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[PMID]:27771388
[Au] Autor:Martinez EC; Garg R; Shrivastava P; Gomis S; van Drunen Littel-van den Hurk S
[Ad] Endereço:Department of Microbiology and Immunology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, 107 Wiggins Road, S7N 5E5, Canada; Vaccine and Infectious Disease Organization-International Vaccine Centre (VIDO-InterVac), University of Saskatchewan, Saskatoon, Saskatchewan, 120 V
[Ti] Título:Intranasal treatment with a novel immunomodulator mediates innate immune protection against lethal pneumonia virus of mice.
[So] Source:Antiviral Res;135:108-119, 2016 11.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Respiratory syncytial virus (RSV) is the leading cause of acute lower respiratory tract infections in infants and young children. There are no licensed RSV vaccines available, and the few treatment options for high-risk individuals are either extremely costly or cause severe side effects and toxicity. Immunomodulation mediated by a novel formulation consisting of the toll-like receptor 3 agonist poly(I:C), an innate defense regulator peptide and a polyphosphazene (P-I-P) was evaluated in the context of lethal infection with pneumonia virus of mice (PVM). Intranasal delivery of a single dose of P-I-P protected adult mice against PVM when given 24 h prior to challenge. These animals experienced minimal weight loss, no clinical disease, 100% survival, and reduced lung pathology. Similar clinical outcomes were observed in mice treated up to 3 days prior to infection. P-I-P pre-treatment induced early mRNA and protein expression of key chemokine and cytokine genes, reduced the recruitment of neutrophils and eosinophils, decreased virus titers in the lungs, and modulated the delayed exacerbated nature of PVM disease without any short-term side effects. On day 14 post-infection, P-I-P-treated mice were confirmed to be PVM-free. These results demonstrate the capacity of this formulation to prevent PVM and possibly other viral respiratory infections.
[Mh] Termos MeSH primário: Imunidade Inata
Fatores Imunológicos/administração & dosagem
Vírus da Pneumonia Murina/imunologia
Compostos Organofosforados/administração & dosagem
Infecções por Pneumovirus/prevenção & controle
Poli I-C/administração & dosagem
Polímeros/administração & dosagem
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos
Administração Intranasal
Animais
Citocinas/imunologia
Fatores Imunológicos/química
Fatores Imunológicos/imunologia
Pulmão/virologia
Camundongos
Camundongos Endogâmicos BALB C
Compostos Organofosforados/imunologia
Infecções por Pneumovirus/imunologia
Poli I-C/imunologia
Receptor 3 Toll-Like/agonistas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Cytokines); 0 (Immunologic Factors); 0 (Organophosphorus Compounds); 0 (Polymers); 0 (Toll-Like Receptor 3); 0 (poly(phosphazene)); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE


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[PMID]:28005954
[Au] Autor:Cortjens B; Lutter R; Boon L; Bem RA; van Woensel JB
[Ad] Endereço:Pediatric Intensive Care Unit, Emma Children's Hospital AMC, Amsterdam, The Netherlands.
[Ti] Título:Pneumovirus-Induced Lung Disease in Mice Is Independent of Neutrophil-Driven Inflammation.
