Acute tropical pulmonary eosinophilia. Characterization of the lower respiratory tract inflammation and its response to therapy.

Abstract

Although acute tropical pulmonary eosinophilia (TPE) is well recognized as a manifestation of filarial infection, the processes that mediate the abnormalities of the lung in TPE are unknown. To evaluate the hypothesis that the derangements of the lower respiratory tract in this disorder are mediated by inflammatory cells in the local milieu we utilized bronchoalveolar lavage to evaluate affected individuals before and after therapy. Inflaminatory cells recovered from the lower respiratory tract of individuals with acute, untreated TPE (a = 8) revealed a striking eosinophilic alveolitis, with marked elevations in both the proportion of eosinophils (TPE 54±5%; normal 2±5%; P < 0.001) and the concentration of eosinophils in the recovered epithelial lining fluid (ELF) (TPE 63±20 X 103/Al; normal 03±0.1 X 103/jl; P < 0.01). Importantly, when individuals (a = 5) with acute TPE were treated with diethylcarbamazine (DEC), there was a marked decrease of the lung eosinophils and concomitant increase in lung function. These observations are consistent with the concept that at least some of the abnormalities found in the lung in acute TPE are mediated by an eosinophil-dominated inflammatory process in the lower respiratory tract.

Eosinophilic Pneumonias

“…These are then ingested by mosquitos taking blood meals, followed by subsequent maturation to thirdstage larvae, completing the life cycle of the organism (126). The pathogenesis of TFPE has not been clarified fully, but a strong eosinophilic immunologic response to microfilariae trapped in the lungs likely plays a pivotal role (129,145,202). Interestingly, only a small percentage of patients affected with lymphatic filariasis develop pulmonary manifestations, and there is a strong male predominance in developing TFPE (126,207).…”

IL-5 Predominant in Bronchoalveolar Lavage Fluid and Peripheral Blood in a Patient with Acute Eosinophilic Pneumonia.

“…The etiology of eosinophilic pneumonia has been described by helminthic infections (2), drugs (3), environmental exposure (4), and collagen diseases (1). The clinical course of these diseases is chronic, and is characterized by persistent or recurrent pulmonary infiltration.…”

Reciprocal Immunomodulatory Effects of Gamma Interferon and Interleukin-4 on Filaria-Induced Airway Hyperresponsiveness

“…However, in certain individuals, the presence of Mf in the lungs is associated with severe asthmatic symptoms and airway hyperresponsiveness (AHR) (5,7). These patients have peripheral blood eosinophilia and increased numbers of highly activated eosinophils in bronchoalveolar lavage (BAL) fluid (30). In addition, lung biopsies from such patients show Mf surrounded by eosinophilic material (7,17,37).…”

“…In addition, lung biopsies from such patients show Mf surrounded by eosinophilic material (7,17,37). Although the mechanisms underlying these processes are not yet understood, parasites trapped in the lung microvasculature are thought to stimulate a localized inflammatory response that leads to the recruitment of eosinophils, eosinophil degranulation, and induction of severe asthmatic symptoms associated with AHR (5,7,30). This condition, termed tropical pulmonary eosinophilia (TPE), can be distinguished from allergic asthma by the effectiveness of anthelmintics in relieving clinical symptoms (25).…”