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Artikel ; Online: Immune Response in Cystic Fibrosis: Interplay between the Host and Microbes.

Boutin, Sébastien / Guillot, Loïc

International journal of molecular sciences

2023 Band 24, Heft 9

Abstract: Cystic fibrosis (CF) is a rare genetic disease caused by genetic variants of the cystic fibrosis transmembrane conductance regulator (CFTR) [ ... ]. ...

Abstract	Cystic fibrosis (CF) is a rare genetic disease caused by genetic variants of the cystic fibrosis transmembrane conductance regulator (CFTR) [...].
Mesh-Begriff(e)	Humans ; Cystic Fibrosis/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics ; Immunity ; Mutation
Chemische Substanzen	Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6)
Sprache	Englisch
Erscheinungsdatum	2023-04-24
Erscheinungsland	Switzerland
Dokumenttyp	Editorial
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24097766
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Modifier Factors of Cystic Fibrosis Phenotypes: A Focus on Modifier Genes.

Mésinèle, Julie / Ruffin, Manon / Guillot, Loïc / Corvol, Harriet

International journal of molecular sciences

2022 Band 23, Heft 22

Abstract: Although cystic fibrosis (CF) is recognized as a monogenic disease, due to variants within ... ...

Abstract	Although cystic fibrosis (CF) is recognized as a monogenic disease, due to variants within the
Mesh-Begriff(e)	Humans ; Cystic Fibrosis/complications ; Cystic Fibrosis/genetics ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Genes, Modifier ; Phenotype
Chemische Substanzen	Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6)
Sprache	Englisch
Erscheinungsdatum	2022-11-17
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms232214205
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Innate Immune Signaling and Proteolytic Pathways in the Resolution or Exacerbation of SARS-CoV-2 in Covid-19: Key Therapeutic Targets?

Sallenave, Jean-Michel / Guillot, Loïc

Frontiers in immunology

2020 Band 11, Seite(n) 1229

Abstract: COVID-19 is caused by the Severe Acute Respiratory Syndrome (SARS) coronavirus (Cov)-2, an enveloped virus with a positive-polarity, single-stranded RNA genome. The initial outbreak of the pandemic began in December 2019, and it is affecting the human ... ...

Abstract	COVID-19 is caused by the Severe Acute Respiratory Syndrome (SARS) coronavirus (Cov)-2, an enveloped virus with a positive-polarity, single-stranded RNA genome. The initial outbreak of the pandemic began in December 2019, and it is affecting the human health of the global community. In common with previous pandemics (Influenza H1N1 and SARS-CoV) and the epidemics of Middle east respiratory syndrome (MERS)-CoV, CoVs target bronchial and alveolar epithelial cells. Virus protein ligands (e.g., haemagglutinin or trimeric spike glycoprotein for Influenza and CoV, respectively) interact with cellular receptors, such as (depending on the virus) either sialic acids, Dipeptidyl peptidase 4 (DPP4), or angiotensin-converting enzyme 2 (ACE2). Host proteases, e.g., cathepsins, furin, or members of the type II transmembrane serine proteases (TTSP) family, such as Transmembrane protease serine 2 (TMPRSS2), are involved in virus entry by proteolytically activating virus ligands. Also involved are Toll Like Receptor (TLR) family members, which upregulate anti-viral and pro-inflammatory mediators [interleukin (IL)-6 and IL-8 and type I and type III Interferons among others], through the activation of Nuclear Factor (NF)-kB. When these events (virus cellular entry and innate immune responses) are uncontrolled, a deleterious systemic response is sometimes encountered in infected patients, leading to the well-described "cytokine storm" and an ensuing multiple organ failure promoted by a downregulation of dendritic cell, macrophage, and T-cell function. We aim to describe how the lung and systemic host innate immune responses affect survival either positively, through downregulating initial viral load, or negatively, by triggering uncontrolled inflammation. An emphasis will be put on host cellular signaling pathways and proteases involved with a view on tackling these therapeutically.
Mesh-Begriff(e)	Animals ; Antiviral Agents/therapeutic use ; Betacoronavirus/immunology ; COVID-19 ; Coronavirus Infections/drug therapy ; Coronavirus Infections/immunology ; Coronavirus Infections/metabolism ; Drug Delivery Systems ; Epithelial Cells/virology ; Humans ; Immunity, Innate ; Lung/immunology ; Lung/virology ; Mice ; Myeloid Cells/virology ; Pandemics ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/immunology ; Pneumonia, Viral/metabolism ; Receptors, Cell Surface/metabolism ; Receptors, Coronavirus ; Receptors, Virus/metabolism ; SARS-CoV-2 ; Serine Proteases/metabolism ; Signal Transduction ; Virus Internalization ; COVID-19 Drug Treatment
Chemische Substanzen	Antiviral Agents ; Receptors, Cell Surface ; Receptors, Coronavirus ; Receptors, Virus ; Serine Proteases (EC 3.4.-)
Schlagwörter	covid19
Sprache	Englisch
Erscheinungsdatum	2020-05-28
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01229
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Septin-dependent defense mechanisms against Pseudomonas aeruginosa are stalled in cystic fibrosis bronchial epithelial cells.