[So] Source:PLoS One;11(12):e0168779, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The human pneumovirus respiratory syncytial virus (RSV) is the most common pathogen causing lower respiratory tract disease in young children worldwide. A hallmark of severe human RSV infection is the strong neutrophil recruitment to the airways and lungs. Massive neutrophil activation has been proven detrimental in numerous diseases, yet in RSV the contribution of neutrophils to disease severity, and thereby, the relevance of targeting them, is largely unknown. To determine the relevance of potential neutrophil targeting therapies, we implemented antibody-mediated neutrophil depletion in a mouse pneumonia virus of mice (PVM) model. PVM is a host specific murine pneumovirus closely related to human RSV, which reproduces many of the features of RSV infection, such as high viral replication and neutrophil recruitment. Clinical disease and markers of lung inflammation and injury were studied in PVM-infected mice treated with either depleting or isotype control antibodies. To confirm our results we performed all experiments in two mice strains: C57Bl6 and BALBc mice. Neutrophil depletion in blood and lungs was efficient throughout the disease. Remarkably, in both mouse strains we found no difference in clinical disease severity between neutrophil-depleted and control arms. In line with this observation, we found no differences between groups in histopathological lung injury and lung viral loads. In conclusion, our study shows that in mice neutrophil recruitment to the lungs does not affect disease outcome or viral clearance during severe PVM infection. As such, this model does not support the notion that neutrophils play a key role in mouse pneumovirus disease.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Vírus da Pneumonia Murina/imunologia
Neutrófilos/imunologia
Pneumonia/imunologia
Infecções por Pneumovirus/imunologia
Infecções por Vírus Respiratório Sincicial/imunologia
[Mh] Termos MeSH secundário: Animais
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Neutrófilos/patologia
Pneumonia/patologia
Infecções por Pneumovirus/patologia
Vírus Sinciciais Respiratórios/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0168779


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[PMID]:27400340
[Au] Autor:Shrivastava P; Sarkar I; Atanley E; Gomis S; van Drunen Littel-van den Hurk S
[Ad] Endereço:VIDO-InterVac, University of Saskatchewan, 120 Veterinary Road, Saskatoon, Saskatchewan, Canada S7N 5E3.
[Ti] Título:IL-12p40 gene-deficient BALB/c mice exhibit lower weight loss, reduced lung pathology and decreased sensitization to allergen in response to infection with pneumonia virus of mice.
[So] Source:Virology;497:1-10, 2016 Oct.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Respiratory syncytial virus (RSV) is a major cause of bronchiolitis and pneumonia in infants and pneumonia virus of mice (PVM) causes similar disease. BALB/c mice are highly susceptible, while C57BL/6 mice are more resistant to PVM. IL-12 was significantly more up-regulated in response to PVM infection in BALB/c than in C57BL/6 mice. IL-12p40-deficient neonatal and adult BALB/c mice showed significantly less weight loss than wild-type mice after PVM challenge. The percentage of regulatory T cells, as well as IFN-ß and IL-18 expression, was higher in the lungs of both neonatal and adult IL-12p40-/- mice. Adult IL-12p40-/- mice also showed enhanced TGF-ß and IL-10 expression and reduced inflammatory responses. Furthermore, IL-12p40-/- mice showed decreased sensitization to inhaled cockroach antigen after PVM infection when compared to wild-type mice. In conclusion, these data suggest that a depressed regulatory capacity in BALB/c mice to PVM infection results in enhanced immunopathology and sensitization to allergen.
[Mh] Termos MeSH primário: Alérgenos/imunologia
Subunidade p40 da Interleucina-12/deficiência
Vírus da Pneumonia Murina/imunologia
Pneumonia Viral/etiologia
Pneumonia Viral/patologia
Perda de Peso
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Expressão Gênica
Interações Hospedeiro-Patógeno/genética
Interações Hospedeiro-Patógeno/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allergens); 0 (Interleukin-12 Subunit p40)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160712
[St] Status:MEDLINE


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[PMID]:27236500
[Au] Autor:Lynch JP; Werder RB; Simpson J; Loh Z; Zhang V; Haque A; Spann K; Sly PD; Mazzone SB; Upham JW; Phipps S
[Ad] Endereço:School of Biomedical Sciences, University of Queensland, Brisbane, Australia.
[Ti] Título:Aeroallergen-induced IL-33 predisposes to respiratory virus-induced asthma by dampening antiviral immunity.
[So] Source:J Allergy Clin Immunol;138(5):1326-1337, 2016 Nov.
