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Andres J Gonzalez, Emmanuel C Ijezie, Onesmo B Balemba, Tanya A Miura
Influenza viruses and rhinoviruses are responsible for a large number of acute respiratory viral infections in human populations and are detected as co-pathogens within hosts. Clinical and epidemiological studies suggest that co-infection by rhinovirus and influenza virus may reduce disease severity and that they may also interfere with each other's spread within a host population. To determine how co-infection by these two unrelated respiratory viruses affects pathogenesis, we established a mouse model using a minor serogroup rhinovirus (RV1B) and mouse-adapted influenza A virus (PR8)...
September 19, 2018: Journal of Virology
Anna Lewandowska-Polak, Małgorzata Brauncajs, Marzanna Jarzębska, Małgorzata Pawełczyk, Marcin Kurowski, Maciej Chałubiński, Joanna Makowska, Marek L Kowalski
BACKGROUND: Impaired regeneration of airway epithelium may lead to persistence of inflammation and remodelling. Regeneration of injured epithelium is a complex phenomenon and the role of toll-like receptors (TLRs) in the stimulation of respiratory virus products in this process has not been established. OBJECTIVE: This study was undertaken to test the hypothesis that the wound repair process in airway epithelium is modulated by microbial products via toll-like receptors...
August 20, 2018: International Journal of Molecular Sciences
Kris Genelyn Dimasuay, Amelia Sanchez, Niccolette Schaefer, Jorge Polanco, Deborah A Ferrington, Hong Wei Chu
Rhinovirus (RV) infection is involved in acute exacerbations of asthma and chronic obstructive pulmonary disease (COPD). RV primarily infects upper and lower airway epithelium. Immunoproteasomes (IP) are proteolytic machineries with multiple functions including the regulation of MHC class I antigen processing during viral infection. However, the role of IP in RV infection has not been explored. We sought to investigate the expression and function of IP during airway RV infection. Primary human tracheobronchial epithelial (HTBE) cells were cultured at air-liquid interface (ALI) and treated with RV16, RV1B, or interferon (IFN)-λ in the absence or presence of an IP inhibitor (ONX-0914)...
August 16, 2018: Clinical Science (1979-)
Sylwia Moskwa, Wojciech Piotrowski, Jerzy Marczak, Małgorzata Pawełczyk, Anna Lewandowska-Polak, Marzanna Jarzębska, Małgorzata Brauncajs, Anna Głobińska, Paweł Górski, Nikolaos G Papadopoulos, Michael R Edwards, Sebastian L Johnston, Marek L Kowalski
PURPOSE: In order to gain an insight into determinants of reported variability in immune responses to respiratory viruses in human bronchial epithelial cells (HBECs) from asthmatics, the responses of HBEC to viral infections were evaluated in HBECs from phenotypically heterogeneous groups of asthmatics and in healthy controls. METHODS: HBECs were obtained during bronchoscopy from 10 patients with asthma (6 atopic and 4 non-atopic) and from healthy controls (n=9) and grown as undifferentiated cultures...
March 2018: Allergy, Asthma & Immunology Research
James T VanLeuven, Benjamin J Ridenhour, Andres J Gonzalez, Craig R Miller, Tanya A Miura
The severity of respiratory viral infections is partially determined by the cellular response mounted by infected lung epithelial cells. Disease prevention and treatment is dependent on our understanding of the shared and unique responses elicited by diverse viruses, yet few studies compare host responses to viruses from different families while controlling other experimental parameters. Murine models are commonly used to study the pathogenesis of respiratory viral infections, and in vitro studies using murine cells provide mechanistic insight into the pathogenesis observed in vivo...
2017: PloS One
Charu Rajput, Tracy Cui, Mingyuan Han, Jing Lei, Joanna L Hinde, Qian Wu, J Kelley Bentley, Marc B Hershenson
Early-life wheezing-associated respiratory tract infection by rhinovirus (RV) is considered a risk factor for asthma development. We have shown that RV infection of 6-day-old BALB/c mice, but not mature mice, induces an asthmalike phenotype that is associated with an increase in the population of type 2 innate lymphoid cells (ILC2s) and dependent on IL-13 and IL-25. We hypothesize that ILC2s are required and sufficient for development of the asthmalike phenotype in immature mice. Mice were infected with RV1B on day 6 of life and treated with vehicle or a chemical inhibitor of retinoic acid receptor-related orphan receptor-α (RORα), SR3335 (15 mg·kg-1 ·day-1 ip for 7 days)...
