the main physiological event in asthma, which leads to worsened clinical symptoms and generates mechanical stress within the airways. Virus infection is the primary cause of exacerbations in people with asthma, however, the impact that bronchoconstriction itself on host antiviral responses and viral replication is currently not well understood. Here we demonstrate how mechanical forces generated during bronchoconstriction may suppress antiviral responses at the airway epithelium without any difference in viral replication. Primary bronchial epithelial cells from donors with asthma were differentiated at the air-liquid interface. Differentiated cells were apically compressed (30 cmH
MeSH term(s)	Humans ; Rhinovirus ; Immunity, Innate ; Asthma/metabolism ; Antiviral Agents/pharmacology ; Epithelial Cells/metabolism ; Picornaviridae Infections
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2023-06-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00074.2022
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Uc I Zs.89: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Severe asthma ILC2s demonstrate enhanced proliferation that is modified by biologics.

Malik, Bilal / Bartlett, Nathan W / Upham, John W / Nichol, Kristy S / Harrington, John / Wark, Peter A B

Respirology (Carlton, Vic.)

2023 Volume 28, Issue 8, Page(s) 758–766

Abstract: Background and objective: Type 2 (T2) innate lymphoid cells (ILC2s) contribute to airway inflammation and disease in asthma. We hypothesize that ILC2s isolated from people with severe allergic and eosinophilic asthma would exhibit an enhanced T2 ... ...

Abstract	Background and objective: Type 2 (T2) innate lymphoid cells (ILC2s) contribute to airway inflammation and disease in asthma. We hypothesize that ILC2s isolated from people with severe allergic and eosinophilic asthma would exhibit an enhanced T2 inflammatory activity that would be altered following treatment with mepolizumab and omalizumab. We compare peripheral blood (PB) isolated ILC2's proliferative capacity, IL-5 and IL-13 secretion and phenotype between healthy without asthma (HC), non-asthma allergic (NAA), mild asthma (MA) and severe allergic and eosinophilic asthma (SA) subjects. We then determined the impact of 6 months treatment with either mepolizumab or omalizumab on ILC2s physiology of SA subjects. Methods: ILC2s were sorted and cultured in the presence of IL-2, IL-25, IL-33 and thymic stromal lymphopoietin (TSLP) for 14 days. ILC2s proliferation, phenotypes and functions were assessed using flowcytometry. The ILC2s response was then reassessed following clinically successful treatment of SA subjects with mepolizumab and omalizumab. Results: SA ILC2s demonstrated increased proliferative capacity, TSLP receptor (TSLPR), GATA3 and NFATc1 protein expressions and increased IL-5 and IL-13 release. ILC2s were also capable of releasing IL-6 in response to stimulation. Mepolizumab treatment reduced ILC2s proliferative capacity and expression of TSLPR, GATA3 and NFATc1. Both mepolizumab and omalizumab were associated with reduced ILC2s release of IL-5 and IL-13, only mepolizumab reduced IL-6. Conclusion: ILC2s from severe allergic and eosinophilic asthma demonstrated an active phenotype typified by increased proliferation, TSLPR, GATA3 and NFATc1 expression and increased IL-5, IL-13 and IL-6 release. Mepolizumab reduced markers of ILC2s activation.
MeSH term(s)	Humans ; Immunity, Innate ; Interleukin-13 ; Biological Products ; Omalizumab ; Interleukin-5 ; Interleukin-6 ; Lymphocytes ; Asthma/drug therapy ; Cytokines/metabolism ; Pulmonary Eosinophilia ; Cell Proliferation
Chemical Substances	Interleukin-13 ; Biological Products ; Omalizumab (2P471X1Z11) ; Interleukin-5 ; Interleukin-6 ; Cytokines
Language	English
Publishing date	2023-04-28
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1435849-9
ISSN	1440-1843 ; 1323-7799
ISSN (online)	1440-1843
ISSN	1323-7799
DOI	10.1111/resp.14506
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Article ; Online: Comparison of commercially available differentiation media on cell morphology, function, and anti-viral responses in conditionally reprogrammed human bronchial epithelial cells.

