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Small Airway Lesions
Published in Philip T. Cagle, Timothy C. Allen, Mary Beth Beasley, Diagnostic Pulmonary Pathology, 2008
Chih-Wei Wang, John R. Muhm, Thomas V. Colby, Kevin O. Leslie
Respiratory bronchiolitis describes the cellular reaction seen in and around respiratory bronchioles that is almost exclusively associated with cigarette smoking (18,19). The characteristic changes of respiratory bronchiolitis include (i) smoker’s macrophages in the lumens of respiratory bronchioles and the surrounding alveolar spaces, (ii) mild chronic bronchiolitis with variable extension into surrounding alveolar parenchyma, and (iii) minimal peribronchiolar fibrosis. The macrophages of respiratory bronchiolitis are commonly referred to as “smoker’s macrophages” and are characterized by the presence of tan-brown cytoplasmic pigment accentuated by fine black punctuate dots and flecks. These cells may show variable positivity with iron stains. Respiratory bronchiolitis is frequently seen in the lung specimens of smokers, and sometimes this may be an incidental finding. Whenever respiratory bronchiolitis is identified in a lung specimen, a careful search for other more significant pathology is warranted. When respiratory bronchiolitis occurs as the only pathologic finding in a surgical lung biopsy, consideration for respiratory bronchiolitis-associated interstitial lung disease is warranted (see later discussion).
Immunopathogenesis and therapeutic potential of macrophage influx in diffuse parenchymal lung diseases
Published in Expert Review of Respiratory Medicine, 2020
Ritu Kulshrestha, Himanshu Dhanda, Apoorva Pandey, Amit Singh, Raj Kumar
DIP is characterized by accumulation of granular-pigmented alveolar macrophages in alveolar lumens and septa secondary to active or passive exposure to tobacco smoke. This light brown pigment, called ‘smoker’s macrophages’ comprises mainly of aluminum silicate (kaolinite) [107]. Such a histologic pattern of DIP may also occur in pneumoconiosis, rheumatologic disease, drug-associated ILD and other inhaled agents, including marijuana smoke [108]. BAL fluid examination of DIP patients reveals a nonspecific increase in eosinophil, neutrophil, lymphocyte, and macrophage counts [109]. Wojtan et al., in 2016, quantified the CD40 and CD163 antigen staining in BALF of DIP patients. They identified three populations of cells: small cells with strong antigen expression (+++), large cells with weak (+), and cells with no expression (–). DIP patients showed a very low proportion of small cells with strong CD40 (M1 phenotype) and CD163 (M2 phenotype) reaction and an elevated proportion of large cells with weak reaction in the BALF [17]. M1 macrophages produced proinflammatory cytokines such as TNF-α and IL-12 and displayed cytotoxic properties while M2 macrophages released inflammatory mediators such as IL-10 and were involved in angiogenesis and wound healing [17,110]. This dual polarization of human alveolar macrophages was seen to progressively increase with smoking severity [111] and remains to be evaluated for progression of DIP.
Smoking-associated interstitial lung disease: update and review
Published in Expert Review of Respiratory Medicine, 2020
Yaser T Dawod, Noah E Cook, William B Graham, Farah Madhani-Lovely, Choua Thao
DIP is relatively uncommon, with the age of onset between 40 and 60 years and a 2:1 male to female predominance. Prevalence of smoking among reported cases is as high as 60–87% [45]. DIP was first described histologically in 1965, with large desquamated epithelial cells filling the alveoli; there were later identified as alveolar macrophages (smoker macrophages) [46]. Diffuse involvement of distal air spaces with these distinctive macrophages, along with mild interstitial thickening and the lack of excessive fibrosis and honeycombing, is characteristic of the disease [47].