An increased incidence of bacterial pneumonia (BP) has been reported in Irish Wolfhounds (IWHs) and the disease typically recurs repeatedly. The aetiology is unclear but the development of bronchiectasis in the absence of clinical findings indicative of interstitial lung disease is common in affected IWHs. This observation led us to hypothesize that the primary cause could be at bronchial level. We evaluated bronchial cartilage structure and composition in IWHs (n=10) with previous episodes of pneumonia compared with IWH control dogs (n=5) and other large-breed control dogs (n=5) without a history of respiratory disease. Histological evaluation of lung sections was performed with haematoxylin and eosin, Masson's trichrome and Prussian blue staining as well as with immunohistochemistry (IHC) for CD3 and CD79a antigens and pancytokeratin. Bronchial cartilage proteoglycan content was evaluated in sections stained with safranin 'O' (SO) and chondrocyte apoptosis by IHC for cleaved caspase-3. Image analysis was used to measure the bronchial cartilage to lumen area ratio as well as the SO staining intensity and caspase-3-positive cell count in digital whole slide images. The most consistent histological finding in the lungs of IWHs with recurrent BP was chronic lymphoplasmacytic inflammation in the peribronchial and perivascular pulmonary interstitium, along with remodelling of the bronchial walls. The bronchial cartilage to lumen area ratio was significantly lower in all IWHs than in control dogs of other breeds (P=0.011), suggesting less cartilage support in the bronchi of the IWH breed. The SO staining intensity of the bronchial cartilage was significantly higher (P=0.008) in affected IWHs than in control dogs of other breeds. Analysis of caspase-3 immunolabelling of large bronchial cartilage revealed significantly fewer apoptotic chondrocytes in affected IWHs than in all control dogs (P=0.045). Based on these findings, altered cartilage metabolism, as a breed-related feature or secondary to chronic inflammation, may play a role in the pathogenesis of bronchiectasis development and recurrent lung infections in IWHs.
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