Awatade, Nikhil T / Reid, Andrew T / Nichol, Kristy S / Budden, Kurtis F / Veerati, Punnam Chander / Pathinayake, Prabuddha S / Grainge, Christopher L / Hansbro, Philip M / Wark, Peter A B

Scientific reports

2023 Volume 13, Issue 1, Page(s) 11200

Abstract: Primary air liquid interface (ALI) cultures of bronchial epithelial cells are used extensively to model airway responses. A recent advance is the development of conditional reprogramming that enhances proliferative capability. Several different media and ...

Abstract	Primary air liquid interface (ALI) cultures of bronchial epithelial cells are used extensively to model airway responses. A recent advance is the development of conditional reprogramming that enhances proliferative capability. Several different media and protocols are utilized, yet even subtle differences may influence cellular responses. We compared the morphology and functional responses, including innate immune responses to rhinovirus infection in conditionally reprogrammed primary bronchial epithelial cells (pBECs) differentiated using two commonly used culture media. pBECs collected from healthy donors (n = 5) were CR using g-irradiated 3T3 fibroblasts and Rho Kinase inhibitor. CRpBECs were differentiated at ALI in either PneumaCult (PN-ALI) or bronchial epithelial growth medium (BEGM)-based differentiation media (BEBM:DMEM, 50:50, Lonza)-(AB-ALI) for 28 days. Transepithelial electrical resistance (TEER), immunofluorescence, histology, cilia activity, ion channel function, and expression of cell markers were analyzed. Viral RNA was assessed by RT-qPCR and anti-viral proteins quantified by LEGENDplex following Rhinovirus-A1b infection. CRpBECs differentiated in PneumaCult were smaller and had a lower TEER and cilia beat frequency compared to BEGM media. PneumaCult media cultures exhibited increased FOXJ1 expression, more ciliated cells with a larger active area, increased intracellular mucins, and increased calcium-activated chloride channel current. However, there were no significant changes in viral RNA or host antiviral responses. There are distinct structural and functional differences in pBECs cultured in the two commonly used ALI differentiation media. Such factors need to be taken into consideration when designing CRpBECs ALI experiments for specific research questions.
MeSH term(s)	Humans ; Bronchi ; Cell Differentiation ; Epithelial Cells ; Chloride Channels ; Cilia ; Culture Media ; Enterovirus Infections
Chemical Substances	Chloride Channels ; Culture Media
Language	English
Publishing date	2023-07-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-37828-0
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Article ; Online: Conditionally reprogrammed asthmatic bronchial epithelial cells express lower <i>FOXJ1</i> at terminal differentiation and lower <i>IFNs</i> following RV-A1 infection.

Veerati, Punnam Chander / Nichol, Kristy S / Read, Jane M / Bartlett, Nathan W / Wark, Peter A B / Knight, Darryl A / Grainge, Christopher L / Reid, Andrew T

American journal of physiology. Lung cellular and molecular physiology

2022 Volume 323, Issue 4, Page(s) L495–L502

Abstract: Primary bronchial epithelial cells (pBECs) obtained from donors have limited proliferation capacity. Recently, conditional reprogramming (CR) technique has overcome this and has provided the potential for extended passaging and subsequent differentiation ...