Brax, Sylvain / Gaudin, Clémence / Calmel, Claire / Boëlle, Pierre-Yves / Corvol, Harriet / Ruffin, Manon / Guillot, Loïc

European journal of cell biology

2024 Band 103, Heft 2, Seite(n) 151416

Abstract: Airway epithelial cells form a physical barrier against inhaled pathogens and coordinate innate immune responses in the lungs. Bronchial cells in people with cystic fibrosis (pwCF) are colonized by Pseudomonas aeruginosa because of the accumulation of ... ...

Abstract	Airway epithelial cells form a physical barrier against inhaled pathogens and coordinate innate immune responses in the lungs. Bronchial cells in people with cystic fibrosis (pwCF) are colonized by Pseudomonas aeruginosa because of the accumulation of mucus in the lower airways and an altered immune response. This leads to chronic inflammation, lung tissue damage, and accelerated decline in lung function. Thus, identifying the molecular factors involved in the host response in the airways is crucial for developing new therapeutic strategies. The septin (SEPT) cytoskeleton is involved in tissue barrier integrity and anti-infective responses. SEPT7 is critical for maintaining SEPT complexes and for sensing pathogenic microbes. In the lungs, SEPT7 may be involved in the epithelial barrier resistance to infection; however, its role in cystic fibrosis (CF) P. aeruginosa infection is unknown. This study aimed to investigate the role of SEPT7 in controlling P. aeruginosa infection in bronchial epithelial cells, particularly in CF. The study findings showed that SEPT7 encages P. aeruginosa in bronchial epithelial cells and its inhibition downregulates the expression of other SEPTs. In addition, P. aeruginosa does not regulate SEPT7 expression. Finally, we found that inhibiting SEPT7 expression in bronchial epithelial cells (BEAS-2B 16HBE14o- and primary cells) resulted in higher levels of internalized P. aeruginosa and decreased IL-6 production during infection, suggesting a crucial role of SEPT7 in the host response against this bacterium. However, these effects were not observed in the CF cells (16HBE14o-/F508del and primary cells) which may explain the persistence of infection in pwCF. The study findings suggest the modification of SEPT7 expression as a potential approach for the anti-infective control of P. aeruginosa, particularly in CF.
Sprache	Englisch
Erscheinungsdatum	2024-04-15
Erscheinungsland	Germany
Dokumenttyp	Journal Article
ZDB-ID	391967-5
ISSN	1618-1298 ; 0070-2463 ; 0171-9335
ISSN (online)	1618-1298
ISSN	0070-2463 ; 0171-9335
DOI	10.1016/j.ejcb.2024.151416
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Airway infections as a risk factor for Pseudomonas aeruginosa acquisition and chronic colonisation in children with cystic fibrosis.

Mésinèle, Julie / Ruffin, Manon / Guillot, Loïc / Boëlle, Pierre-Yves / Corvol, Harriet

Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society

2023 Band 22, Heft 5, Seite(n) 901–908

Abstract: Background: Pseudomonas aeruginosa (Pa) infection is detrimental to people with cystic fibrosis (pwCF). Several clinical and genetic factors predispose to early Pa infections. However, the role of earlier infections with other pathogens on the risk of ... ...