June 1, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
Annika Bergauer, Nina Sopel, Bettina Kroß, Tytti Vuorinen, Paraskevi Xepapadaki, Scott T Weiss, Ashley Blau, Himanshu Sharma, Cornelia Kraus, Rebekka Springel, Manfred Rauh, Susanne Mittler, Anna Graser, Theodor Zimmermann, Volker O Melichar, Alexander Kiefer, Marek L Kowalski, Anna Sobanska, Tuomas Jartti, Heikki Lukkarinen, Nikolaos G Papadopoulos, Susetta Finotto
We analysed the influence of rhinovirus (RV) in nasopharyngeal fluid (NPF) on type I and III interferon (IFN) responses (e.g. IFN-α and IFN -: λ) and their signal transduction, at baseline and during disease exacerbation, in cohorts of pre-school children with and without asthma.At the time of recruitment into the Europe-wide study PreDicta, and during symptoms, NPF was collected and the local RV colonisation was analysed. Peripheral blood mononuclear cells (PBMCs) were challenged in vitro with RV or not...
February 2017: European Respiratory Journal: Official Journal of the European Society for Clinical Respiratory Physiology
Jason L Girkin, Luke M Hatchwell, Adam M Collison, Malcolm R Starkey, Philip M Hansbro, Hideo Yagita, Paul S Foster, Joerg Mattes
the aim of this study is to elucidate the role of TRAIL during rhinovirus (RV) infection in vivo. Naïve wild-type and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-deficient (Tnfsf10-/- ) BALB/c mice were infected intranasally with RV1B. In separate experiments, Tnfsf10-/- mice were sensitized and challenged via the airway route with house dust mite (HDM) to induce allergic airways disease and then challenged with RVIB or UV-RVIB. Airway hyperreactivity (AHR) was invasively assessed as total airways resistance in response to increasing methacholine challenge and inflammation was assessed in bronchoalveolar lavage fluid at multiple time points postinfection...
January 1, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
A Głobińska, M Pawełczyk, A Piechota-Polańczyk, A Olszewska-Ziąber, S Moskwa, A Mikołajczyk, A Jabłońska, P K Zakrzewski, M Brauncajs, M Jarzębska, S Taka, N G Papadopoulos, M L Kowalski
The aim of this study was to assess the immune response to parainfluenza virus type 3 (PIV3), rhinovirus 1B (RV1B) and intracellular Toll-like receptors (TLR) agonists in nasal epithelial cells (NECs) from patients with allergic rhinitis and healthy controls. NECs were obtained from eight patients with allergic rhinitis (AR) and 11 non-atopic healthy controls (HC) by nasal scraping, grown to confluence and exposed to PIV3, RV1B infection or TLR-3 and TLR-7/8 agonists. Interferon (IFN)-λ1, IFN-α, IFN-β and regulated on activation, normal T expressed and secreted (RANTES) release into the cell culture supernatants was assessed at 8, 24 and 48 h upon infection or 8 and 24 h after stimulation with poly(I:C) and R848...
January 2017: Clinical and Experimental Immunology
C Huang, D Jiang, D Francisco, R Berman, Q Wu, J G Ledford, C M Moore, Y Ito, C Stevenson, D Munson, L Li, M Kraft, H W Chu
BACKGROUND: Rhinovirus (RV) infection in asthma induces varying degrees of airway inflammation (e.g. neutrophils), but the underlying mechanisms remain unclear. OBJECTIVE: The major goal was to determine the role of genetic variation [e.g. single nucleotide polymorphisms (SNPs)] of Toll-interacting protein (Tollip) in airway epithelial responses to RV in a type 2 cytokine milieu. METHODS: DNA from blood of asthmatic and normal subjects was genotyped for Tollip SNP rs5743899 AA, AG and GG genotypes...
