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Article ; Online: Oxidative profile, inflammatory responses and δ-aminolevulinate dehydratase enzyme activity in influenza B virus infection.

Bulegon, Jovana Simonetti / Weber, Andressa de Azambuja Pias / de Souza, Manoela Dias / Viero, Fernanda Tibolla / Pillat, Micheli Mainardi / Gonçalves, Thissiane de Lima

Pathogens and disease

2023 Volume 81

Abstract: ... with influenza B virus (IBV). To evaluate the activity of the δ-ALA-D enzyme, lipid peroxidation was estimated ... understanding of oxidative and inflammatory pathways during IBV infection. ...

Abstract	The aim of the current study was to determine the activity of the delta-aminolevulinate dehydratase (δ-ALA-D) enzyme, oxidative stress biomarkers and the expression of cytokines in those infected with influenza B virus (IBV). To evaluate the activity of the δ-ALA-D enzyme, lipid peroxidation was estimated as levels of thiobarbituric acid reactive substances, protein and non-protein thiol groups, ferric-reducing antioxidant power (FRAP), vitamin C concentration and cytokine levels in IBV-infected individuals (n = 50) and a control group (n = 30). δ-ALA-D activity was significantly lower in IBV-infected individuals compared with controls, as well as levels of thiols, vitamin C and FRAP. Lipid peroxidation and cytokine levels of IL-6, IL-10, IL-17A and IFN-y were statistically higher in the IBV group. In conclusion, we found evidence of the generation of oxidants, the depletion of the antioxidant system, decrease in the activity of the δ-ALA-D enzyme and an increase in the synthesis of cytokines, thus contributing to a better understanding of oxidative and inflammatory pathways during IBV infection.
MeSH term(s)	Humans ; Antioxidants ; Porphobilinogen Synthase/metabolism ; Influenza B virus/metabolism ; Influenza, Human ; Oxidative Stress ; Ascorbic Acid ; Iron ; Cytokines/metabolism ; Herpesviridae Infections
Chemical Substances	Antioxidants ; Porphobilinogen Synthase (EC 4.2.1.24) ; Ascorbic Acid (PQ6CK8PD0R) ; Iron (E1UOL152H7) ; Cytokines
Language	English
Publishing date	2023-10-10
Publishing country	United States
Document type	Journal Article
ISSN	2049-632X
ISSN (online)	2049-632X
DOI	10.1093/femspd/ftad028
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Article ; Online: The pro-inflammatory response to influenza A virus infection is fueled by endothelial cells.

Bauer, Lisa / Rijsbergen, Laurine C / Leijten, Lonneke / Benavides, Feline Fw / Noack, Danny / Lamers, Mart M / Haagmans, Bart L / de Vries, Rory D / de Swart, Rik L / van Riel, Debby

Life science alliance

2023 Volume 6, Issue 7

Abstract: ... Endothelial cells play a key role in systemic inflammatory responses during severe influenza A virus (IAV ... and H3N2 viruses and assessed the associated pro-inflammatory responses. Despite the detection of IAV ... Morbidity and mortality from influenza are associated with high levels of systemic inflammation ...

Abstract	Morbidity and mortality from influenza are associated with high levels of systemic inflammation. Endothelial cells play a key role in systemic inflammatory responses during severe influenza A virus (IAV) infections, despite being rarely infected in humans. How endothelial cells contribute to systemic inflammatory responses is unclear. Here, we developed a transwell system in which airway organoid-derived differentiated human lung epithelial cells were co-cultured with primary human lung microvascular endothelial cells (LMECs). We compared the susceptibility of LMECs to pandemic H1N1 virus and recent seasonal H1N1 and H3N2 viruses and assessed the associated pro-inflammatory responses. Despite the detection of IAV nucleoprotein in LMEC mono-cultures, there was no evidence for productive infection. In epithelial-endothelial co-cultures, abundant IAV infection of epithelial cells resulted in the breakdown of the epithelial barrier, but infection of LMECs was rarely detected. We observed a significantly higher secretion of pro-inflammatory cytokines in LMECs when co-cultured with IAV-infected epithelial cells than LMEC mono-cultures exposed to IAV. Taken together, our data show that LMECs are abortively infected by IAV but can fuel the inflammatory response.
MeSH term(s)	Humans ; Influenza, Human/metabolism ; Endothelial Cells/metabolism ; Influenza A Virus, H1N1 Subtype ; Influenza A Virus, H3N2 Subtype ; Influenza A virus
Language	English
Publishing date	2023-04-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202201837
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Article ; Online: Inflammatory and antiviral responses to influenza A virus infection are dysregulated in pregnant mice with allergic airway disease.