Abstract	Primary bronchial epithelial cells (pBECs) obtained from donors have limited proliferation capacity. Recently, conditional reprogramming (CR) technique has overcome this and has provided the potential for extended passaging and subsequent differentiation of cells at air-liquid interface (ALI). However, there has been no donor-specific comparison of cell morphology, baseline gene expression, barrier function, and antiviral responses compared with their "parent" pBECs, especially cells obtained from donors with asthma. We, therefore, collected and differentiated pBECs at ALI from mild donors with asthma (n = 6) for the parent group. The same cells were conditionally reprogrammed and later differentiated at ALI. Barrier function was measured during the differentiation phase. Morphology and baseline gene expression were compared at terminal differentiation. Viral replication kinetics and antiviral responses were assessed following rhinovirus (RV) infection over 96 h. Barrier function during the differentiation phase and cell structural morphology at terminal differentiation appear similar in both parent and CR groups, however, there were elongated cell structures superficial to basal cells and significantly lower FOXJ1 expression in CR group. IFN gene expression was also significantly lower in CR group compared with parent asthma group following RV infection. The CR technique is a beneficial tool to proliferate pBECs over extended passages. Considering lower FOXJ1 expression, viral replication kinetics and antiviral responses, a cautious approach should be taken while choosing CR cells for experiments. In addition, as lab-to-lab cell culture techniques vary, the most appropriate technique must be utilized to best match individual cell functions and morphologies to address specific research questions and experimental reproducibility across the labs.
MeSH term(s)	Antiviral Agents/metabolism ; Asthma/metabolism ; Cells, Cultured ; Epithelial Cells/metabolism ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Humans ; Picornaviridae Infections ; Reproducibility of Results ; Rhinovirus/physiology
Chemical Substances	Antiviral Agents ; FOXJ1 protein, human ; Forkhead Transcription Factors
Language	English
Publishing date	2022-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00230.2022
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Uc I Zs.89: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Human coronaviruses 229E and OC43 replicate and induce distinct antiviral responses in differentiated primary human bronchial epithelial cells.

Loo, Su-Ling / Wark, Peter A B / Esneau, Camille / Nichol, Kristy S / Hsu, Alan C-Y / Bartlett, Nathan W

American journal of physiology. Lung cellular and molecular physiology

2020 Volume 319, Issue 6, Page(s) L926–L931

Abstract: The recurrent emergence of novel, pathogenic coronaviruses (CoVs) severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1; 2002), Middle East respiratory syndrome (MERS)-CoV (2012), and most recently SARS-CoV-2 (2019) has highlighted the need for ... ...

Abstract	The recurrent emergence of novel, pathogenic coronaviruses (CoVs) severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1; 2002), Middle East respiratory syndrome (MERS)-CoV (2012), and most recently SARS-CoV-2 (2019) has highlighted the need for physiologically informative airway epithelial cell infection models for studying immunity to CoVs and development of antiviral therapies. To address this, we developed an in vitro infection model for two human coronaviruses; alphacoronavirus 229E-CoV (229E) and betacoronavirus OC43-CoV (OC43) in differentiated primary human bronchial epithelial cells (pBECs). Primary BECs from healthy subjects were grown at air-liquid interface (ALI) and infected with 229E or OC43, and replication kinetics and time-course expression of innate immune mediators were assessed. OC43 and 229E-CoVs replicated in differentiated pBECs but displayed distinct replication kinetics: 229E replicated rapidly with viral load peaking at 24 h postinfection, while OC43 replication was slower peaking at 96 h after infection. This was associated with diverse antiviral response profiles defined by increased expression of type I/III interferons and interferon-stimulated genes (ISGs) by 229E compared with no innate immune activation with OC43 infection. Understanding the host-virus interaction for previously established coronaviruses will give insight into pathogenic mechanisms underpinning SARS-CoV-2-induced respiratory disease and other future coronaviruses that may arise from zoonotic sources.
MeSH term(s)	Antiviral Agents/pharmacology ; Bronchi/drug effects ; Bronchi/immunology ; Bronchi/virology ; Cells, Cultured ; Coronavirus 229E, Human/drug effects ; Coronavirus 229E, Human/immunology ; Coronavirus Infections/drug therapy ; Coronavirus Infections/immunology ; Coronavirus Infections/virology ; Epithelial Cells/drug effects ; Epithelial Cells/immunology ; Epithelial Cells/virology ; Humans ; Interferons/metabolism ; Virus Replication/drug effects
Chemical Substances	Antiviral Agents ; interferon type III ; Interferons (9008-11-1)
Keywords	covid19
Language	English
Publishing date	2020-09-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00374.2020
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Zs.A 2749: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)

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Article ; Online: IL-25 blockade augments antiviral immunity during respiratory virus infection.