[Is] ISSN:1097-6825
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Frequent viral lower respiratory infections in early life are an independent risk factor for asthma onset. This risk and the development of persistent asthma are significantly greater in children who later become sensitized. OBJECTIVE: We sought to elucidate the pathogenic processes that underlie the synergistic interplay between allergen exposures and viral infections. METHODS: Mice were inoculated with a murine-specific Pneumovirus species (pneumonia virus of mice [PVM]) and exposed to low-dose cockroach extract (CRE) in early and later life, and airway inflammation, remodeling, and hyperreactivity assessed. Mice were treated with anti-IL-33 or apyrase to neutralize or block IL-33 release. RESULTS: PVM infection or CRE exposure alone did not induce disease, whereas PVM/CRE coexposure acted synergistically to induce the hallmark features of asthma. CRE exposure during viral infection in early life induced a biphasic IL-33 response and impaired IFN-α and IFN-λ production, which in turn increased epithelial viral burden, airway smooth muscle growth, and type 2 inflammation. These features were ameliorated when CRE-induced IL-33 release was blocked or neutralized, whereas substitution of CRE with exogenous IL-33 recapitulated the phenotype observed in PVM/CRE-coexposed mice. Mechanistically, IL-33 downregulated viperin and interferon regulatory factor 7 gene expression and rapidly degraded IL-1 receptor-associated kinase 1 expression in plasmacytoid dendritic cells both in vivo and in vitro, leading to Toll-like receptor 7 hyporesponsiveness and impaired IFN-α production. CONCLUSION: We identified a hitherto unrecognized function of IL-33 as a potent suppressor of innate antiviral immunity and demonstrate that IL-33 contributes significantly to the synergistic interplay between respiratory virus and allergen exposures in the onset and progression of asthma.
[Mh] Termos MeSH primário: Alérgenos/imunologia
Asma/imunologia
Baratas
Citocinas/imunologia
Proteínas de Insetos/imunologia
Vírus da Pneumonia Murina
Infecções por Pneumovirus/imunologia
[Mh] Termos MeSH secundário: Poluentes Atmosféricos/imunologia
Animais
Asma/virologia
Líquido da Lavagem Broncoalveolar/imunologia
Líquido da Lavagem Broncoalveolar/virologia
Células Dendríticas/imunologia
Pulmão/virologia
Camundongos Endogâmicos BALB C
Infecções por Pneumovirus/virologia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants); 0 (Allergens); 0 (Cytokines); 0 (Insect Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160530
[St] Status:MEDLINE


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[PMID]:26621546
[Au] Autor:Shrivastava P; Watkiss E; van Drunen Littel-van den Hurk S
[Ad] Endereço:VIDO-InterVac, University of Saskatchewan, 120 Veterinary Road, Saskatoon, Saskatchewan S7N 5E3, Canada.
[Ti] Título:The response of aged mice to primary infection and re-infection with pneumonia virus of mice depends on their genetic background.
[So] Source:Immunobiology;221(3):494-502, 2016 Mar.
[Is] ISSN:1878-3279
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The pneumonia virus of mice (PVM) model is used to study respiratory syncytial virus (RSV) pathogenesis. The outcome of PVM infection varies in different inbred mouse strains, BALB/c being highly susceptible and C57BL/6 more resistant. As the disease symptoms induced by RSV infection can become more severe as people age, we examined the primary and secondary immune responses to infection with PVM in aged BALB/c and C57BL/6 mice. Based on clinical parameters, aged C57BL/6 mice displayed less severe disease than young adult mice when infected with 3000pfu of PVM-15, while BALB/c mice were equally susceptible at both ages showing significant weight loss and high levels of virus replication. Furthermore, after primary infection the CD4(+) T cell numbers in the lungs were higher in young adult mice, while the CD8(+) T cell numbers were comparable in both age groups and strains. When either C57BL/6 or BALB/c mice were infected with PVM as young adults and then re-infected as aged mice, they were protected from clinical disease, while virus replication was reduced. In contrast to mice with a primary PVM-infection, re-infected mice did not have infiltration of neutrophils or inflammatory mediators in the lung. BALB/c mice had higher virus neutralizing antibody levels in the serum and lung than C57BL/6 mice upon re-infection. Re-infection with PVM led to significant influx of effector CD4(+) T cells into the lungs when compared to aged mice with a primary infection, while this cell population was decreased in the lung draining lymph nodes in both mouse strains. After re-infection the effector CD8(+) T cell population was also decreased in the lung draining lymph nodes in both mouse strain when compared to aged mice after primary infection. However, the central memory CD4(+) and CD8(+) T cells were significantly enhanced in numbers in the lungs and draining lymph nodes of both mouse strains after re-infection, and these numbers were higher for C57BL/6 mice.