Abstract	Background: Pseudomonas aeruginosa (Pa) infection is detrimental to people with cystic fibrosis (pwCF). Several clinical and genetic factors predispose to early Pa infections. However, the role of earlier infections with other pathogens on the risk of Pa infection in paediatric pwCF remains unknown. Methods: Using Kaplan-Meier method, we computed the cumulative incidences of bacterial and fungal initial acquisition (IA) and chronic colonisation (CC) in 1,231 French pwCF under 18 years of age for methicillin-susceptible and resistant Staphylococcus aureus (MSSA and MRSA), Stenotrophomonas maltophilia, Haemophilus influenzae, Achromobacter xylosoxidans, and Aspergillus species. Previous infections were analysed as Pa-IA and Pa-CC risk factors using Cox regression models. Results: By 2 years of age, 65.5% pwCF had experienced at least one bacterial or fungal IA, and 27.9% had experienced at least one CC. The median age of Pa-IA was 5.1 years, and Pa-CC was present in 25% pwCF by 14.7 years. While 50% acquired MSSA at 2.1 years, 50% progressed to chronic MSSA colonisation at 8.4 years. At 7.9 and 9.7 years, 25% pwCF were infected by S. maltophilia and Aspergillus spp., respectively. The risk of Pa-IA and Pa-CC increased with IAs of all other species, with hazard ratios (HR) up to 2.19 (95% Confidence interval (CI) 1.18-4.07). The risk of Pa-IA increased with the number of previous bacterial/fungal IAs (HR=1.89, 95% CI 1.57-2.28), with a 16% increase per additional pathogen; same trend was noted for Pa-CC. Conclusions: This study establishes that the microbial community in CF airways can modulate Pa occurrence. At the dawn of targeted therapies, it paves the way for characterizing future trends and evolution of infections.
Mesh-Begriff(e)	Child ; Humans ; Adolescent ; Child, Preschool ; Aged ; Cystic Fibrosis/complications ; Cystic Fibrosis/epidemiology ; Cystic Fibrosis/microbiology ; Pseudomonas aeruginosa ; Methicillin-Resistant Staphylococcus aureus ; Respiratory System ; Pseudomonas Infections/diagnosis ; Pseudomonas Infections/epidemiology ; Pseudomonas Infections/microbiology ; Staphylococcus aureus ; Bacteria ; Risk Factors
Sprache	Englisch
Erscheinungsdatum	2023-07-06
Erscheinungsland	Netherlands
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2084724-5
ISSN	1873-5010 ; 1569-1993
ISSN (online)	1873-5010
ISSN	1569-1993
DOI	10.1016/j.jcf.2023.06.007
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Innate Immune Signaling and Proteolytic Pathways in the Resolution or Exacerbation of SARS-CoV-2 in Covid-19

Sallenave, Jean-Michel / Guillot, Loïc

Frontiers in Immunology

Key Therapeutic Targets?

2020 Band 11

Schlagwörter	covid19
Verlag	Frontiers Media SA
Erscheinungsland	ch
Dokumenttyp	Artikel ; Online
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01229
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel: Innate Immune Signaling and Proteolytic Pathways in the Resolution or Exacerbation of SARS-CoV-2 in Covid-19: Key Therapeutic Targets?

Sallenave, Jean-Michel / Guillot, Loïc

Front Immunol

Abstract	COVID-19 is caused by the Severe Acute Respiratory Syndrome (SARS) coronavirus (Cov)-2, an enveloped virus with a positive-polarity, single-stranded RNA genome. The initial outbreak of the pandemic began in December 2019, and it is affecting the human health of the global community. In common with previous pandemics (Influenza H1N1 and SARS-CoV) and the epidemics of Middle east respiratory syndrome (MERS)-CoV, CoVs target bronchial and alveolar epithelial cells. Virus protein ligands (e.g., haemagglutinin or trimeric spike glycoprotein for Influenza and CoV, respectively) interact with cellular receptors, such as (depending on the virus) either sialic acids, Dipeptidyl peptidase 4 (DPP4), or angiotensin-converting enzyme 2 (ACE2). Host proteases, e.g., cathepsins, furin, or members of the type II transmembrane serine proteases (TTSP) family, such as Transmembrane protease serine 2 (TMPRSS2), are involved in virus entry by proteolytically activating virus ligands. Also involved are Toll Like Receptor (TLR) family members, which upregulate anti-viral and pro-inflammatory mediators [interleukin (IL)-6 and IL-8 and type I and type III Interferons among others], through the activation of Nuclear Factor (NF)-kB. When these events (virus cellular entry and innate immune responses) are uncontrolled, a deleterious systemic response is sometimes encountered in infected patients, leading to the well-described "cytokine storm" and an ensuing multiple organ failure promoted by a downregulation of dendritic cell, macrophage, and T-cell function. We aim to describe how the lung and systemic host innate immune responses affect survival either positively, through downregulating initial viral load, or negatively, by triggering uncontrolled inflammation. An emphasis will be put on host cellular signaling pathways and proteases involved with a view on tackling these therapeutically.
Schlagwörter	covid19
Verlag	WHO
Dokumenttyp	Artikel
Anmerkung	WHO #Covidence: #612918
Datenquelle	COVID19

