Distribution and quantitation of lung parenchymal contractile tissue in ovine lentivirus-induced lymphoid interstitial pneumonia. Do tissue forces limit lung distensibility?
BACKGROUND
Lymphoid interstitial pneumonia (LIP) is frequently identified in sheep infected with the ovine lentivirus, maedi-visna virus (MVV). Functional consequences of this condition include a reduction in lung distensibility that cannot be explained by the density of surface forces within the lung parenchyma. A potential source of tissue forces to account for this functional deficit is the substantial parenchymal smooth muscle hyperplasia that is a feature of the lung pathology. This investigation examines the relationship between lung distensibility and the quantity and distribution of smooth muscle hyperplasia in MVV-induced LIP.


METHODS
Immunohistochemical localization of alpha-smooth muscle actin (ASMA) was used to identify parenchymal contractile tissue. The distribution and morphometric quantitation of ASMA in lung parenchyma was determined in normal sheep lungs and in lungs from sheep seropositive for MVV. The relationship between the volume density of ASMA in lung parenchyma (Vv'ASMA') and static lung compliance (Cst) and lung distensibility (K) was examined.


RESULTS
In normal lungs, ASMA was expressed by typical smooth muscle cells surrounding airways and blood vessels, by cells at the alveolar septal tips protruding into the alveolar ducts, and, rarely, by individual cells within septa. In MVV-seropositive sheep with minimal histopathology, increased ASMA expression occurred in association with early interstitial infiltrates and was located both at septal tips and within septa. With more severe pathology, ASMA-expressing cells became organized into bundles within obviously thickened septa and septal tips. In maedi, Vv'ASMA' is negatively correlated with K and Cst (rs = -0.614; p < 0.005; and rs = -0.504; p < 0.025, respectively). However, partial correlation coefficients indicate that Vv'ASMA' and lung parenchymal tissue density (Vvt) are strongly interdependent.


CONCLUSIONS
ASMA expression in normal sheep lung parenchyma follows a similar pattern of distribution to that described for human lungs. The quantity of ASMA in lung parenchyma in LIP associated with MVV infection is negatively correlated with lung distensibility; however, whether this is a causal association remains undetermined.
Collie
D D
DD
Department of Veterinary Pathology, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Scotland.
Pyrah
I
I
Watt
N J
NJ
D000199:Actins / Q000032:analysis; D000818:Animals; D005260:Female; D006965:Hyperplasia / Q000473:pathology; D008168:Lung / Q000737:chemistry / Q000473:pathology*; D009130:Muscle, Smooth / Q000737:chemistry / Q000473:pathology*; D011021:Pneumonia, Progressive Interstitial, of Sheep / Q000503:physiopathology*; D012129:Respiratory Function Tests; D012756:Sheep; D014790:Visna-maedi virus / Q000472:pathogenicity
D000199:Actins