Vanders, Rebecca L / Gomez, Henry M / Hsu, Alan C / Daly, Katie / Wark, Peter A B / Horvat, Jay C / Hansbro, Philip M

American journal of physiology. Lung cellular and molecular physiology

2023 Volume 325, Issue 3, Page(s) L385–L398

Abstract: Influenza A virus (IAV) infections are increased during pregnancy especially with asthma ... we induced IAV infection. We assessed viral titers, airway inflammation, lung antiviral responses, mucus ... hypersecretion, and airway hyperresponsiveness (AHR). During early IAV infection, pregnant mice with AAD had ...

Abstract	Influenza A virus (IAV) infections are increased during pregnancy especially with asthma as a comorbidity, leading to asthma exacerbations, secondary bacterial infections, intensive care unit admissions, and mortality. We aimed to define the processes involved in increased susceptibility and severity of IAV infections during pregnancy, especially with asthma. We sensitized mice to house dust mite (HDM), induced pregnancy, and challenged with HDM to induce allergic airway disease (AAD). At midpregnancy, we induced IAV infection. We assessed viral titers, airway inflammation, lung antiviral responses, mucus hypersecretion, and airway hyperresponsiveness (AHR). During early IAV infection, pregnant mice with AAD had increased mRNA expression of the inflammatory markers
MeSH term(s)	Pregnancy ; Female ; Mice ; Animals ; Humans ; Cytokines/metabolism ; Hyperplasia/pathology ; beta-Defensins ; Asthma/pathology ; Lung/metabolism ; Respiration Disorders ; Respiratory Hypersensitivity/pathology ; Influenza A virus ; Influenza, Human/pathology ; Antiviral Agents/therapeutic use ; RNA, Messenger ; Pyroglyphidae ; Disease Models, Animal
Chemical Substances	Cytokines ; beta-Defensins ; Antiviral Agents ; RNA, Messenger
Language	English
Publishing date	2023-07-18
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.00232.2022
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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: Influenza A Virus Exacerbates Group A Streptococcus Infection and Thwarts Anti-Bacterial Inflammatory Responses in Murine Macrophages.

Aleith, Johann / Brendel, Maria / Weipert, Erik / Müller, Michael / Schultz, Daniel / Ko-Infekt Study Group / Müller-Hilke, Brigitte

Pathogens (Basel, Switzerland)

2022 Volume 11, Issue 11

Abstract: ... accumulating evidence revealed that influenza A virus (IAV) renders the host vulnerable to bacterial ... Seasonal influenza epidemics pose a considerable hazard for global health. In the past decades ... of influenza on anti-bacterial innate immunity is restricted to the vicinity of the lung or systemically ...

Abstract	Seasonal influenza epidemics pose a considerable hazard for global health. In the past decades, accumulating evidence revealed that influenza A virus (IAV) renders the host vulnerable to bacterial superinfections which in turn are a major cause for morbidity and mortality. However, whether the impact of influenza on anti-bacterial innate immunity is restricted to the vicinity of the lung or systemically extends to remote sites is underexplored. We therefore sought to investigate intranasal infection of adult C57BL/6J mice with IAV H1N1 in combination with bacteremia elicited by intravenous application of Group A Streptococcus (GAS). Co-infection in vivo was supplemented in vitro by challenging murine bone marrow derived macrophages and exploring gene expression and cytokine secretion. Our results show that viral infection of mice caused mild disease and induced the depletion of CCL2 in the periphery. Influenza preceding GAS infection promoted the occurrence of paw edemas and was accompanied by exacerbated disease scores. In vitro co-infection of macrophages led to significantly elevated expression of TLR2 and CD80 compared to bacterial mono-infection, whereas CD163 and CD206 were downregulated. The GAS-inducible upregulation of inflammatory genes, such as Nos2, as well as the secretion of TNFα and IL-1β were notably reduced or even abrogated following co-infection. Our results indicate that IAV primes an innate immune layout that is inadequately equipped for bacterial clearance.
Language	English
Publishing date	2022-11-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2695572-6
ISSN	2076-0817
ISSN	2076-0817
DOI	10.3390/pathogens11111320
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Article ; Online: NMP4: a nuclear driver of innate inflammatory responses during influenza A virus infection.