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Artikel ; Online: Innate Immune Signaling and Proteolytic Pathways in the Resolution or Exacerbation of SARS-CoV-2 in Covid-19

Sallenave, Jean-Michel / Guillot, Loïc

ISSN: 1664-3224 ; EISSN: 1664-3224 ; Frontiers in Immunology ; https://hal.sorbonne-universite.fr/hal-02898083 ; Frontiers in Immunology, Frontiers, 2020, 11, pp.1229. ⟨10.3389/fimmu.2020.01229⟩

Key Therapeutic Targets?

2020

Abstract: International audience ... COVID-19 is caused by the Severe Acute Respiratory Syndrome (SARS) coronavirus (Cov)-2, an enveloped virus with a positive-polarity, single-stranded RNA genome. The initial outbreak of the pandemic began in December 2019, and it ... ...

Abstract	International audience COVID-19 is caused by the Severe Acute Respiratory Syndrome (SARS) coronavirus (Cov)-2, an enveloped virus with a positive-polarity, single-stranded RNA genome. The initial outbreak of the pandemic began in December 2019, and it is affecting the human health of the global community. In common with previous pandemics (Influenza H1N1 and SARS-CoV) and the epidemics of Middle east respiratory syndrome (MERS)-CoV, CoVs target bronchial and alveolar epithelial cells. Virus protein ligands (e.g., haemagglutinin or trimeric spike glycoprotein for Influenza and CoV, respectively) interact with cellular receptors, such as (depending on the virus) either sialic acids, Dipeptidyl peptidase 4 (DPP4), or angiotensin-converting enzyme 2 (ACE2). Host proteases, e.g., cathepsins, furin, or members of the type II transmembrane serine proteases (TTSP) family, such as Transmembrane protease serine 2 (TMPRSS2), are involved in virus entry by proteolytically activating virus ligands. Also involved are Toll Like Receptor (TLR) family members, which upregulate anti-viral and pro-inflammatory mediators [interleukin (IL)-6 and IL-8 and type I and type III Interferons among others], through the activation of Nuclear Factor (NF)-kB. When these events (virus cellular entry and innate immune responses) are uncontrolled, a deleterious systemic response is sometimes encountered in infected patients, leading to the well-described "cytokine storm" and an ensuing multiple organ failure promoted by a downregulation of dendritic cell, macrophage, and T-cell function. We aim to describe how the lung and systemic host innate immune responses affect survival either positively, through downregulating initial viral load, or negatively, by triggering uncontrolled inflammation. An emphasis will be put on host cellular signaling pathways and proteases involved with a view on tackling these therapeutically.
Schlagwörter	COVID-19 ; SARS-CoV-2 ; coronavirus ; lung innate immunity ; protease ; [SDV]Life Sciences [q-bio] ; [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology ; covid19
Thema/Rubrik (Code)	572
Sprache	Englisch
Erscheinungsdatum	2020-05-28
Verlag	HAL CCSD
Erscheinungsland	fr
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel ; Online: Innate Immune Signaling and Proteolytic Pathways in the Resolution or Exacerbation of SARS-CoV-2 in Covid-19

Sallenave, Jean-Michel / Guillot, Loïc

ISSN: 1664-3224 ; EISSN: 1664-3224 ; Frontiers in Immunology ; https://hal.sorbonne-universite.fr/hal-02898083 ; Frontiers in Immunology, Frontiers, 2020, 11, pp.1229. ⟨10.3389/fimmu.2020.01229⟩

Key Therapeutic Targets?

