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Article ; Online: Environmentally persistent free radicals enhance SARS-CoV-2 replication in respiratory epithelium.

Yamamoto, Ayaho / Sly, Peter D / Chew, Keng Yih / Khachatryan, Lavrent / Begum, Nelufa / Yeo, Abrey J / Vu, Luan D / Short, Kirsty R / Cormier, Stephania A / Fantino, Emmanuelle

Experimental biology and medicine (Maywood, N.J.)

2023 Volume 248, Issue 3, Page(s) 271–279

Abstract: Epidemiological evidence links lower air quality with increased incidence and severity of COVID-19; however, mechanistic data have yet to be published. We hypothesized air pollution-induced oxidative stress in the nasal epithelium increased viral ... ...

Abstract	Epidemiological evidence links lower air quality with increased incidence and severity of COVID-19; however, mechanistic data have yet to be published. We hypothesized air pollution-induced oxidative stress in the nasal epithelium increased viral replication and inflammation. Nasal epithelial cells (NECs), collected from healthy adults, were grown into a fully differentiated epithelium. NECs were infected with the ancestral strain of SARS-CoV-2. An oxidant combustion by-product found in air pollution, the environmentally persistent free radical (EPFR) DCB230, was used to mimic pollution exposure four hours prior to infection. Some wells were pretreated with antioxidant, astaxanthin, for 24 hours prior to EPFR-DCB230 exposure and/or SARS-CoV-2 infection. Outcomes included viral replication, epithelial integrity, surface receptor expression (
MeSH term(s)	Humans ; SARS-CoV-2/metabolism ; COVID-19/metabolism ; Antioxidants/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Angiotensin-Converting Enzyme 2/metabolism ; Free Radicals/metabolism ; Cytokines/metabolism ; Respiratory Mucosa/metabolism ; Oxidants/metabolism
Chemical Substances	Antioxidants ; Tumor Necrosis Factor-alpha ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; astaxanthine (8XPW32PR7I) ; Free Radicals ; Cytokines ; Oxidants
Language	English
Publishing date	2023-01-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	4015-0
ISSN	1535-3699 ; 1525-1373 ; 0037-9727
ISSN (online)	1535-3699 ; 1525-1373
ISSN	0037-9727
DOI	10.1177/15353702221142616
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Article ; Online: Deficiency in ST2 signaling ameliorates RSV-associated pulmonary hypertension.

Vu, Luan D / Saravia, Jordy / Jaligama, Sridhar / Baboeram Panday, Rajshri V / Sullivan, Ryan D / Mancarella, Salvatore / Cormier, Stephania A / Kimura, Dai

American journal of physiology. Heart and circulatory physiology

2021 Volume 321, Issue 2, Page(s) H309–H317

Abstract: Pulmonary hypertension (PH) observed during respiratory syncytial virus (RSV) bronchiolitis is associated with morbidity and mortality, especially in children with congenital heart disease. Yet, the pathophysiological mechanisms of RSV-associated PH ... ...

