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. 2013 Nov;49(5):808-13.
doi: 10.1165/rcmb.2013-0096OC.

Viral Bronchiolitis in Young Rats Causes Small Airway Lesions That Correlate With Reduced Lung Function

Free PMC article

Viral Bronchiolitis in Young Rats Causes Small Airway Lesions That Correlate With Reduced Lung Function

Ronald L Sorkness et al. Am J Respir Cell Mol Biol. .
Free PMC article


Viral illness with wheezing during infancy is associated with the inception of childhood asthma. Small airway dysfunction is a component of childhood asthma, but little is known about how viral illness at an early age may affect the structure and function of small airways. We used a well-characterized rat model of postbronchiolitis chronic airway dysfunction to address how postinfectious small airway lesions affect airway physiological function and if the structure/function correlates persist into maturity. Brown Norway rats were sham- or virus inoculated at 3 to 4 weeks of age and allowed to recover from the acute illness. At 3 to 14 months of age, physiology (respiratory system resistance, Newtonian resistance, tissue damping, and static lung volumes) was assessed in anesthetized, intubated rats. Serial lung sections revealed lesions in the terminal bronchioles that reduced luminal area and interrupted further branching, affecting 26% (range, 13-39%) of the small airways at 3 months of age and 22% (range, 6-40%) at 12 to 14 months of age. At 3 months of age (n = 29 virus; n = 7 sham), small airway lesions correlated with tissue damping (rs = 0.69) but not with Newtonian resistance (rs = 0.23), and Newtonian resistance was not elevated compared with control rats, indicating that distal airways were primarily responsible for the airflow obstruction. Older rats (n = 7 virus; n = 6 sham) had persistent small airway dysfunction and significantly increased Newtonian resistance in the postbronchiolitis group. We conclude that viral airway injury at an early age may induce small airway lesions that are associated quantitatively with small airway physiological dysfunction early on and that these defects persist into maturity.


<i>Figure 1.</i>
Figure 1.
Serial lung sections at intervals of 25 μm, representing the coursing of a normal bronchiole, obtained from a normal control Brown Norway (BN) rat, and an affected bronchiole, obtained from a BN rat that recovered from respiratory viral illness at an early age. Sections are numbered from medial to lateral planes, spanning a total of 300 μm. Lungs were harvested at 10 months of age.
<i>Figure 2.</i>
Figure 2.
The associations of respiratory system resistance (Rrs) (A), Newtonian resistance (RN) (B), and tissue damping (G) (C) with the prevalence of small airway lesions (%Airways Affected) in BN rats at 3 months of age. Triangles indicate sham-inoculated control rats (n = 7); circles indicate virus-inoculated rats (n = 29).
<i>Figure 3.</i>
Figure 3.
Comparisons between sham-inoculated control and virus-inoculated rats at 3 months of age (n = 7 control rats; n = 29 virus-inoculated rats) and at 10 to 14 months of age (n = 6 control rats; n = 7 virus-inoculated rats) regarding the percentage of airways affected (A), Rrs (B), G (C), residual lung volume/total lung capacity (RV/TLC) ratio (D), and Newtonian resistance (E). Triangles indicate sham-inoculated control rats; circles indicate virus-inoculated rats. All rats were inoculated at 3 to 4 weeks of age. *Virus group significantly different compared with the control group. CTRL, control.

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