Immunopathological studies in patients with farmer's lung

Abstract

Summary Immunohistological study of lung biopsies from four palients with farmer's lung revealed histological evidence of vasculilis along with deposits of immunoglobulins and C3 in and around the affected vessels in the biopsies from two palients. Both these patients were exposed to mouldy hay antigens shortly before biopsy. Both these patients also had considerable numbers of eosinophils in their lung lesions. Immune‐complex mediated vasculitis is probably an early event in the pathogenesis of farmer's lung and might not be detectable in the absence of recent exposure to relevant antigens. The presence of large numbers of eosinophits in these lesions suggests a type I reaction acting as the trigger for a type 3 reaction.

Experimental Hypersensitivity Pneumonitis

“…Precipitating antibody specific for antigens of M. faeni occurs in the serum of cattle with some evidence to support an increased incidence during periods of maximum exposure to mouldy hay, a major source of M. faeni antigen [15], The association of bovine immunoglobulin, complement components and M. faeni antigen within sections of lung from naturally occurring bovine interstitial pneu monia of the farmer's lung type, suggests that either or both reaction types II and III of Gell and Coombs [9, see also 21] may play a role in the patho genesis of the pneumonitis. Similar observations have been made upon human lung obtained from patients with farmer's lung [10].…”

Hypersensitivity pneumonia: the role of lung biopsy in diagnosis and management

“…Rare reports describe a patchy airspace filling process resembling bronchopneumonia, in which both neutrophils and eosinophils are present with an associated necrotizing small vessel vasculitis. 25,33 Lung biopsy often has a critical role in separating chronic hypersensitivity pneumonia from other forms of diffuse interstitial lung disease, especially in patients for whom no specific antigenic exposure is identified. 6 Histological diagnosis of hypersensitivity pneumonia is predicated on recognition of a classical triad: 1) bronchiolocentric cellular chronic interstitial pneumonia, 2) chronic bronchiolitis, and 3) non-necrotizing granulomatous inflammation affecting the peribronchiolar interstitium.…”

In vitro release of arachidonic acid and in vivo responses to respirable fractions of cotton dust.

“…Lung biopsies as in farmer's lung (10) and pigeon breeder's lung (11) may not reflect very early cellular changes, since most are undertaken with hospitalized patients and taken some time after last exposure, i.e., the acute PMN response which is largely absent 4 days after dust exposure may not be observed.…”