Abstract	Pulmonary hypertension (PH) observed during respiratory syncytial virus (RSV) bronchiolitis is associated with morbidity and mortality, especially in children with congenital heart disease. Yet, the pathophysiological mechanisms of RSV-associated PH remain unclear. Therefore, this study aimed to investigate the pathophysiological mechanism of RSV-associated PH. We used a translational mouse model of RSV-associated PH, in which wild-type (WT) and suppression of tumorigenicity 2 (ST2) knockout neonatal mice were infected with RSV at 5 days old and reinfected 4 wk later. The development of PH in WT mice following RSV reinfection was evidenced by elevated right ventricle systolic pressure, shortened pulmonary artery acceleration time (PAT), and decreased PAT/ejection time (ET) ratio. It coincided with the augmentation of periostin and IL-13 expression and increased arginase bioactivity by both arginase 1 and 2 as well as induction of nitric oxide synthase (NOS) uncoupling. Absence of ST2 signaling prevented RSV-reinfected mice from developing PH by suppressing NOS uncoupling. In summary, ST2 signaling was involved in the development of RSV-associated PH. ST2 signaling inhibition may be a novel therapeutic target for RSV-associated PH.
MeSH term(s)	Animals ; Animals, Newborn ; Arginase/genetics ; Arginase/metabolism ; Bronchiolitis, Viral/complications ; Bronchiolitis, Viral/genetics ; Bronchiolitis, Viral/metabolism ; Cell Adhesion Molecules/genetics ; Cell Adhesion Molecules/metabolism ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/metabolism ; Interleukin-1 Receptor-Like 1 Protein/genetics ; Interleukin-13/genetics ; Interleukin-13/metabolism ; Lung/metabolism ; Mice ; Mice, Knockout ; Nitric Oxide Synthase Type I/genetics ; Nitric Oxide Synthase Type I/metabolism ; Nitric Oxide Synthase Type II/genetics ; Nitric Oxide Synthase Type II/metabolism ; Nitric Oxide Synthase Type III/genetics ; Nitric Oxide Synthase Type III/metabolism ; Reinfection ; Respiratory Syncytial Virus Infections/complications ; Respiratory Syncytial Virus Infections/genetics ; Respiratory Syncytial Virus Infections/metabolism ; Respiratory Syncytial Viruses
Chemical Substances	Cell Adhesion Molecules ; Il1rl1 protein, mouse ; Interleukin-1 Receptor-Like 1 Protein ; Interleukin-13 ; Postn protein, mouse ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos1 protein, mouse (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39) ; Nos3 protein, mouse (EC 1.14.13.39) ; Arg1 protein, mouse (EC 3.5.3.1) ; Arg2 protein, mouse (EC 3.5.3.1) ; Arginase (EC 3.5.3.1)
Language	English
Publishing date	2021-06-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00018.2021
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Article ; Online: IL-1β Promotes Expansion of IL-33

Vu, Luan D / Phan, Anh T Q / Hijano, Diego R / Siefker, David T / Tillman, Heather / Cormier, Stephania A

American journal of respiratory cell and molecular biology

2021 Volume 66, Issue 3, Page(s) 312–322

Abstract: Respiratory syncytial virus (RSV)-induced immunopathogenesis and disease severity in neonatal mice and human infants have been related to elevated pulmonary IL-33. Thus, targeting IL-33 has been suggested as a potential therapy for respiratory viral ... ...

Abstract	Respiratory syncytial virus (RSV)-induced immunopathogenesis and disease severity in neonatal mice and human infants have been related to elevated pulmonary IL-33. Thus, targeting IL-33 has been suggested as a potential therapy for respiratory viral infections. Yet, the regulatory mechanisms on IL-33 during early life remain unclear. Here, using a neonatal mouse model of RSV, we demonstrate that IL-1β positively regulates but is not required for RSV-induced expression of pulmonary IL-33 in neonatal mice early after the initial infection. Exogenous IL-1β upregulates RSV-induced IL-33 expression by promoting the proliferation of IL-33
MeSH term(s)	Animals ; Humans ; Interleukin-1beta/pharmacology ; Interleukin-33 ; Lung/pathology ; Mice ; Mice, Inbred BALB C ; Respiratory Syncytial Virus Infections/pathology ; Respiratory Syncytial Virus, Human ; Stem Cells/pathology
Chemical Substances	Interleukin-1beta ; Interleukin-33
Language	English
Publishing date	2021-12-03
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.2021-0313OC
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Article ; Online: Role of Type I Interferon (IFN) in the Respiratory Syncytial Virus (RSV) Immune Response and Disease Severity.

Hijano, Diego R / Vu, Luan D / Kauvar, Lawrence M / Tripp, Ralph A / Polack, Fernando P / Cormier, Stephania A

Frontiers in immunology

2019 Volume 10, Page(s) 566

Abstract: Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract disease in children <2 years of age. Increased morbidity and mortality have been reported in high-risk patients, such as premature infants, patients with cardiac ... ...

