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Human Rhinovirus In Bronchial Epithelium Of Infants With

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Vol. 118. Tari: Lindahl, Harry & Haahtela; 2006. Human rhinovirus in bronchial epithelium of infants with recurrent respiratory symptoms; pp. 591–596. [DOI] Introduction Rhinovirus (RV) is the leading cause of exacerbations of lung disease. A sensory neuronal model, derived from human dental pulp stem cells and differentiated into peripheral neuronal equivalents (PNEs), was used to examine RV’s effects on airway sensory nerves. We investigated whether RV can directly infect and alter PNEs or whether it exerts effects indirectly

Association of Rhinovirus Infections with Asthma

ABSTRACT: Human respiratory syncytial virus (HRSV) is the main cause of bronchiolitis during the first year of life, but other viruses such as rhinovirus also occur and are clinically indistinguishable. In hospitalized infants with bronchiolitis, the analysis of the peripheral blood mononuclear cells (PBMC) gene expression might be useful for identification the etiologies In another set of experiments, bronchial epitheliums were cultured with EVs and infected with human rhinovirus RV16 at a multiplicity of infection

Computer illustration of human rhinovirus particles (blue) in the ...

We evaluated the use of nasal epithelial cells (NEC) as surrogate of bronchial epithelial cells (BEC) for rhinovirus (RV) studies. We found that NEC are a suitable alternative cellular system to BEC Human rhinovirus in bronchial epithelium of infants with recurrent respiratory symptoms. K. Malmström A. Pitkäranta +8 authors M. Mäkelä Medicine The Journal of allergy and clinical immunology 2006

Malmström K., Pitkäranta A., Carpen O., Pelkonen A., Malmberg L.P., Turpeinen M. Human rhinovirus in bronchial epithelium of infants with recurrent respiratory symptoms.

Subauste MC, Proud D. Effects of tumor necrosis factor-alpha, epidermal growth factor and transforming growth factor-alpha on interleukin-8 production by, and human rhinovirus replication in, bronchial epithelial cells.

Human rhinovirus in bronchial epithelium of infants with recurrent respiratory symptoms Rhinovirus Human rhinovirus is a picornavirus that is the most frequent cause of the common cold in the general population. In SOT recipients, rhinovirus is the respiratory virus most commonly identified in prospective studies assessing the incidence of CARV infections [9]. Infections with rhinovirus are usually mild and self-limiting, although some cases of severe LRT disease and

  • The ABCs of Rhinoviruses, Wheezing, and Asthma
  • Recent advances in understanding rhinovirus immunity
  • Pathogenesis of rhinovirus infection
  • Rhinovirus and Asthma Exacerbations

Kristiina Malmström, Anne Pitkäranta, Olli Carpen, Anna Pelkonen, Pekka Malmberg, Markku Turpeinen, Merja Kajosaari, Seppo Sarna, Harry Lindahl, Tari Haahtela, Mika J Mäkelä Kliniken för hud- och könssjukdomar Korva-, nenä- ja kurkkutautien klinikka Lastentautien yksikkö Avdelningen för folkhälsovetenskap Lastenkirurgian yksikkö Forskningsoutput: Tidskriftsbidrag Coinfection with respiratory syncytial virus and rhinovirus increases IFN-λ1 and CXCL10 expression in human primary bronchial epithelial cells Nipaporn Sankuntaw1*, Nuntaya Punyadee2,3, Wasun Chantratita4, Viraphong Lulitanond5

The mechanisms by which rhinovirus influences asthma are not fully established, but current evidence indicates that the immune response to this virus is critical in this process. Many airway cell types are involved in the immune response to rhinovirus, but most important are respiratory epithelial cells and possibly macrophages.

Rhinovirus is commonly associated with bronchiolitis – only second to RSV during the first year life. The prevalence of HRV-bronchiolitis may be very high in predisposed infants. HRV diagnosis is almost exclusively based on PCR, which detects respiratory Here we describe three novel mouse models of rhinovirus infection: minor-group rhinovirus infection of BALB/c mice, major-group rhinovirus infection of transgenic BALB/c mice expressing a mouse-human ICAM-1 chimera and rhinovirus-induced exacerbation of Epigenetic training of human bronchial epithelium cells by repeated rhinovirus infections Marua Abu Risha, Karosham D. Reddy, Sai Sneha Priya Nemani,

Background Human rhinoviruses (HRV) cause the majority of colds and trigger exacerbations of chronic lower airway diseases. Airway epithelial cells are the primary site for HRV infection and replication, and the initiation of host inflammatory responses. At present, the molecular mechanisms that underpin HRV responses in airway epithelial cells are incompletely Rhinovirus (RV) is among the most frequent causative agents of upper respiratory tract infections in children and adults and is linked to a broad spectrum of clinical syndromes. Generally, by 2 years of age, approximately 90% of children have antibodies against RV [1]. The “common cold” is the colloquial term given for mild, self-limiting upper respiratory infections,