December 2016: Clinical and Experimental Allergy: Journal of the British Society for Allergy and Clinical Immunology
Sung Bu Lee, Jeong-Ah Song, Go-Eun Choi, Hun Sik Kim, Yong Ju Jang
BACKGROUND: Patients with chronic rhinosinusitis (CRS) commonly experience aggravation of their symptoms after viral upper respiratory infection (URI). Rhinovirus (RV) is the most common URI-causing virus. However, there is a lack of a mouse model of RV infection and in vivo studies investigating the effect of RV infection on CRS. METHODS: A mouse model of chronic allergic rhinosinusitis (CARS) was established by sensitizing to ovalbumin (OVA) through intraperitoneal injection followed by nasal challenges with OVA for 5 weeks...
November 2016: International Forum of Allergy & Rhinology
Mingyuan Han, Yutein Chung, Jun Young Hong, Charu Rajput, Jing Lei, Joanna L Hinde, Qiang Chen, Steven P Weng, J Kelley Bentley, Marc B Hershenson
BACKGROUND: We have shown that rhinovirus, a cause of asthma exacerbation, colocalizes with CD68+ and CD11b+ airway macrophages after experimental infection in human subjects. We have also shown that rhinovirus-induced cytokine expression is abolished in Toll-like receptor (TLR2)-/- bone marrow-derived macrophages. OBJECTIVE: We hypothesize that TLR2+ macrophages are required and sufficient for rhinovirus-induced airway inflammation in vivo. METHODS: Naive and ovalbumin (OVA)-sensitized and challenged C57BL/6 wild-type and TLR2-/- mice were infected with RV1B, followed by IgG or anti-TLR2, to determine the requirement and sufficiency of TLR2 for rhinovirus-induced airway responses...
December 2016: Journal of Allergy and Clinical Immunology
Michael R Edwards, Fabrizio Facchinetti, Maurizio Civelli, Gino Villetti, Sebastian L Johnston
Respiratory virus infections precipitate asthma and chronic obstructive pulmonary disease (COPD) exacerbations, with most exacerbations due to rhinovirus infection. Both asthma and COPD exacerbations are not well controlled by steroid therapies, and there is a much research interest in finding improved therapies or combinations of therapies for controlling exacerbations. CHF6001 is a new, inhaled highly potent and selective phosphodiesterase type 4 (PDE4) inhibitor. Using in vitro human bronchial epithelial cells (BEAS-2B), we investigated the potential anti-inflammatory effects of CHF6001 on rhinovirus (RV1B)-induced cytokines...
February 2016: Pharmacology Research & Perspectives
A Graser, A B Ekici, N Sopel, V O Melichar, T Zimmermann, N G Papadopoulos, S Taka, F Ferrazzi, T Vuorinen, S Finotto
The proinflammatory cytokine interleukin-17A (IL-17A) is known to mediate antimicrobial activity, but its role during rhinovirus (RV) infections and in asthma needs further investigation. Therefore, we addressed the role of IL-17A during allergic asthma and antiviral immune response in human and murine immunocompetent cells. In this study we found that asthmatic children with a RV infection in their upper airways have upregulated mRNA levels of the antiviral cytokine interferon type I (IFN)-β and the transcription factor T-box 21 (TBX21) and reduced levels of IL-17A protein in their peripheral blood mononuclear cells (PBMCs)...
September 2016: Mucosal Immunology
Marco P Alves, Aline Schögler, Simone Ebener, Nathalie J Vielle, Carmen Casaulta, Andreas Jung, Alexander Moeller, Thomas Geiser, Nicolas Regamey
BACKGROUND AND OBJECTIVE: Rhinoviruses (RV) replicate in both upper and lower airway epithelial cells. We evaluated the possibility of using nasal epithelial cells (NEC) as surrogate of bronchial epithelial cells (BEC) for RV pathogenesis cell culture studies. METHODS: We used primary paired NEC and BEC cultures established from healthy subjects and compared the replication of RV belonging to the major (RV16) and minor (RV1B) group, and the cellular antiviral and proinflammatory cytokine responses towards these viruses...