Abstract	Respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract disease in children <2 years of age. Increased morbidity and mortality have been reported in high-risk patients, such as premature infants, patients with cardiac disease, and severely immune compromised patients. Severe disease is associated with the virulence of the virus as well as host factors specifically including the innate immune response. The role of type I interferons (IFNs) in the response to RSV infection is important in regulating the rate of virus clearance and in directing the character of the immune response, which is normally associated with protection and less severe disease. Two RSV non-structural proteins, NS1 and NS2, as well as the envelope G glycoprotein are known to suppress type I IFN production and a robust type I IFN response to RSV does not occur in human infants or neonatal mouse models of RSV infection. Additionally, presence of type I IFNs are associated with mild symptoms in infants and administration of IFN-α prior to infection of neonatal mice with RSV reduces immunopathology. This evidence has driven RSV prophylaxis and therapeutic efforts to consider strategies for enhancing type I IFN production.
MeSH term(s)	Animals ; Humans ; Interferon Type I/immunology ; Interleukin-33/physiology ; Mice ; Respiratory Syncytial Virus Infections/immunology ; Respiratory Syncytial Virus Vaccines/immunology ; Toll-Like Receptors/physiology
Chemical Substances	Interferon Type I ; Interleukin-33 ; Respiratory Syncytial Virus Vaccines ; Toll-Like Receptors
Language	English
Publishing date	2019-03-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.00566
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Article ; Online: Elevated Levels of Type 2 Respiratory Innate Lymphoid Cells in Human Infants with Severe Respiratory Syncytial Virus Bronchiolitis.

Vu, Luan D / Siefker, David / Jones, Tamekia L / You, Dahui / Taylor, Ryleigh / DeVincenzo, John / Cormier, Stephania A

American journal of respiratory and critical care medicine

2019 Volume 200, Issue 11, Page(s) 1414–1423

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Bronchiolitis, Viral/immunology ; Bronchiolitis, Viral/pathology ; Female ; Gestational Age ; Humans ; Immunity, Innate ; Infant ; Infant, Newborn ; Interleukins/metabolism ; Lymphocytes/immunology ; Lymphocytes/pathology ; Male ; Respiratory Mucosa/immunology ; Respiratory Mucosa/pathology ; Respiratory Syncytial Virus Infections/immunology ; Respiratory Syncytial Virus Infections/pathology ; Respiratory Syncytial Viruses ; Severity of Illness Index ; Viral Load
Chemical Substances	Interleukins
Language	English
Publishing date	2019-07-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.201812-2366OC
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Article ; Online: Absence of antibody responses to SARS-CoV-2 N protein in COVID-19 vaccine breakthrough cases.

Vu, Luan D / Wallace, Shonta / Phan, Anh Tq / Christofferson, Rebecca C / Turner, Erik / Parker, Sean / Elkind-Hirsch, Karen / Landry, Darrell / Stansbury, Austin / Rose, Rebecca / Nolan, David J / Lamers, Susanna L / Hirezi, Michael / Ogden, Beverly / Cormier, Stephania A

Experimental biology and medicine (Maywood, N.J.)

2022 Volume 247, Issue 21, Page(s) 1923–1936

Abstract: Understanding the risk factors for breakthrough coronavirus disease 2019 (COVID-19) (BC19) is critical to inform policy. Herein, we assessed Delta (Lineage B.1.617.2) variant-specific effectiveness of the BNT162b2 (Pfizer) vaccine and characterized Delta- ...