[Mh] Termos MeSH primário: Patrimônio Genético
Predisposição Genética para Doença
Vírus da Pneumonia Murina/fisiologia
Infecções por Pneumovirus/genética
Infecções por Pneumovirus/virologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Fatores Etários
Animais
Linhagem Celular
Citocinas/metabolismo
Memória Imunológica
Mediadores da Inflamação/metabolismo
Pulmão/imunologia
Pulmão/patologia
Pulmão/virologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Infecções por Pneumovirus/imunologia
Infecções por Pneumovirus/metabolismo
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151202
[St] Status:MEDLINE


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[PMID]:26537680
[Au] Autor:Dyer KD; Drummond RA; Rice TA; Percopo CM; Brenner TA; Barisas DA; Karpe KA; Moore ML; Rosenberg HF
[Ad] Endereço:Inflammation Immunobiology Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
[Ti] Título:Priming of the Respiratory Tract with Immunobiotic Lactobacillus plantarum Limits Infection of Alveolar Macrophages with Recombinant Pneumonia Virus of Mice (rK2-PVM).
[So] Source:J Virol;90(2):979-91, 2015 Nov 04.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Pneumonia virus of mice (PVM) is a natural rodent pathogen that replicates in bronchial epithelial cells and reproduces many clinical and pathological features of the more severe forms of disease associated with human respiratory syncytial virus. In order to track virus-target cell interactions during acute infection in vivo, we developed rK2-PVM, bacterial artificial chromosome-based recombinant PVM strain J3666 that incorporates the fluorescent tag monomeric Katushka 2 (mKATE2). The rK2-PVM pathogen promotes lethal infection in BALB/c mice and elicits characteristic cytokine production and leukocyte recruitment to the lung parenchyma. Using recombinant virus, we demonstrate for the first time PVM infection of both dendritic cells (DCs; CD11c(+) major histocompatibility complex class II(+)) and alveolar macrophages (AMs; CD11c(+) sialic acid-binding immunoglobulin-like lectin F(+)) in vivo and likewise detect mKATE2(+) DCs in mediastinal lymph nodes from infected mice. AMs support both active virus replication and production of infectious virions. Furthermore, we report that priming of the respiratory tract with immunobiotic Lactobacillus plantarum, a regimen that results in protection against the lethal inflammatory sequelae of acute respiratory virus infection, resulted in differential recruitment of neutrophils, DCs, and lymphocytes to the lungs in response to rK2-PVM and a reduction from ∼ 40% to <10% mKATE2(+) AMs in association with a 2-log drop in the release of infectious virions. In contrast, AMs from L. plantarum-primed mice challenged with virus ex vivo exhibited no differential susceptibility to rK2-PVM. Although the mechanisms underlying Lactobacillus-mediated viral suppression remain to be fully elucidated, this study provides insight into the cellular basis of this response. IMPORTANCE: Pneumonia virus of mice (PVM) is a natural mouse pathogen that serves as a model for severe human respiratory syncytial virus disease. We have developed a fully functional recombinant PVM strain with a fluorescent reporter protein (rK2-PVM) that permits us to track infection of target cells in vivo. With rK2-PVM, we demonstrate infection of leukocytes in the lung, notably, dendritic cells and alveolar macrophages. Alveolar macrophages undergo productive infection and release infectious virions. We have shown previously that administration of immunobiotic Lactobacillus directly to the respiratory mucosa protects mice from the lethal sequelae of PVM infection in association with profound suppression of the virus-induced inflammatory response. We show here that Lactobacillus administration also limits infection of leukocytes in vivo and results in diminished release of infectious virions from alveolar macrophages. This is the first study to provide insight into the cellular basis of the antiviral impact of immunobiotic L. plantarum.