Boehme, Julia D / Frentzel, Sarah / Bruder, Dunja

Cellular & molecular immunology

2020 Volume 17, Issue 12, Page(s) 1220–1221

MeSH term(s)	Animals ; Humans ; Inflammation/immunology ; Influenza A virus/immunology ; Influenza, Human/immunology ; Influenza, Human/virology ; Lung/immunology ; Lung/virology ; Mice ; Organ Specificity ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/virology ; Transcription Factors/deficiency ; Transcription Factors/metabolism
Chemical Substances	Transcription Factors
Keywords	covid19
Language	English
Publishing date	2020-08-03
Publishing country	China
Document type	Journal Article
ZDB-ID	2435097-7
ISSN	2042-0226 ; 1672-7681
ISSN (online)	2042-0226
ISSN	1672-7681
DOI	10.1038/s41423-020-0517-5
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Zs.A 6681: Show issues

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bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Pyruvate affects inflammatory responses of macrophages during influenza A virus infection.

Abusalamah, Hazar / Reel, Jessica M / Lupfer, Christopher R

Virus research

2020 Volume 286, Page(s) 198088

Abstract: ... with influenza A virus impaired cytokine production (IL-6, IL-1β, and TNF-α). Sodium pyruvate did not inhibit viral RNA ... the immune response produced by macrophages but does not inhibit virus replication. ... of sodium pyruvate in culture media during infection of mouse bone marrow derived macrophages ...

Abstract	Pyruvate is the end product of glycolysis and transported into the mitochondria for use in the tricarboxylic acid (TCA) cycle. It is also a common additive in cell culture media. We discovered that inclusion of sodium pyruvate in culture media during infection of mouse bone marrow derived macrophages with influenza A virus impaired cytokine production (IL-6, IL-1β, and TNF-α). Sodium pyruvate did not inhibit viral RNA replication. Instead, the addition of sodium pyruvate alters cellular metabolism and diminished mitochondrial reactive oxygen species (ROS) production and lowered immune signaling. Overall, sodium pyruvate affects the immune response produced by macrophages but does not inhibit virus replication.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Cells, Cultured ; Culture Media/chemistry ; Gene Expression ; Immunity, Innate/drug effects ; Inflammasomes/drug effects ; Inflammasomes/metabolism ; Inflammation/immunology ; Inflammation/virology ; Influenza A virus/drug effects ; Macrophages/drug effects ; Macrophages/immunology ; Macrophages/virology ; Mice ; Mice, Inbred C57BL ; Pyruvic Acid/pharmacology ; Virus Replication/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Culture Media ; Inflammasomes ; Pyruvic Acid (8558G7RUTR)
Keywords	covid19
Language	English
Publishing date	2020-07-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605780-9
ISSN	1872-7492 ; 0168-1702
ISSN (online)	1872-7492
ISSN	0168-1702
DOI	10.1016/j.virusres.2020.198088
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Zs.A 1965: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article: Infectious Bronchitis Virus Infection Increases Pathogenicity of H9N2 Avian Influenza Virus by Inducing Severe Inflammatory Response.