Abstract	Understanding the risk factors for breakthrough coronavirus disease 2019 (COVID-19) (BC19) is critical to inform policy. Herein, we assessed Delta (Lineage B.1.617.2) variant-specific effectiveness of the BNT162b2 (Pfizer) vaccine and characterized Delta-driven BC19 cases (fully vaccinated individuals who get infected) with known-time-since-vaccination. In this longitudinal prospective study (January 21-October 30, 2021), 90 naïve and 15 convalescent individuals were enrolled at the initiation of vaccination. Samples from 27 unvaccinated individuals with previous laboratory-confirmed COVID-19 diagnosis were collected at a single time point. Longitudinal serology profile (antibodies against severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] S and N proteins) and live-virus-based neutralization capacities were assessed while controlling for age. Sex, age, history of reactions to the COVID-19 vaccine, and viral neutralization capacities were identified as significant risk factors for breakthrough COVID-19. At 8 months postvaccination, male sex, individuals ⩾65 years of age, and individuals who experienced noticeable side effects with the COVID-19 vaccine were at 5.47 (
MeSH term(s)	Male ; Humans ; COVID-19 Vaccines ; Antibody Formation ; SARS-CoV-2 ; BNT162 Vaccine ; COVID-19 Testing ; Prospective Studies ; COVID-19/prevention & control ; Antibodies
Chemical Substances	COVID-19 Vaccines ; BNT162 Vaccine ; Antibodies
Language	English
Publishing date	2022-11-19
Publishing country	England
Document type	Journal Article
ZDB-ID	4015-0
ISSN	1535-3699 ; 1525-1373 ; 0037-9727
ISSN (online)	1535-3699 ; 1525-1373
ISSN	0037-9727
DOI	10.1177/15353702221134097
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Article ; Online: Reduced turnaround times through multi-sectoral community collaboration during the first surge of SARS-CoV-2 and associated effect on patient care and hospital operations.

Christofferson, Rebecca C / O'Neal, Hollis R / Jagneaux, Tonya / O'Neal, Catherine / Walsh, Christine S / Mayton, E Handly / Vu, Luan D / Fish, Abigail I / Phan, Anh / Stoufflet, Thaya E / Schroeder, Jonathan R / Walker, Morgan / Turner, Erik A / Pierce, Christi / Wester, K Scott / DeLeo, Connie / Tenreiro, Edgardo / Ogden, Beverly / Cormier, Stephania A

PloS one

2021 Volume 16, Issue 10, Page(s) e0257302

Abstract: Background: In March 2020, an influx of admissions in COVID-19 positive patients threatened to overwhelm healthcare facilities in East Baton Rouge Parish, Louisiana. Exacerbating this problem was an overall shortage of diagnostic testing capability at ... ...

Abstract	Background: In March 2020, an influx of admissions in COVID-19 positive patients threatened to overwhelm healthcare facilities in East Baton Rouge Parish, Louisiana. Exacerbating this problem was an overall shortage of diagnostic testing capability at that time, resulting in a delay in time-to-result return. An improvement in diagnostic testing availability and timeliness was necessary to improve the allocation of resources and ultimate throughput of patients. The management of a COVID-19 positive patient or patient under investigation requires infection control measures that can quickly consume personal protective equipment (PPE) stores and personnel available to treat these patients. Critical shortages of both PPE and personnel also negatively impact care in patients admitted with non-COVID-19 illnesses. Methods: A multisectoral partnership of healthcare providers, facilities and academicians created a molecular diagnostic lab within an academic research facility dedicated to testing inpatients and healthcare personnel for SARS-CoV-2. The purpose of the laboratory was to provide a temporary solution to the East Baton Rouge Parish healthcare community until individual facilities were self-sustaining in testing capabilities. We describe the partnership and the impacts of this endeavor by developing a model derived from a combination of data sources, including electronic health records, hospital operations, and state and local resources. Findings: Our model demonstrates two important principles: the impact of reduced turnaround times (TAT) on potential differences in inpatient population numbers for COVID-19 and savings in PPE attributed to the more rapid TAT.
MeSH term(s)	COVID-19/epidemiology ; COVID-19/prevention & control ; COVID-19/therapy ; Delivery of Health Care ; Disease Outbreaks ; Female ; Health Personnel ; Humans ; Inpatients ; Louisiana/epidemiology ; Male ; Patient Care ; Personal Protective Equipment ; SARS-CoV-2
Language	English
Publishing date	2021-10-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0257302
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Article ; Online: New mouse model of pulmonary hypertension induced by respiratory syncytial virus bronchiolitis.