Williams, Teresa C / Loo, Su-Ling / Nichol, Kristy S / Reid, Andrew T / Veerati, Punnam C / Esneau, Camille / Wark, Peter A B / Grainge, Christopher L / Knight, Darryl A / Vincent, Thomas / Jackson, Crystal L / Alton, Kirby / Shimkets, Richard A / Girkin, Jason L / Bartlett, Nathan W

Communications biology

2022 Volume 5, Issue 1, Page(s) 415

Abstract: IL-25 is implicated in the pathogenesis of viral asthma exacerbations. However, the effect of IL-25 on antiviral immunity has yet to be elucidated. We observed abundant expression and colocalization of IL-25 and IL-25 receptor at the apical surface of ... ...

Abstract	IL-25 is implicated in the pathogenesis of viral asthma exacerbations. However, the effect of IL-25 on antiviral immunity has yet to be elucidated. We observed abundant expression and colocalization of IL-25 and IL-25 receptor at the apical surface of uninfected airway epithelial cells and rhinovirus infection increased IL-25 expression. Analysis of immune transcriptome of rhinovirus-infected differentiated asthmatic bronchial epithelial cells (BECs) treated with an anti-IL-25 monoclonal antibody (LNR125) revealed a re-calibrated response defined by increased type I/III IFN and reduced expression of type-2 immune genes CCL26, IL1RL1 and IL-25 receptor. LNR125 treatment also increased type I/III IFN expression by coronavirus infected BECs. Exogenous IL-25 treatment increased viral load with suppressed innate immunity. In vivo LNR125 treatment reduced IL-25/type 2 cytokine expression and increased IFN-β expression and reduced lung viral load. We define a new immune-regulatory role for IL-25 that directly inhibits virus induced airway epithelial cell innate anti-viral immunity.
MeSH term(s)	Antiviral Agents/pharmacology ; Asthma/metabolism ; Humans ; Immunity, Innate ; Interleukin-17/immunology ; Rhinovirus ; Virus Diseases
Chemical Substances	Antiviral Agents ; IL25 protein, human ; Interleukin-17
Language	English
Publishing date	2022-05-04
Publishing country	England
Document type	Journal Article
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-022-03367-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Blocking Notch3 Signaling Abolishes MUC5AC Production in Airway Epithelial Cells from Individuals with Asthma.

Reid, Andrew T / Nichol, Kristy S / Chander Veerati, Punnam / Moheimani, Fatemeh / Kicic, Anthony / Stick, Stephen M / Bartlett, Nathan W / Grainge, Chris L / Wark, Peter A B / Hansbro, Philip M / Knight, Darryl A

American journal of respiratory cell and molecular biology

2020 Volume 62, Issue 4, Page(s) 513–523

Abstract: In asthma, goblet cell numbers are increased within the airway epithelium, perpetuating the production of mucus that is more difficult to clear and results in airway mucus plugging. Notch1, Notch2, or Notch3, or a combination of these has been shown to ... ...

Abstract	In asthma, goblet cell numbers are increased within the airway epithelium, perpetuating the production of mucus that is more difficult to clear and results in airway mucus plugging. Notch1, Notch2, or Notch3, or a combination of these has been shown to influence the differentiation of airway epithelial cells. How the expression of specific Notch isoforms differs in fully differentiated adult asthmatic epithelium and whether Notch influences mucin production after differentiation is currently unknown. We aimed to quantify different Notch isoforms in the airway epithelium of individuals with severe asthma and to examine the impact of Notch signaling on mucin MUC5AC. Human lung sections and primary bronchial epithelial cells from individuals with and without asthma were used in this study. Primary bronchial epithelial cells were differentiated at the air-liquid interface for 28 days. Notch isoform expression was analyzed by Taqman quantitative PCR. Immunohistochemistry was used to localize and quantify Notch isoforms in human airway sections. Notch signaling was inhibited
MeSH term(s)	Aged ; Asthma/metabolism ; Bronchi/metabolism ; Cell Differentiation/physiology ; Cells, Cultured ; Epithelial Cells/metabolism ; Female ; Goblet Cells/metabolism ; Humans ; Lung/metabolism ; Male ; Middle Aged ; Mucin 5AC/metabolism ; RNA, Small Interfering/metabolism ; Receptor, Notch3/metabolism ; Respiratory Mucosa/metabolism ; Signal Transduction/physiology
Chemical Substances	MUC5AC protein, human ; Mucin 5AC ; NOTCH3 protein, human ; RNA, Small Interfering ; Receptor, Notch3
Language	English
Publishing date	2020-01-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2019-0069OC
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Zs.A 2851: Show issues

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Article ; Online: Airway Epithelial Cell Immunity Is Delayed During Rhinovirus Infection in Asthma and COPD.

