Comparison of paired human nasal and bronchial airway epithelial cell responses to rhinovirus infection and IL-13 treatment

Clinical and Translational Medicine - Tập 7 - Trang 1-10 - 2018
Nicole Roberts1, Reem Al Mubarak1, David Francisco2, Monica Kraft2, Hong Wei Chu1
1Department of Medicine, National Jewish Health, Denver, USA
2Department of Medicine, University of Arizona, Tucson, USA

Tóm tắt

Because of its advantage as a minimally invasive procedure, nasal brushings have been increasingly used and proposed as a valuable approach to study lower airway diseases in lieu of bronchial epithelial cells. However, there is limited or conflicting evidence pertaining to whether nasal samples can be surrogates to bronchial samples. The goal of the present study is to test whether nasal epithelial cells have similar antiviral and inflammatory responses to IL-13 treatment and rhinovirus infection, a condition mimicking virally induced asthma exacerbation. Nasal and bronchial airway epithelial cells taken from the same patient were cultured under submerged and air–liquid interface (ALI) culture in the absence or presence of rhinovirus and IL-13 treatment. Inflammatory cytokines IP-10 and eotaxin-3, antiviral gene Mx1 and viral levels were measured. In the absence of IL-13 treatment, nasal and bronchial cells showed a similar IP-10 response in both ALI and submerged cultures. Under the ALI culture, short term (e.g., 3 days) IL-13 treatment had a minimal effect on viral and Mx1 levels in both cell types. However, prolonged (e.g., 14 days) IL-13 treatments in both cell types decreased viral load and Mx1 expression. Under the submerged culture, IL-13 treatment in both cell types has minimal effects on viral load, IP-10 and Mx1. IL-13-induced eotaxin-3 production was similar in both types of cells under either submerged or ALI culture, which was not affected by viral infection. Our data suggest that nasal epithelial cells could serve as a surrogate to bronchial epithelial cells in future studies aimed at defining the role of type 2 cytokine IL-13 in regulating pro-inflammatory and antiviral responses.

Tài liệu tham khảo

Hackner K et al (2017) Fever after bronchoscopy: serum procalcitonin enables early diagnosis of post-interventional bacterial infection. BMC Pulm Med 17:156 Chanez P et al (1999) Comparison between nasal and bronchial inflammation in asthmatic and control subjects. Am J Respir Crit Care Med 159:588–595 Lachowicz-Scroggins ME, Boushey HA, Finkbeiner WE, Widdicombe JH (2010) Interleukin-13-induced mucous metaplasia increases susceptibility of human airway epithelium to rhinovirus infection. Am J Respir Cell Mol Biol 43:652–661 Lopez-Souza N (2009) et al. In vitro susceptibility to rhinovirus infection is greater for bronchial than for nasal airway epithelial cells in human subjects. J Allergy Clin Immunol 123:1384–1390 McDougall CM et al (2008) Nasal epithelial cells as surrogates for bronchial epithelial cells in airway inflammation studies. Am J Respir Cell Mol Biol 39:560–568 Thavagnanam S et al (2014) Nasal epithelial cells can act as a physiological surrogate for paediatric asthma studies. PLoS ONE 9:e85802 Suzuki K et al (2016) IP-10 is elevated in virus-induced acute exacerbations in childhood asthma. Tokai J Exp Clin Med 41:210–217 Berman R et al (2016) MUC18 regulates lung rhinovirus infection and inflammation. PLoS ONE 11:e0163927 Stokes AB et al (2014) Comparison of three different brushing techniques to isolate and culture primary nasal epithelial cells from human subjects. Exp Lung Res 40:327–332 Chu HW et al (2015) CRISPR-Cas9-mediated gene knockout in primary human airway epithelial cells reveals a proinflammatory role for MUC18. Gene Ther 22:822–829 Suprynowicz FA et al (2012) Conditionally reprogrammed cells represent a stem-like state of adult epithelial cells. Proc Natl Acad Sci USA 109:20035–20040 Devalia JL, Sapsford RJ, Wells CW, Richman P, Davies RJ (1990) Culture and comparison of human bronchial and nasal epithelial cells in vitro. Respir Med 84:303–312 Laitinen LA, Heino M, Laitinen A, Kava T, Haahtela T (1985) Damage of the airway epithelium and bronchial reactivity in patients with asthma. Am Rev Respir Dis 131:599–606 Davies DE (2001) The bronchial epithelium in chronic and severe asthma. Curr Allergy Asthma Rep 1:127–133 Pringle EJ et al (2012) Nasal and bronchial airway epithelial cell mediator release in children. Pediatr Pulmonol 47:1215–1225 Comer DM, Elborn JS, Ennis M (2012) Comparison of nasal and bronchial epithelial cells obtained from patients with COPD. PLoS ONE 7:e32924 Jakiela B et al (2014) Th2-type cytokine-induced mucus metaplasia decreases susceptibility of human bronchial epithelium to rhinovirus infection. Am J Respir Cell Mol Biol 51:229–241 Wynn TA (2003) IL-13 effector functions. Annu Rev Immunol 21:425–456 Wark PA et al (2005) Asthmatic bronchial epithelial cells have a deficient innate immune response to infection with rhinovirus. J Exp Med 201:937–947 Sykes A et al (2014) Rhinovirus-induced interferon production is not deficient in well controlled asthma. Thorax 69:240–246 Moskwa S et al (2018) Innate immune response to viral infections in primary bronchial epithelial cells is modified by the atopic status of asthmatic patients. Allergy Asthma Immunol Res 10:144–154 Zhou W et al (2006) IL-13 is associated with reduced illness and replication in primary respiratory syncytial virus infection in the mouse. Microbes Infect 8:2880–2889 Foxman EF et al (2015) Temperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells. Proc Natl Acad Sci USA 112:827–832 Seng LG, Daly J, Chang KC, Kuchipudi SV (2014) High basal expression of interferon-stimulated genes in human bronchial epithelial (BEAS-2B) cells contributes to influenza A virus resistance. PLoS ONE 9:e109023 Wark PA et al (2007) IFN-gamma-induced protein 10 is a novel biomarker of rhinovirus-induced asthma exacerbations. J Allergy Clin Immunol 120:586–593 Li L et al (1999) Effects of Th2 cytokines on chemokine expression in the lung: IL-13 potently induces eotaxin expression by airway epithelial cells. J Immunol 162:2477–2487 van Wetering S et al (2007) Epithelial differentiation is a determinant in the production of eotaxin-2 and -3 by bronchial epithelial cells in response to IL-4 and IL-13. Mol Immunol 44:803–811 Coleman JM et al (2012) Epithelial eotaxin-2 and eotaxin-3 expression: relation to asthma severity, luminal eosinophilia and age at onset. Thorax 67:1061–1066 Huang C et al (2016) Tollip SNP rs5743899 modulates human airway epithelial responses to rhinovirus infection. Clin Exp Allergy 46:1549–1563 Papadopoulos NG et al (2001) Rhinovirus infection up-regulates eotaxin and eotaxin-2 expression in bronchial epithelial cells. Clin Exp Allergy 31:1060–1066 Rajan D, Gaston KA, McCracken CE, Erdman DD, Anderson LJ (2013) Response to rhinovirus infection by human airway epithelial cells and peripheral blood mononuclear cells in an in vitro two-chamber tissue culture system. PLoS ONE 8:e66600 Meyer JE et al (2006) Nasal RANTES and eotaxin production pattern in response to rhinovirus infection. Rhinology 44:140–144