Kimura, Dai / Saravia, Jordy / Jaligama, Sridhar / McNamara, Isabella / Vu, Luan D / Sullivan, Ryan D / Mancarella, Salvatore / You, Dahui / Cormier, Stephania A

American journal of physiology. Heart and circulatory physiology

2018 Volume 315, Issue 3, Page(s) H581–H589

Abstract: Pulmonary hypertension (PH) has been observed in up to 75% of infants with moderate to severe respiratory syncytial virus (RSV) bronchiolitis and is associated with significant morbidity and mortality in infants with congenital heart disease. The purpose ...

Abstract	Pulmonary hypertension (PH) has been observed in up to 75% of infants with moderate to severe respiratory syncytial virus (RSV) bronchiolitis and is associated with significant morbidity and mortality in infants with congenital heart disease. The purpose of the present study was to establish a mouse model of PH secondary to RSV bronchiolitis that mimics the disease etiology as it occurs in infants. Neonatal mice were infected with RSV at 5 days of age and then reinfected 4 wk later. Serum-free medium was administered to age-matched mice as a control. Echocardiography and right ventricular systolic pressure (RVSP) measurements via right jugular vein catheterization were conducted 5 and 6 days after the second infection, respectively. Peripheral capillary oxygen saturation monitoring did not indicate hypoxia at 2-4 days post-RSV infection, before reinfection, and at 2-7 days after reinfection. RSV-infected mice had significantly higher RVSP than control mice. Pulsed-wave Doppler recording of the pulmonary blood flow by echocardiogram demonstrated a significantly shortened pulmonary artery acceleration time and decreased pulmonary artery acceleration time-to-ejection time ratio in RSV-infected mice. Morphometry showed that RSV-infected mice exhibited a significantly higher pulmonary artery medial wall thickness and had an increased number of muscularized pulmonary arteries compared with control mice. These findings, confirmed by RVSP measurements, demonstrate the development of PH in the lungs of mice infected with RSV as neonates. This animal model can be used to study the pathogenesis of PH secondary to RSV bronchiolitis and to assess the effect of treatment interventions. NEW & NOTEWORTHY This is the first mouse model of respiratory syncytial virus-induced pulmonary hypertension, to our knowledge. This model will allow us to decipher molecular mechanisms responsible for the pathogenesis of pulmonary hypertension secondary to respiratory syncytial virus bronchiolitis with the use of knockout and/or transgenic animals and to monitor therapeutic effects with echocardiography.
MeSH term(s)	Animals ; Blood Pressure ; Bronchiolitis, Viral/complications ; Bronchiolitis, Viral/pathology ; Disease Models, Animal ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/pathology ; Hypertension, Pulmonary/virology ; Mice ; Mice, Inbred BALB C ; Pulmonary Artery/pathology ; Respiratory Syncytial Virus Infections/complications ; Respiratory Syncytial Virus Infections/pathology
Language	English
Publishing date	2018-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00627.2017
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Article ; Online: Type I Interferon Potentiates IgA Immunity to Respiratory Syncytial Virus Infection During Infancy.

Hijano, Diego R / Siefker, David T / Shrestha, Bishwas / Jaligama, Sridhar / Vu, Luan D / Tillman, Heather / Finkelstein, David / Saravia, Jordy / You, Dahui / Cormier, Stephania A

Scientific reports

2018 Volume 8, Issue 1, Page(s) 11034

Abstract: Respiratory syncytial virus (RSV) infection is the most frequent cause of hospitalization in infants and young children worldwide. Although mucosal RSV vaccines can reduce RSV disease burden, little is known about mucosal immune response capabilities in ... ...