February 2016: Respirology: Official Journal of the Asian Pacific Society of Respirology
Luke Hatchwell, Adam Collison, Jason Girkin, Kristy Parsons, Junyao Li, Jie Zhang, Simon Phipps, Darryl Knight, Nathan W Bartlett, Sebastian L Johnston, Paul S Foster, Peter A B Wark, Joerg Mattes
BACKGROUND: Asthma exacerbations represent a significant disease burden and are commonly caused by rhinovirus (RV), which is sensed by Toll-like receptors (TLR) such as TLR7. Some asthmatics have impaired interferon (IFN) responses to RV, but the underlying mechanisms of this clinically relevant observation are poorly understood. OBJECTIVES: To investigate the importance of intact TLR7 signalling in vivo during RV exacerbation using mouse models of house dust mite (HDM)-induced allergic airways disease exacerbated by a superimposed RV infection...
September 2015: Thorax
Amit K Mehta, Wei Duan, Astrid M Doerner, Suzanne L Traves, David H Broide, David Proud, Bruce L Zuraw, Michael Croft
BACKGROUND: Rhinovirus infection at an early age has been associated with development of asthma, but how rhinovirus influences the immune response is not clear. OBJECTIVE: Tolerance to inhaled antigen is mediated through induction of regulatory T (Treg) cells, and we examined whether rhinovirus infection of the respiratory tract can block airway tolerance by modulating Treg cells. METHODS: The immune response to intranasal ovalbumin in mice was assessed with concomitant infection with RV1B, and the factors induced in vivo were compared with those made by human lung epithelial cells infected in vitro with RV16...
January 2016: Journal of Allergy and Clinical Immunology
Aran Singanayagam, Nicholas Glanville, Ross P Walton, Julia Aniscenko, Rebecca M Pearson, James W Pinkerton, Jay C Horvat, Philip M Hansbro, Nathan W Bartlett, Sebastian L Johnston
Viral exacerbations of chronic obstructive pulmonary disease (COPD), commonly caused by rhinovirus (RV) infections, are poorly controlled by current therapies. This is due to a lack of understanding of the underlying immunopathological mechanisms. Human studies have identified a number of key immune responses that are associated with RV-induced exacerbations including neutrophilic inflammation, expression of inflammatory cytokines and deficiencies in innate anti-viral interferon. Animal models of COPD exacerbation are required to determine the contribution of these responses to disease pathogenesis...
August 2015: Clinical Science (1979-)
Jun Young Hong, Yutein Chung, Jessica Steenrod, Qiang Chen, Jing Lei, Adam T Comstock, Adam M Goldsmith, J Kelley Bentley, Uma S Sajjan, Marc B Hershenson
BACKGROUND: The mechanisms by which viruses cause asthma exacerbations are not precisely known. Previously, we showed that, in ovalbumin (OVA)-sensitized and -challenged mice with allergic airway inflammation, rhinovirus (RV) infection increases type 2 cytokine production from alternatively-activated (M2) airway macrophages, enhancing eosinophilic inflammation and airways hyperresponsiveness. In this paper, we tested the hypothesis that IL-4 signaling determines the state of macrophage activation and pattern of RV-induced exacerbation in mice with allergic airways disease...
2014: Respiratory Research
Eugene Kim, Huisu Lee, Hyun Sook Kim, Sulmui Won, Eu Kyoung Lee, Hwan Soo Kim, Kyongwon Bang, Yoon Hong Chun, Jong-Seo Yoon, Hyun Hee Kim, Jin Tack Kim, Joon Sung Lee
PURPOSE: The aim of the present study was to investigate the differences in lower airway inflammatory immune responses, including cellular responses and responses in terms of inflammatory mediators in bronchoalveolar lavage fluid (BALF) and the airway, to rhinovirus (RV) infection on asthma exacerbation by comparing a control and a murine asthma model, with or without RV infection. METHODS: BALB/c mice were intraperitoneally injected with a crude extract of Dermatophagoides farinae (Df) or phosphate buffered saline (PBS) and were subsequently intranasally treated with a crude extract of Df or PBS...
November 2013: Korean Journal of Pediatrics
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