[Mh] Termos MeSH primário: Fatores Imunológicos/administração & dosagem
Lactobacillus plantarum/imunologia
Macrófagos Alveolares/imunologia
Macrófagos Alveolares/virologia
Vírus da Pneumonia Murina/imunologia
Probióticos/administração & dosagem
Sistema Respiratório/imunologia
[Mh] Termos MeSH secundário: Animais
Células Dendríticas/imunologia
Células Dendríticas/virologia
Feminino
Linfonodos/imunologia
Camundongos Endogâmicos BALB C
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (Immunologic Factors)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:161203
[Lr] Data última revisão:
161203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151106
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.02279-15


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[PMID]:26529077
[Au] Autor:Maunder HE; Taylor G; Leppard KN; Easton AJ
[Ad] Endereço:School of Life Sciences, University of Warwick, Coventry CV4 7AL, UK. Electronic address: H.Maunder@oxfordbiomedica.co.uk.
[Ti] Título:Intranasal immunisation with recombinant adenovirus vaccines protects against a lethal challenge with pneumonia virus of mice.
[So] Source:Vaccine;33(48):6641-9, 2015 Nov 27.
[Is] ISSN:1873-2518
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Pneumonia virus of mice (PVM) infection of BALB/c mice induces bronchiolitis leading to a fatal pneumonia in a dose-dependent manner, closely paralleling the development of severe disease during human respiratory syncytial virus infection in man, and is thus a recognised model in which to study the pathogenesis of pneumoviruses. This model system was used to investigate delivery of the internal structural proteins of PVM as a potential vaccination strategy to protect against pneumovirus disease. Replication-deficient recombinant human adenovirus serotype 5 (rAd5) vectors were constructed that expressed the M or N gene of PVM pathogenic strain J3666. Intranasal delivery of these rAd5 vectors gave protection against a lethal challenge dose of PVM in three different mouse strains, and protection lasted for at least 20 weeks post-immunisation. Whilst the PVM-specific antibody response in such animals was weak and inconsistent, rAd5N primed a strong PVM-specific CD8(+) T cell response and, to a lesser extent, a CD4(+) T cell response. These findings suggest that T-cell responses may be more important than serum IgG in the observed protection induced by rAd5N.
[Mh] Termos MeSH primário: Adenovírus Humanos/genética
Portadores de Fármacos
Vírus da Pneumonia Murina/imunologia
Pneumonia Viral/veterinária
Infecções por Pneumovirus/prevenção & controle
Vacinas Virais/administração & dosagem
Vacinas Virais/imunologia
[Mh] Termos MeSH secundário: Administração Intranasal
Animais
Anticorpos Antivirais/sangue
Antígenos Virais/genética
Antígenos Virais/imunologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Feminino
Masculino
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C3H
Camundongos Endogâmicos C57BL
Vírus da Pneumonia Murina/genética
Pneumonia Viral/prevenção & controle
Análise de Sobrevida
Vacinas Sintéticas/administração & dosagem
Vacinas Sintéticas/genética
Vacinas Sintéticas/imunologia
Proteínas Estruturais Virais/genética
Proteínas Estruturais Virais/imunologia
Vacinas Virais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Viral); 0 (Antigens, Viral); 0 (Drug Carriers); 0 (Vaccines, Synthetic); 0 (Viral Structural Proteins); 0 (Viral Vaccines)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151104
[St] Status:MEDLINE


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[PMID]:26298860
[Au] Autor:Shrivastava P; Atanley E; Sarkar I; Watkiss E; Gomis S; van Drunen Littel-van den Hurk S
[Ad] Endereço:VIDO-InterVac, University of Saskatchewan, 120 Veterinary Road, Saskatoon, Saskatchewan, Canada S7N 5E3.