Abstract	Respiratory syncytial virus (RSV) infection is the most frequent cause of hospitalization in infants and young children worldwide. Although mucosal RSV vaccines can reduce RSV disease burden, little is known about mucosal immune response capabilities in children. Neonatal or adult mice were infected with RSV; a subset of neonatal mice received interferon alpha (IFN-α) (intranasal) prior to RSV infection. B cells, B cell activating factor (BAFF) and IgA were measured by flow cytometry. RSV specific IgA was measured in nasal washes. Nasal associated lymphoid tissue (NALT) and lungs were stained for BAFF and IgA. Herein, we show in a mouse model of RSV infection that IFN-α plays a dual role as an antiviral and immune modulator and age-related differences in IgA production upon RSV infection can be overcome by IFN-α administration. IFN-α administration before RSV infection in neonatal mice increased RSV-specific IgA production in the nasal mucosa and induced expression of the B-cell activating factor BAFF in NALT. These findings are important, as mucosal antibodies at the infection site, and not serum antibodies, have been shown to protect human adults from experimental RSV infection.
MeSH term(s)	Animals ; B-Cell Activating Factor/metabolism ; Flow Cytometry ; Immunoglobulin A/immunology ; Immunoglobulin A/metabolism ; Interferon Type I/metabolism ; Mice ; Mice, Inbred BALB C ; Palivizumab/therapeutic use ; Real-Time Polymerase Chain Reaction ; Respiratory Syncytial Virus Infections/drug therapy ; Respiratory Syncytial Virus Infections/immunology ; Respiratory Syncytial Virus Infections/metabolism
Chemical Substances	B-Cell Activating Factor ; Immunoglobulin A ; Interferon Type I ; Palivizumab (DQ448MW7KS)
Language	English
Publishing date	2018-07-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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/s41598-018-29456-w
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Article ; Online: Specific inhibition of NLRP3 in chikungunya disease reveals a role for inflammasomes in alphavirus-induced inflammation.

Chen, Weiqiang / Foo, Suan-Sin / Zaid, Ali / Teng, Terk-Shin / Herrero, Lara J / Wolf, Stefan / Tharmarajah, Kothila / Vu, Luan D / van Vreden, Caryn / Taylor, Adam / Freitas, Joseph R / Li, Rachel W / Woodruff, Trent M / Gordon, Richard / Ojcius, David M / Nakaya, Helder I / Kanneganti, Thirumala-Devi / O'Neill, Luke A J / Robertson, Avril A B /

King, Nicholas J / Suhrbier, Andreas / Cooper, Matthew A / Ng, Lisa F P / Mahalingam, Suresh

Nature microbiology

2017 Volume 2, Issue 10, Page(s) 1435–1445

Abstract: Mosquito-borne viruses can cause severe inflammatory diseases and there are limited therapeutic solutions targeted specifically at virus-induced inflammation. Chikungunya virus (CHIKV), a re-emerging alphavirus responsible for several outbreaks worldwide ...

Abstract	Mosquito-borne viruses can cause severe inflammatory diseases and there are limited therapeutic solutions targeted specifically at virus-induced inflammation. Chikungunya virus (CHIKV), a re-emerging alphavirus responsible for several outbreaks worldwide in the past decade, causes debilitating joint inflammation and severe pain. Here, we show that CHIKV infection activates the NLRP3 inflammasome in humans and mice. Peripheral blood mononuclear cells isolated from CHIKV-infected patients showed elevated NLRP3, caspase-1 and interleukin-18 messenger RNA expression and, using a mouse model of CHIKV infection, we found that high NLRP3 expression was associated with peak inflammatory symptoms. Inhibition of NLRP3 activation using the small-molecule inhibitor MCC950 resulted in reduced CHIKV-induced inflammation and abrogated osteoclastogenic bone loss and myositis, but did not affect in vivo viral replication. Mice treated with MCC950 displayed lower expression levels of the cytokines interleukin-6, chemokine ligand 2 and tumour necrosis factor in joint tissue. Interestingly, MCC950 treatment abrogated disease signs in mice infected with a related arthritogenic alphavirus, Ross River virus, but not in mice infected with West Nile virus-a flavivirus. Here, using mouse models of alphavirus-induced musculoskeletal disease, we demonstrate that NLRP3 inhibition in vivo can reduce inflammatory pathology and that further development of therapeutic solutions targeting inflammasome function could help treat arboviral diseases.
Language	English
Publishing date	2017-10
Publishing country	England
Document type	Journal Article
ISSN	2058-5276
ISSN (online)	2058-5276
DOI	10.1038/s41564-017-0015-4
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