Veerati, Punnam Chander / Troy, Niamh M / Reid, Andrew T / Li, Ngan Fung / Nichol, Kristy S / Kaur, Parwinder / Maltby, Steven / Wark, Peter A B / Knight, Darryl A / Bosco, Anthony / Grainge, Chris L / Bartlett, Nathan W

Frontiers in immunology

2020 Volume 11, Page(s) 974

Abstract: Respiratory viral infections, particularly those caused by rhinovirus, exacerbate chronic respiratory inflammatory diseases, such as asthma and chronic obstructive pulmonary disease (COPD). Airway epithelial cells are the primary site of rhinovirus ... ...

Abstract	Respiratory viral infections, particularly those caused by rhinovirus, exacerbate chronic respiratory inflammatory diseases, such as asthma and chronic obstructive pulmonary disease (COPD). Airway epithelial cells are the primary site of rhinovirus replication and responsible of initiating the host immune response to infection. Numerous studies have reported that the anti-viral innate immune response (including type I and type III interferon) in asthma is less effective or deficient leading to the conclusion that epithelial innate immunity is a key determinant of disease severity during a rhinovirus induced exacerbation. However, deficient rhinovirus-induced epithelial interferon production in asthma has not always been observed. We hypothesized that disparate
MeSH term(s)	Aged ; Asthma/immunology ; Asthma/virology ; Cells, Cultured ; Epithelial Cells/immunology ; Epithelial Cells/virology ; Female ; Gene Expression ; Humans ; Immunity, Innate ; Male ; Middle Aged ; Pulmonary Disease, Chronic Obstructive/immunology ; Pulmonary Disease, Chronic Obstructive/virology ; Respiratory Mucosa/cytology ; Respiratory Mucosa/immunology ; Respiratory Mucosa/virology ; Rhinovirus
Language	English
Publishing date	2020-05-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.00974
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Article: Human coronaviruses 229E and OC43 replicate and induce distinct anti-viral responses in differentiated primary human bronchial epithelial cells

Loo, Su-Ling / Wark, Peter A B / Esneau, Camille / Nichol, Kristy S / Hsu, Alan C-Y / Bartlett, Nathan W

Abstract: The recurrent emergence of novel, pathogenic coronaviruses (CoVs) SARS-CoV-1 (2002), MERS-CoV (2012) and most recently SARS-CoV-2 (2019) has highlighted the need for physiologically informative airway epithelial cell infection models for studying ... ...

Abstract	The recurrent emergence of novel, pathogenic coronaviruses (CoVs) SARS-CoV-1 (2002), MERS-CoV (2012) and most recently SARS-CoV-2 (2019) has highlighted the need for physiologically informative airway epithelial cell infection models for studying immunity to CoVs and development of anti-viral therapies. To address this, we developed an in-vitro infection model for two human coronaviruses; alphacoronavirus 229E-CoV (229E) and betacoronavirus OC43-CoV (OC43) in differentiated primary human bronchial epithelial cells (pBECs). Primary BECs from healthy subjects were grown at air liquid interface (ALI) and infected with 229E or OC43, and replication kinetics and time-course expression of innate immune mediators were assessed. OC43 and 229E-CoVs replicated in differentiated pBECs but displayed distinct replication kinetics: 229E replicated rapidly with viral load peaking at 24 hours post-infection, whilst OC43 replication was slower peaking at 7 days after infection. This was associated with diverse anti-viral response profiles defined by increased expression of type I/III interferons and interferon-stimulated genes (ISGs) by 229E compared to OC43. Understanding the host-virus interaction for previously established coronaviruses will give insight into pathogenic mechanisms underpinning SARS-CoV-2-induced respiratory disease and other future coronaviruses that may arise from zoonotic sources.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #751458
Database	COVID19

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