[Ti] Título:Blunted inflammatory and mucosal IgA responses to pneumonia virus of mice in C57BL/6 neonates are correlated to reduced protective immunity upon re-infection as elderly mice.
[So] Source:Virology;485:233-43, 2015 Nov.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Respiratory syncytial virus is a major cause of bronchiolitis in infants and pneumonia virus of mice (PVM) causes similar disease in mice. The impact of PVM infection in BALB/c and C57BL/6 neonates, and upon re-infection as elderly mice, was compared. As previously shown for adult mice, PVM caused more disease in BALB/c than in C57BL/6 neonates. After PVM-15 infection BALB/c neonates showed higher production of inflammatory mediators, more influx of plasmacytoid dendritic cells and higher IFN-α expression, and more IgA in the lungs than C57BL/6 neonates. After re-infection as elderly, BALB/c mice developed virus neutralizing antibodies in serum and lung, and were protected from clinical disease, whereas C57BL/6 mice did not develop an anamnestic response and were not protected. These results suggest that an effective local innate response, as well as priming of mucosal adaptive responses in neonates after PVM-15 infection is correlated to decreased susceptibility and protection upon re-infection.
[Mh] Termos MeSH primário: Imunoglobulina A/imunologia
Vírus da Pneumonia Murina/imunologia
Pneumonia Viral
Infecções por Pneumovirus/imunologia
Infecções por Pneumovirus/virologia
Mucosa Respiratória/imunologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Anticorpos Antivirais/imunologia
Citocinas/metabolismo
Células Dendríticas/imunologia
Células Dendríticas/metabolismo
Mediadores da Inflamação/metabolismo
Pulmão/imunologia
Pulmão/metabolismo
Pulmão/patologia
Pulmão/virologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Infecções por Pneumovirus/metabolismo
Mucosa Respiratória/metabolismo
Mucosa Respiratória/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Viral); 0 (Cytokines); 0 (Immunoglobulin A); 0 (Inflammation Mediators)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:151023
[Lr] Data última revisão:
151023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150824
[St] Status:MEDLINE


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[PMID]:26145728
[Au] Autor:Percopo CM; Rice TA; Brenner TA; Dyer KD; Luo JL; Kanakabandi K; Sturdevant DE; Porcella SF; Domachowske JB; Keicher JD; Rosenberg HF
[Ad] Endereço:Inflammation Immunobiology Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
[Ti] Título:Immunobiotic Lactobacillus administered post-exposure averts the lethal sequelae of respiratory virus infection.
[So] Source:Antiviral Res;121:109-19, 2015 Sep.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We reported previously that priming of the respiratory tract with immunobiotic Lactobacillus prior to virus challenge protects mice against subsequent lethal infection with pneumonia virus of mice (PVM). We present here the results of gene microarray which document differential expression of proinflammatory mediators in response to PVM infection alone and those suppressed in response to Lactobacillus plantarum. We also demonstrate for the first time that intranasal inoculation with live or heat-inactivated L. plantarum or Lactobacillus reuteri promotes full survival from PVM infection when administered within 24h after virus challenge. Survival in response to L. plantarum administered after virus challenge is associated with suppression of proinflammatory cytokines, limited virus recovery, and diminished neutrophil recruitment to lung tissue and airways. Utilizing this post-virus challenge protocol, we found that protective responses elicited by L. plantarum at the respiratory tract were distinct from those at the gastrointestinal mucosa, as mice devoid of the anti-inflammatory cytokine, interleukin (IL)-10, exhibit survival and inflammatory responses that are indistinguishable from those of their wild-type counterparts. Finally, although L. plantarum interacts specifically with pattern recognition receptors TLR2 and NOD2, the respective gene-deleted mice were fully protected against lethal PVM infection by L. plantarum, as are mice devoid of type I interferon receptors. Taken together, L. plantarum is a versatile and flexible agent that is capable of averting the lethal sequelae of severe respiratory infection both prior to and post-virus challenge via complex and potentially redundant mechanisms.
