Publications
447 results found
Nguyen-Van-Tam JS, Openshaw PJM, Nicholson KG, 2014, Neuraminidase inhibitors for influenza complications Reply, LANCET, Vol: 384, Pages: 1261-1262, ISSN: 0140-6736
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- Citations: 1
Goritzka M, Makris S, Kausar F, et al., 2014, Alveolar macrophages modulate innate immune responses to Respiratory Syncytial Virus (RSV) infection through MAVS signalling and type I interferons, 9th European-Mucosal-Immunology-Group Meeting, Publisher: WILEY-BLACKWELL, Pages: 7-8, ISSN: 0019-2805
Openshaw P, 2014, Protective and inflammatory responses in respiratory virus infections, 9th European-Mucosal-Immunology-Group Meeting, Publisher: WILEY-BLACKWELL, Pages: 8-8, ISSN: 0019-2805
Lambert L, Sagfors AM, Openshaw PJM, et al., 2014, Immunity to RSV in early-life, FRONTIERS IN IMMUNOLOGY, Vol: 5, ISSN: 1664-3224
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- Citations: 132
Nguyen-Van-Tam JS, Openshaw PJM, Nicholson KG, 2014, Antivirals for influenza: where now for clinical practice and pandemic preparedness?, LANCET, Vol: 384, Pages: 386-387, ISSN: 0140-6736
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- Citations: 11
Schiavoni I, Fedele G, Quattrini A, et al., 2014, Live Attenuated <i>B</i>. <i>pertussis</i> BPZE1 Rescues the Immune Functions of Respiratory Syncytial Virus Infected Human Dendritic Cells by Promoting Th1/Th17 Responses, PLOS ONE, Vol: 9, ISSN: 1932-6203
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- Citations: 11
Goritzka M, Durant LR, Pereira C, et al., 2014, Alpha/Beta Interferon Receptor Signaling Amplifies Early Proinflammatory Cytokine Production in the Lung during Respiratory Syncytial Virus Infection, Journal of Virology, Vol: 88, Pages: 6128-6136, ISSN: 0022-538X
Type I interferons (IFNs) are produced early upon virus infection and signal through the alpha/beta interferon (IFN-α/β) receptor (IFNAR) to induce genes that encode proteins important for limiting viral replication and directing immune responses. To investigate the extent to which type I IFNs play a role in the local regulation of inflammation in the airways, we examined their importance in early lung responses to infection with respiratory syncytial virus (RSV). IFNAR1-deficient (IFNAR1−/−) mice displayed increased lung viral load and weight loss during RSV infection. As expected, expression of IFN-inducible genes was markedly reduced in the lungs of IFNAR1−/− mice. Surprisingly, we found that the levels of proinflammatory cytokines and chemokines in the lungs of RSV-infected mice were also greatly reduced in the absence of IFNAR signaling. Furthermore, low levels of proinflammatory cytokines were also detected in the lungs of IFNAR1−/− mice challenged with noninfectious innate immune stimuli such as selected Toll-like receptor (TLR) agonists. Finally, recombinant IFN-α was sufficient to potentiate the production of inflammatory mediators in the lungs of wild-type mice challenged with innate immune stimuli. Thus, in addition to its well-known role in antiviral resistance, type I IFN receptor signaling acts as a central driver of early proinflammatory responses in the lung. Inhibiting the effects of type I IFNs may therefore be useful in dampening inflammation in lung diseases characterized by enhanced inflammatory cytokine production.
Goritzka M, Durant LR, Pereira C, et al., 2014, Interferon-a/b receptor signalling is amplifying early proinflammatory cytokine production in the lung during Respiratory Syncytial Virus (RSV) infection, Annual Congress of the British-Society-for-Immunology, Publisher: Wiley, Pages: 6128-6136, ISSN: 0019-2805
Type I interferons (IFNs) are produced early upon virus infection and signal through the alpha/beta interferon (IFN-/) receptor(IFNAR) to induce genes that encode proteins important for limiting viral replication and directing immune responses. Toinvestigate the extent to which type I IFNs play a role in the local regulation of inflammation in the airways, we examined theirimportance in early lung responses to infection with respiratory syncytial virus (RSV). IFNAR1-deficient (IFNAR1 / ) mice displayedincreased lung viral load and weight loss during RSV infection. As expected, expression of IFN-inducible genes was markedlyreduced in the lungs of IFNAR1 / mice. Surprisingly, we found that the levels of proinflammatory cytokines and chemokinesin the lungs of RSV-infected mice were also greatly reduced in the absence of IFNAR signaling. Furthermore, low levels ofproinflammatory cytokines were also detected in the lungs of IFNAR1 / mice challenged with noninfectious innate immunestimuli such as selected Toll-like receptor (TLR) agonists. Finally, recombinant IFN- was sufficient to potentiate the productionof inflammatory mediators in the lungs of wild-type mice challenged with innate immune stimuli. Thus, in addition to itswell-known role in antiviral resistance, type I IFN receptor signaling acts as a central driver of early proinflammatory responsesin the lung. Inhibiting the effects of type I IFNs may therefore be useful in dampening inflammation in lung diseases characterizedby enhanced inflammatory cytokine production.
