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Table 1 Rhinovirus Studies

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

Hakonarson 1998 [73]; Van Ly 2013 [50], Shariff 2017 [53];

Co-cultures of airway cells

Integrated response of multiple cell types

Few studies elucidating modulation of RV-induced AHR

Korpi-Steiner 2010 [52]; Van Ly 2013 [50]; Rajan 2013 [51]

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]