[Mh] Termos MeSH primário: Fatores Imunológicos/administração & dosagem
Lactobacillus plantarum/imunologia
Lactobacillus reuteri/imunologia
Vírus da Pneumonia Murina/imunologia
Infecções por Pneumovirus/patologia
Infecções por Pneumovirus/terapia
Probióticos/administração & dosagem
[Mh] Termos MeSH secundário: Administração Intranasal
Animais
Modelos Animais de Doenças
Feminino
Perfilação da Expressão Gênica
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Immunologic Factors)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:161203
[Lr] Data última revisão:
161203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150707
[St] Status:MEDLINE


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[PMID]:25398130
[Au] Autor:Scheer S; Krempl C; Kallfass C; Frey S; Jakob T; Mouahid G; Moné H; Schmitt-Gräff A; Staeheli P; Lamers MC
[Ad] Endereço:Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany; International Max Planck Research School of Molecular and Cellular Biology, Freiburg, Germany; University of Freiburg, Freiburg, Germany.
[Ti] Título:S. mansoni bolsters anti-viral immunity in the murine respiratory tract.
[So] Source:PLoS One;9(11):e112469, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The human intestinal parasite Schistosoma mansoni causes a chronic disease, schistosomiasis or bilharzia. According to the current literature, the parasite induces vigorous immune responses that are controlled by Th2 helper cells at the expense of Th1 helper cells. The latter cell type is, however, indispensable for anti-viral immune responses. Remarkably, there is no reliable literature among 230 million patients worldwide describing defective anti-viral immune responses in the upper respiratory tract, for instance against influenza A virus or against respiratory syncitial virus (RSV). We therefore re-examined the immune response to a human isolate of S. mansoni and challenged mice in the chronic phase of schistosomiasis with influenza A virus, or with pneumonia virus of mice (PVM), a mouse virus to model RSV infections. We found that mice with chronic schistosomiasis had significant, systemic immune responses induced by Th1, Th2, and Th17 helper cells. High serum levels of TNF-α, IFN-γ, IL-5, IL-13, IL-2, IL-17, and GM-CSF were found after mating and oviposition. The lungs of diseased mice showed low-grade inflammation, with goblet cell hyperplasia and excessive mucus secretion, which was alleviated by treatment with an anti-TNF-α agent (Etanercept). Mice with chronic schistosomiasis were to a relative, but significant extent protected from a secondary viral respiratory challenge. The protection correlated with the onset of oviposition and TNF-α-mediated goblet cell hyperplasia and mucus secretion, suggesting that these mechanisms are involved in enhanced immune protection to respiratory viruses during chronic murine schistosomiasis. Indeed, also in a model of allergic airway inflammation mice were protected from a viral respiratory challenge with PVM.
[Mh] Termos MeSH primário: Coinfecção/imunologia
Vírus da Influenza A/imunologia
Vírus da Pneumonia Murina/imunologia
Infecções por Orthomyxoviridae/imunologia
Schistosoma mansoni/imunologia
Esquistossomose mansoni/imunologia
[Mh] Termos MeSH secundário: Animais
Lavagem Broncoalveolar
Citocinas/sangue
Etanercepte
Citometria de Fluxo
Pulmão/patologia
Camundongos
Mucina-5AC/metabolismo
Mucina-5B/metabolismo
Infecções por Orthomyxoviridae/patologia
Estatísticas não Paramétricas
Linfócitos T Auxiliares-Indutores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Muc5ac protein, mouse); 0 (Muc5b protein, mouse); 0 (Mucin 5AC); 0 (Mucin-5B); OP401G7OJC (Etanercept)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141115
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0112469



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