2020

Abstract	International audience COVID-19 is caused by the Severe Acute Respiratory Syndrome (SARS) coronavirus (Cov)-2, an enveloped virus with a positive-polarity, single-stranded RNA genome. The initial outbreak of the pandemic began in December 2019, and it is affecting the human health of the global community. In common with previous pandemics (Influenza H1N1 and SARS-CoV) and the epidemics of Middle east respiratory syndrome (MERS)-CoV, CoVs target bronchial and alveolar epithelial cells. Virus protein ligands (e.g., haemagglutinin or trimeric spike glycoprotein for Influenza and CoV, respectively) interact with cellular receptors, such as (depending on the virus) either sialic acids, Dipeptidyl peptidase 4 (DPP4), or angiotensin-converting enzyme 2 (ACE2). Host proteases, e.g., cathepsins, furin, or members of the type II transmembrane serine proteases (TTSP) family, such as Transmembrane protease serine 2 (TMPRSS2), are involved in virus entry by proteolytically activating virus ligands. Also involved are Toll Like Receptor (TLR) family members, which upregulate anti-viral and pro-inflammatory mediators [interleukin (IL)-6 and IL-8 and type I and type III Interferons among others], through the activation of Nuclear Factor (NF)-kB. When these events (virus cellular entry and innate immune responses) are uncontrolled, a deleterious systemic response is sometimes encountered in infected patients, leading to the well-described "cytokine storm" and an ensuing multiple organ failure promoted by a downregulation of dendritic cell, macrophage, and T-cell function. We aim to describe how the lung and systemic host innate immune responses affect survival either positively, through downregulating initial viral load, or negatively, by triggering uncontrolled inflammation. An emphasis will be put on host cellular signaling pathways and proteases involved with a view on tackling these therapeutically.
Schlagwörter	COVID-19 ; SARS-CoV-2 ; coronavirus ; lung innate immunity ; protease ; [SDV]Life Sciences [q-bio] ; [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology ; covid19
Thema/Rubrik (Code)	572
Sprache	Englisch
Erscheinungsdatum	2020-05-28
Verlag	HAL CCSD
Erscheinungsland	fr
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Buch ; Online: Host signaling and proteolytic pathways in the resolution or the exacerbation of coronavirus (CoV-2) infection in COVID-19 disease

SALLENAVE, Jean-Michel / Guillot, Loic

what therapeutic targets?

2020

Abstract: COVID-19 is caused by the Severe Acute Respiratory Syndrome (SARS) coronavirus (Cov)-2, an enveloped virus with a positive single-stranded RNA genome. Pandemic initial outbreak began in December 2019 and is threatening the health of the global community. ...

Abstract	COVID-19 is caused by the Severe Acute Respiratory Syndrome (SARS) coronavirus (Cov)-2, an enveloped virus with a positive single-stranded RNA genome. Pandemic initial outbreak began in December 2019 and is threatening the health of the global community. In common with previous pandemics (Influenza H1N1, SARS-CoV-1) and the epidemics of Middle east respiratory syndrome (MERS)-CoV, CoVs target bronchial and alveolar epithelial cells. Virus proteins ligands (eg haemagglutinin or spike protein for Influenza and CoV, respectively) interact with cellular receptors such as (depending on the virus), either sialic acids, Dipeptidyl peptidase 4 (DPP4), or angiotensin-converting enzyme 2 (ACE2). Host proteases, eg cathepsins, furin, or members of the type II transmembrane serine proteases (TTSP) family such as Transmembrane protease serine 2 (TMPRSS2) are involved in virus entry by proteolytically activating virus ligands. Also involved are Toll Like Receptor (TLR) familly members which up-regulate anti-viral and pro-inflammatory mediators (interleukin (IL)-6 and IL-8...), through the activation of Nuclear Factor (NF)-kB. When these events (virus cellular entry and innate immune responses) are uncontrolled, a deleterious systemic response is sometimes encountered in infected patients, leading to the well described ‘cytokine storm’ and an ensuing multiple organ failure, promoted by a down-regulation of dendritic cells, macrophage and T cell function.We aim to describe how the lung and systemic host innate immune responses affect survival either positively, through down-regulating initial viral load, or negatively, by triggering uncontrolled inflammation. An emphasis will be put on host cellular signaling pathways and proteases involved, with a view on tackling these therapeutically.
Schlagwörter	covid19
Verlag	Center for Open Science
Erscheinungsland	us
Dokumenttyp	Buch ; Online
DOI	10.31219/osf.io/rtfmx
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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