Hypersensitivity pneumonitis: A fibrosing alveolitis produced by inhalation of diverse antigens

Abstract

Hypersensitivity pneumonitis (HP) is a T H 1 lymphocyte-biased fibrosing alveolitis caused by antigens ranging from avian excreta, fungi, thermophilic bacteria, and protozoa to reactive chemicals found in the workplace. Mimicking a viral syndrome, acute exposures to inciting antigens cause abrupt onset of nonproductive cough, dyspnea, and chills with arthralgias or malaise usually from 4 to 8 hours later so that the temporal relationship between antigen exposure and symptoms might be unsuspected. The histology of HP reveals prominent lymphocyte infiltrates that thicken the alveolar septa with poorly formed granulomas or giant cells. Bronchoalveolar lavage fluid demonstrates greater than 20% lymphocytes in nearly all patients. Abnormalities on high-resolution computed tomographic examinations range from nodular centrilobular opacities in acute/subacute disease to increased reticular markings and honeycombing fibrosis, which typically are predominant in the upper lobes, in patients with advanced disease. Descriptors include ''mosaic'' attenuation and groundglass opacities. Repeated episodes can result in nodular pulmonary infiltrates and suspected nonspecific interstitial pneumonia or idiopathic pulmonary fibrosis. Clinicians require a high level of suspicion to make an early diagnosis of HP before extensive pulmonary fibrosis or restrictive lung disease has occurred.

Therapeutic Effect of Neuraminidase-1–Selective Inhibition in Mouse Models of Bleomycin-Induced Pulmonary Inflammation and Fibrosis

“…Pulmonary fibrosis, a defining feature of interstitial lung disease, complicates a spectrum of illnesses (Spagnolo et al, 2018;Fischer and Distler, 2019;Perelas et al, 2020;Varone et al, 2020). It develops as a consequence of environmental or professional exposures (Khazdair et al, 2015;Trethewey and Walters, 2018;Greenberger, 2019;Hanania et al, 2019;Hoy and Chambers, 2020) or infections (Naik and Moore, 2010;George et al, 2020) or in its most severe forms emerges This work was supported by National Institutes of Health National Heart, Lung, and Blood Institute [Grant R01-HL126897]; Department of Veterans Affairs [Grant I01CX000101] and [Grant I01BX002499]; and GlycoNet . We thank T. Guo (University of Alberta) for providing samples of CG33300.…”

Acute hypersensitivity pneumonitis in woodworkers caused by inhalation of birch dust contaminated with <i>Pantoea agglomerans</i> and <i>Microbacterium barkeri</i>

“…For establishing proper diagnosis, a detailed anamnesis aimed at identifying exposure agents suspected to cause the disease, characteristic symptoms and type of relation between the potential etiological agents and particular symptoms, is very important. Five patients who developed disease after occupational exposure to the inhalation of wood dust displayed dyspnea, dry cough, fever and malaise, reported as typical symptoms for the acute stage of HP [1][2][3][4][5][6]. Physical examination revealed rales over lung fields, regarded as characteristic for HP, in all the patients.…”

“…Hypersensitivity pneumonitis (HP) is an infrequent, immune-mediated disease of the lower parts of the lungs, initiated by the interaction of immunocompetent cells with large quantities of offending allergens, mostly belonging to fungi, actinobacteria, nontuberculous mycobacteria and bird proteins, which are repeatedly inhaled on exposure to various organic dusts. This interaction leads to lymphocytic and often granulomatous inflammation of the peripheral airways, alveoli and surrounding interstitial tissue and at long-lasting exposure, to fibrosis [1][2][3][4][5][6]. The immunopathogenic allergens are usually inhaled at work, hence the subunits of the disease are named after occupation at risk, such as farmer's lung or bird breeder's lung [1,4,6].…”

Timber-colonizing gram-negative bacteria as potential causative agents of respiratory diseases in woodworkers

“…The disease is caused by the interaction of immunocompetent cells, classified as Th1 allergic response, with the large quantities of microbial or animal allergens associated with organic dusts. The pathogenic reaction leads to lymphocytic and often granulomatous inflammation of the lower parts of lungs and finally to fibrosis (Selman et al 2012;Quirce et al 2016;Sforza and Marinou 2017;Nogueira et al 2019;Greenberger 2019).…”