From: Modulation of airway hyperresponsiveness by rhinovirus exposure
Method/Study | Advantages | Disadvantages | References |
---|---|---|---|
ASM cells | Primary cell modulating AHR and airway tone | Direct infection with RV not likely given architecture of the lung | |
Co-cultures of airway cells | Integrated response of multiple cell types | Few studies elucidating modulation of RV-induced AHR | |
Clinical isolates | Tissue from infected patients with and without asthma/COPD | Inconsistent findings with respect to susceptibility to infection/symptoms | Marin 2000 [94]; Corne 2002 [95]; Greene 2002; de Kluijver 2003 [108]; DeMore 2009 [109]; Schneider 2010 [96]; Kennedy 2014 [18] |
PCLS | Intact architecture of the lung tissue/airways | No circulating immune cells | Kennedy and Koziol-White 2018 [24] |
Murine studies | Easy to manipulate genetically to understand mechanisms of RV-induced AHR | Only susceptible to RV-B infection, a serotype not associated severe RV infections/symptoms. Model with human ICAM-1 limited to RV infection in the context of allergic airways disease. | Tuthill 2003 [28]; Bartlett 2008 [27]; Meurs 2008 [31]; Calvo 2009 [34]; Lau 2009 [35]; Miller 2009 [36]; Bizzintino 2011 [33] |
Pediatric in vivo studies | • Correlation between RV exposure and wheeze in a large population of pediatric subjects. • Identification of potential targets for abrogation of RV-induced AHR/development of asthma. • Experimental RV challenge to study relationship between IgE levels and exacerbation severity. | • Primarily performed in subjects with European ethnic background. • Little extrapolation to other ethnic groups due to prevalency of polymorphism associated with wheeze. | Lemanske 2002 [16]; Kotaniemi-Syrjänen 2003 [80]; Zambrano 2003 [25]; Bisgaard 2004 [15]; Jackson 2008 [64]; Calişkan 2013 [89] |