Guvenel AK, Chiu C, Openshaw PJM, 2014, Current concepts and progress in RSV vaccine development, EXPERT REVIEW OF VACCINES, Vol: 13, Pages: 333-344, ISSN: 1476-0584
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- Citations: 42
Schnoeller C, Roux X, Sawant D, et al., 2014, Attenuated <i>Bordetella pertussis</i> Vaccine Protects against Respiratory Syncytial Virus Disease via an IL-17-Dependent Mechanism, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 189, Pages: 194-202, ISSN: 1073-449X
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- Citations: 37
Harker JA, Yamaguchi Y, Culley FJ, et al., 2014, Delayed sequelae of neonatal RSV infection are dependent on cells of the innate immune system, Journal of Virology, ISSN: 0022-538X
Infection with respiratory syncytial virus (RSV) in neonatal mice leads to exacerbated disease if mice are re-infected with the same virus as adults. Both T cells and host MHC genotype contribute to this phenomenon, but the part played by innate immunity has not been defined. Since macrophages and natural killer (NK) cells play key roles in regulating inflammation during RSV infection of adult mice, we studied the role of these cells in exacerbated inflammation following neonatal RSV sensitization/adult re-infection. Compared to those undergoing primary adult infection, neonatally sensitized mice showed enhanced airway fluid levels of interleukin-6 (IL-6), interferon alpha (IFNα), CXCL1 (KC) and tumor necrosis factor alpha (TNFα) at 12-24h, and IL-4, IL-5, IFNγ and CCL11 (eotaxin) at day 4 after re-infection. Weight loss during re-infection was accompanied by an initial influx of NK cells and granulocytes into the airways and lungs, followed by T cells. NK depletion during re-infection attenuated weight loss, but did not alter T cell responses. Depleting alveolar macrophages with inhaled clodronate liposomes reduced both NK and T cell numbers and attenuated weight loss. These findings indicate a hitherto unappreciated role for the innate immune response in governing the pathogenic recall responses to RSV infection.
Dunning JW, Merson L, Rohde GGU, et al., 2014, Open source clinical science for emerging infections, The Lancet Infectious Diseases, Vol: 14, Pages: 8-9, ISSN: 1473-3099
Farhadi N, Lambert L, Triulzi C, et al., 2013, Natural Killer cell NKG2D and granzyme B are critical for allergic pulmonary inflammation, Journal of Allergy and Clinical Immunology
BackgroundThe diverse roles of innate immune cells in the pathogenesis of asthma remain to be fully defined. Natural killer (NK) cells are innate lymphocytes which can regulate adaptive immune responses. NK cells are activated in asthma; however, their role in allergic airway inflammation is not fully understood.ObjectiveWe investigated the importance of NK cells in house dust mite (HDM) triggered allergic pulmonary inflammation. Specifically, we aimed to determine the role of the major NK cell activating receptor NKG2D and NK cell effector functions mediated by granzyme B.MethodsAllergic airway inflammation was induced in the airways of mice by repeated intranasal HDM extract administration and responses in wild type and NKG2D deficient mice were compared. Adoptive transfer studies were used to identify the cells and mechanisms involved.ResultsMice lacking NKG2D were resistant to the induction of allergic inflammation and showed little pulmonary eosinophilia, few airway Th2 cells and no rise in serum IgE after multiple HDM allergen exposures. However, NKG2D was not required for pulmonary inflammation after a single inoculation of allergen. NKG2D deficient mice showed no alteration in responses to respiratory virus infection. Transfer of wild type NK cells (but not CD3+ cells) into NKG2D deficient mice restored allergic inflammatory responses only if the NK cells expressed granzyme B. ConclusionThese studies establish a pivotal role for NK cell NKG2D and granzyme B in the pathogenesis of HDM induced allergic lung disease, and identify novel therapeutic targets for the prevention and treatment of asthma.