Kong, Lingchen / You, Renrong / Zhang, Dianchen / Yuan, Qingli / Xiang, Bin / Liang, Jianpeng / Lin, Qiuyan / Ding, Chan / Liao, Ming / Chen, Libin / Ren, Tao

Frontiers in veterinary science

2022 Volume 8, Page(s) 824179

Abstract: Infectious bronchitis virus (IBV) and H9N2 avian influenza virus (AIV) are frequently identified ... H9N2 groups. In general, a higher virus load and a more intense inflammatory response were observed ... of respiratory disease in chickens, and secondary infection with H9N2 virus further enhances the pathogenicity ...

Abstract	Infectious bronchitis virus (IBV) and H9N2 avian influenza virus (AIV) are frequently identified in chickens with respiratory disease. However, the role and mechanism of IBV and H9N2 AIV co-infection remain largely unknown. Specific-pathogen-free (SPF) chickens were inoculated with IBV 2 days before H9N2 virus inoculation (IBV/H9N2); with IBV and H9N2 virus simultaneously (IBV+H9N2); with H9N2 virus 2 days before IBV inoculation (H9N2/IBV); or with either IBV or H9N2 virus alone. Severe respiratory signs, pathological damage, and higher morbidity and mortality were observed in the co-infection groups compared with the IBV and H9N2 groups. In general, a higher virus load and a more intense inflammatory response were observed in the three co-infection groups, especially in the IBV/H9N2 group. The same results were observed in the transcriptome analysis of the trachea of the SPF chickens. Therefore, IBV might play a major role in the development of respiratory disease in chickens, and secondary infection with H9N2 virus further enhances the pathogenicity by inducing a severe inflammatory response. These findings may provide a reference for the prevention and control of IBV and H9N2 AIV in the poultry industry and provide insight into the molecular mechanisms of IBV and H9N2 AIV co-infection in chickens.
Language	English
Publishing date	2022-02-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2834243-4
ISSN	2297-1769
ISSN	2297-1769
DOI	10.3389/fvets.2021.824179
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Article ; Online: Human C1q Regulates Influenza A Virus Infection and Inflammatory Response via Its Globular Domain.

Varghese, Praveen M / Kishore, Uday / Rajkumari, Reena

International journal of molecular sciences

2022 Volume 23, Issue 6

Abstract: The Influenza A virus (IAV) is a severe respiratory pathogen. C1q is the first subcomponent ... independent modulation by C1q and its individual recombinant globular heads against IAV infection ... response in H1N1 and pro-inflammatory response in H3N2-infected cells as evident from differential ...

Abstract	The Influenza A virus (IAV) is a severe respiratory pathogen. C1q is the first subcomponent of the complement system's classical pathway. C1q is composed of 18 polypeptide chains. Each of these chains contains a collagen-like region located at the N terminus, and a C-terminal globular head region organized as a heterotrimeric structure (ghA, ghB and ghC). This study was aimed at investigating the complement activation-independent modulation by C1q and its individual recombinant globular heads against IAV infection. The interaction of C1q and its recombinant globular heads with IAV and its purified glycoproteins was examined using direct ELISA and far-Western blotting analysis. The effect of the complement proteins on IAV replication kinetics and immune modulation was assessed by qPCR. The IAV entry inhibitory properties of C1q and its recombinant globular heads were confirmed using cell binding and luciferase reporter assays. C1q bound IAV virions via HA, NA and M1 IAV proteins, and suppressed replication in H1N1, while promoting replication in H3N2-infected A549 cells. C1q treatment further triggered an anti-inflammatory response in H1N1 and pro-inflammatory response in H3N2-infected cells as evident from differential expression of TNF-α, NF-κB, IFN-α, IFN-β, IL-6, IL-12 and RANTES. Furthermore, C1q treatment was found to reduce luciferase reporter activity of MDCK cells transfected with H1N1 pseudotyped lentiviral particles, indicative of an entry inhibitory role of C1q against infectivity of IAV. These data appear to demonstrate the complement-independent subtype specific modulation of IAV infection by locally produced C1q.
MeSH term(s)	Complement C1q ; Complement System Proteins ; Humans ; Influenza A Virus, H1N1 Subtype ; Influenza A Virus, H3N2 Subtype ; Influenza A virus ; Influenza, Human
Chemical Substances	Complement C1q (80295-33-6) ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2022-03-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23063045
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Article ; Online: Influenza A Virus Exacerbates Group A Streptococcus Infection and Thwarts Anti-Bacterial Inflammatory Responses in Murine Macrophages