Human rhinoviruses (HRVs) were discovered as common cold pathogens over 50 years ago. Recent advances in molecular viral diagnostics have led to an appreciation of their role in more-significant respiratory illnesses, including bronchiolitis in infancy, childhood pneumonia, and acute exacerbations of chronic respiratory diseases such as asthma, chronic obstructive lung Images of bronchial epithelium from an adult subject without asthma who was experimentally infected with rhinovirus-16. (a) Hematoxylin and eosin stain shows an intact epithelium. (b) Tissue was stained for RV16 capsid protein (red) and DAPI, a nuclear stain. Note that some cells are stained with RV and others are not.

For example, as previously discussed, blockade of the IL-25 receptor in murine models correlated with decreased T2 biasing response during RV infections (27). Similarly, in an in vitro study utilizing human asthma bronchial epithelial cells experimentally infected with RV-A16, antibodies to IL-33 resulted in attenuated T2 cytokine production (33). A recent prospective study investigated the differences in the nasopharyngeal microbiome during acute respiratory tract infections due to human rhinovirus or RSV in 135 infants aged less than 6 months [38]. By contrast to previous studies, S. aureus was Replication kinetics of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and human rhinovirus (HRV) in air-liquid interface cultures of human bronchial epithelial cells coinfected simultaneously with SARS-CoV-2 and HRV in the presence or absence of BX795.

Abstract Human rhinovirus (HRV) remains a leading cause of several human diseases including the common cold. Despite considerable research over the

Introduction Rhinovirus (RV) is the leading cause of exacerbations of lung disease. A sensory neuronal model, derived from human dental pulp stem cells and differentiated into peripheral neuronal equivalents (PNEs), was used to examine RV’s effects on airway sensory nerves. We investigated whether RV can directly infect and alter PNEs or whether it exerts New molecular diagnostic tools have recently allowed the discovery of human rhinovirus species C (HRV-C) that may be overrepresented in children with A new and potentially more pathogenic group of human rhinovirus (HRV), group C (HRVC), has recently been discovered. We hypothesised that HRVC would be present in children with acute asthma and cause more severe attacks than other viruses or HRV groups. Children with acute asthma (n = 128; age 2–16 yrs) were recruited on presentation to an emergency department.

Human monocytic cells direct the robust release of CXCL10 by bronchial epithelial cells during rhinovirus infection. Clin Exp Allergy. 2010;40:1203–13 This study used a co-culture model of bronchial epithelial cells and monocytes to demonstrate synergistic chemokine production during rhinovirus infection. In the second model, transgenic BALB/c mice, expressing a mouse‐human ICAM‐1 chimera, were inoculated with the major group HRV‐16. Rhinovirus‐induced exacerbation of allergic airway inflammation is mimicked in the third model. Studies utilizing cultured human nasal epithelial cells showed decreased zona occluden-1, claudin-1, and E-cadherin mRNA and protein levels after infection with RV [24••]. This is consistent with observations regarding the disruption

Methods Epithelial cell culture Major group HRV species, which use intercellular adhesion molecule-1 (ICAM-1) as a receptor, do not infect more than 5-10% of primary human bronchial epithelial cells in culture [26]. This review examines the epidemiologic association between rhinovirus infections and exacerbations of asthma and outlines current information on immune responses to rhinovirus infection and potential connections between antiviral

Rationale: No studies have assessed the effects of HRV infection on epithelial tight junctions (TJ) and resultant barrier function. Aim: To correlate viral infection with TJ disassembly, epithelial barrier integrity and function. Methods: Human airway epithelial cells were infected with HRV-1B at various Tissue Culture Infectivity Doses (TCID50) over 72 hours. HRV replication was However, rhinovirus-driven asthma exacerbations are additionally characterised by an amplified Th2 immune response and airway neutrophilia. This commentary focuses on recent advances in understanding immunity toward rhinovirus infection and how innate and adaptive immune responses drive rhinovirus-induced asthma exacerbations.

This is potentially important, since it has recently been shown that rhinovirus can induce NO‐synthase expression in human primary bronchial epithelial cells in vitro [48], and that such NO can reduce rhinovirus replication and the induced inflammatory cytokine release by Background Human rhinovirus C (HRV-C) accounts for a large proportion of HRV-related illnesses, but the immune response to HRV-C infection has not been elucidated. Our objective was to assess the effect of HRV-C on cytokine secretion in human bronchial epithelial (HBE) cells grown at air–liquid interface (ALI) and compare it with that of respiratory syncytial