Guvenal A, Jozwik A, Paras A, et al., 2013, CD4+ T cell subsets in experimental human infection with Respiratory Syncytial Virus, Annual Congress of the British-Society-for-Immunology, Publisher: WILEY-BLACKWELL, Pages: 123-123, ISSN: 0019-2805
Guvenel A, Jozwik A, Paras A, et al., 2013, CD4 Virus + T cell subsets in experimental human infection with respiratory syncytial, Annual Congress of the British-Society-for-Immunology, Publisher: WILEY-BLACKWELL, Pages: 123-124, ISSN: 0019-2805
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- Citations: 1
Tregoning JS, Wang B, McDonald JU, et al., 2013, Respiratory syncytial virus (RSV) infection during early life suppresses antibody responses by the induction of interferon gamma, Annual Congress of the British-Society-for-Immunology, Publisher: WILEY-BLACKWELL, Pages: 104-104, ISSN: 0019-2805
Openshaw PJM, 2013, A Gene Expression Signature for RSV: Clinical Implications and Limitations, PLOS MEDICINE, Vol: 10, ISSN: 1549-1277
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- Citations: 4
Durant LR, Makris S, Voorburg CM, et al., 2013, Regulatory T Cells Prevent Th2 Immune Responses and Pulmonary Eosinophilia during Respiratory Syncytial Virus Infection in Mice, JOURNAL OF VIROLOGY, Vol: 87, Pages: 10946-10954, ISSN: 0022-538X
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- Citations: 78
Semple MG, Myles PR, Nicholson KG, et al., 2013, An Evaluation of Community Assessment Tools (CATs) in Predicting Use of Clinical Interventions and Severe Outcomes during the A(H1N1)pdm09 Pandemic, PLOS ONE, Vol: 8, ISSN: 1932-6203
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- Citations: 4
Openshaw PJ, Chiu C, 2013, Protective and dysregulated T cell immunity in RSV infection, CURRENT OPINION IN VIROLOGY, Vol: 3, Pages: 468-474, ISSN: 1879-6257
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- Citations: 81
Dodd JS, Clark D, Muir R, et al., 2013, Endogenous IL-21 regulates pathogenic mucosal CD4 T-cell responses during enhanced RSV disease in mice, MUCOSAL IMMUNOLOGY, Vol: 6, Pages: 704-717, ISSN: 1933-0219
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- Citations: 10
Tregoning JS, Wang BL, McDonald JU, et al., 2013, Neonatal antibody responses are attenuated by interferon-γ produced by NK and T cells during RSV infection, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 110, Pages: 5576-5581, ISSN: 0027-8424
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- Citations: 32
Myles P, Nguyen-Van-Tam JS, Semple MG, et al., 2013, Differences between asthmatics and nonasthmatics hospitalised with influenza A infection, EUROPEAN RESPIRATORY JOURNAL, Vol: 41, Pages: 824-831, ISSN: 0903-1936
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- Citations: 40
Openshaw P, 2013, Dr Brigitte Askonas (1923-2012), EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 43, Pages: 865-866, ISSN: 0014-2980
Hansel TT, Johnston SL, Openshaw PJ, 2013, Microbes and mucosal immune responses in asthma, LANCET, Vol: 381, Pages: 861-873, ISSN: 0140-6736
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- Citations: 121
Loebbermann J, Durant L, Thornton H, et al., 2013, Defective immunoregulation in RSV vaccine-augmented viral lung disease restored by selective chemoattraction of regulatory T cells, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 110, Pages: 2987-2992, ISSN: 0027-8424
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- Citations: 52
Farhadi N, Guerra N, Openshaw PJ, et al., 2013, The Role Of Nk Cells In Allergic Inflammation Of The Lung, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 187, ISSN: 1073-449X
Openshaw PJ, 2013, The Mouse Model of Respiratory Syncytial Virus Disease, CHALLENGES AND OPPORTUNITIES FOR RESPIRATORY SYNCYTIAL VIRUS VACCINES, Vol: 372, Pages: 359-369, ISSN: 0070-217X
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- Citations: 25
Habibi MS, Openshaw PJM, 2012, Benefit and harm from immunity to respiratory syncytial virus: implications for treatment, CURRENT OPINION IN INFECTIOUS DISEASES, Vol: 25, Pages: 687-694, ISSN: 0951-7375
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- Citations: 18
Pollard AJ, Savulescu J, Oxford J, et al., 2012, Human microbial challenge: the ultimate animal model, LANCET INFECTIOUS DISEASES, Vol: 12, Pages: 903-905, ISSN: 1473-3099
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- Citations: 30
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