Aleith, Johann / Brendel, Maria / Weipert, Erik / Müller, Michael / Schultz, Daniel / Ko-Infekt Study Group / Müller-Hilke, Brigitte / Ko-Infekt Study Group: / Methling, Karen / Lalk, Michael / Blohm, Ulrike / Schäfer, Alexander / Kreikemeyer, Bernd

2022

Abstract	Seasonal influenza epidemics pose a considerable hazard for global health. In the past decades, accumulating evidence revealed that influenza A virus (IAV) renders the host vulnerable to bacterial superinfections which in turn are a major cause for morbidity and mortality. However, whether the impact of influenza on anti-bacterial innate immunity is restricted to the vicinity of the lung or systemically extends to remote sites is underexplored. We therefore sought to investigate intranasal infection of adult C57BL/6J mice with IAV H1N1 in combination with bacteremia elicited by intravenous application of Group A Streptococcus (GAS). Co-infection in vivo was supplemented in vitro by challenging murine bone marrow derived macrophages and exploring gene expression and cytokine secretion. Our results show that viral infection of mice caused mild disease and induced the depletion of CCL2 in the periphery. Influenza preceding GAS infection promoted the occurrence of paw edemas and was accompanied by exacerbated disease scores. In vitro co-infection of macrophages led to significantly elevated expression of TLR2 and CD80 compared to bacterial mono-infection, whereas CD163 and CD206 were downregulated. The GAS-inducible upregulation of inflammatory genes, such as Nos2, as well as the secretion of TNFα and IL-1β were notably reduced or even abrogated following co-infection. Our results indicate that IAV primes an innate immune layout that is inadequately equipped for bacterial clearance.
Keywords	Text ; ddc:570 ; influenza A virus -- Group A Streptococcus -- co-infection -- inflammation -- sepsis -- macrophage -- innate immunity
Subject code	570
Language	English
Publishing date	2022-11-10
Publishing country	de
Document type	Article ; Online
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Article ; Online: Influenza A Virus Exacerbates Group A Streptococcus Infection and Thwarts Anti-Bacterial Inflammatory Responses in Murine Macrophages

Johann Aleith / Maria Brendel / Erik Weipert / Michael Müller / Daniel Schultz / Ko-Infekt Study Group / Brigitte Müller-Hilke

Pathogens, Vol 11, Iss 1320, p

2022 Volume 1320

Abstract	Seasonal influenza epidemics pose a considerable hazard for global health. In the past decades, accumulating evidence revealed that influenza A virus (IAV) renders the host vulnerable to bacterial superinfections which in turn are a major cause for morbidity and mortality. However, whether the impact of influenza on anti-bacterial innate immunity is restricted to the vicinity of the lung or systemically extends to remote sites is underexplored. We therefore sought to investigate intranasal infection of adult C57BL/6J mice with IAV H1N1 in combination with bacteremia elicited by intravenous application of Group A Streptococcus (GAS). Co-infection in vivo was supplemented in vitro by challenging murine bone marrow derived macrophages and exploring gene expression and cytokine secretion. Our results show that viral infection of mice caused mild disease and induced the depletion of CCL2 in the periphery. Influenza preceding GAS infection promoted the occurrence of paw edemas and was accompanied by exacerbated disease scores. In vitro co-infection of macrophages led to significantly elevated expression of TLR2 and CD80 compared to bacterial mono-infection, whereas CD163 and CD206 were downregulated. The GAS-inducible upregulation of inflammatory genes, such as Nos2, as well as the secretion of TNFα and IL-1β were notably reduced or even abrogated following co-infection. Our results indicate that IAV primes an innate immune layout that is inadequately equipped for bacterial clearance.
Keywords	influenza A virus ; Group A Streptococcus ; co-infection ; inflammation ; sepsis ; macrophage ; Medicine ; R
Subject code	570
Language	English
Publishing date	2022-11-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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