Hypersensitivity pneumonitis: Antigen diversity and disease implications

Abstract

Hypersensitivity pneumonitis (HP) is an immune-mediated syndrome triggered by inhalation of a wide variety of allergens, to which an individual has previously been sensitized. More than 200 agents responsible for the disease have already been identified; however, HP occurs only in a small number of individuals exposed to causal antigens. The present report provides an overview of the role of antigen role in HP, highlighting its diversity, research methods, and prevention strategies, as well as the impact on disease prognosis following elimination of antigen. HP is an underdiagnosed disease and, therefore, it is difficult to accurately estimate its incidence. Triggering antigens can be divided into six broad categories: bacteria, fungi, mycobacteria, animal and plant proteins, chemicals, and metals, represented by disease prototypes. The identification of causal antigen is a major challenge; it is impossible to obtain in about 30-60% of cases. The acute form of HP, with early detection and immediate eviction of causal antigen, tends to have an excellent prognosis. In the chronic form, partial recovery of disease is still possible; however, some cases tend to progress to fibrosis, even after removal from exposure. In conclusion, HP diagnosis should be based on a proactive search for potential antigen sources, although their identification is hampered by the lack of standardized methods of demonstrating the specific antigen sensitization. Antigen avoidance is a critical determinant in disease prognosis.

The value of serum precipitins against specific antigens in patients diagnosed with hypersensitivity pneumonitis – retrospective study

“…Molds can induce farmer's lung in large agriculture regions, especially during wet and warm seasons [24]. Most frequently involved are Alternaria, Aspergillus, and Botrytis species [24], and in some geographic regions, Absidia (Lichtheimia corymbifera) and Wallemia were suggested as the cause of farmer's lung disease [26,27]. As molds' antigens were not included in our laboratory set, this type of allergy could be missed out in our material.…”

“…In our study group, an important observation concerned patients with unproved contact with birds' allergens in whom ssIgG were positive (35%) mostly to poultry and pigeons. According to other studies, ssIgG presence in HP patients denying the contact with birds' allergens may serve as a proof of exposition [22][23][24]. One of neglected by patients forms of exposition to birds' allergens is the contact with feather filling of pillows and clothing (feather duvet lung) [25].…”

“…We did not confirm the allergy to thermophilic actinomycetes in most of our patients who reported the exposition to hay or hay products. The data from literature indicate that farmer's lung may be caused either by thermophilic bacteria or by molds [10,24,26,27]. Molds can induce farmer's lung in large agriculture regions, especially during wet and warm seasons [24].…”

“…The data from literature indicate that farmer's lung may be caused either by thermophilic bacteria or by molds [10,24,26,27]. Molds can induce farmer's lung in large agriculture regions, especially during wet and warm seasons [24]. Most frequently involved are Alternaria, Aspergillus, and Botrytis species [24], and in some geographic regions, Absidia (Lichtheimia corymbifera) and Wallemia were suggested as the cause of farmer's lung disease [26,27].…”

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

“…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].…”