Tropical Eosinophilia Demonstration of Microfilariæ in Lung, Liver, and Lymph-Nodes

Webb, Jessica; Job, C. K.; Gault, Edward W.

doi:10.1016/s0140-6736(60)90730-3

Cited by 104 publications

(38 citation statements)

References 11 publications

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“…Furthermore, when these individuals were treated with DEC, the lung eosinophilia rapidly began to resolve within the first 2 wk oftherapy, and this resolution was paralleled by an improvement in lung function. Importantly, reevaluation 1 (6,9,10,12,13).…”

Section: Resultsmentioning

confidence: 99%

“…In this context, serial sectioning ofthe few available lung biopsies from individuals with acute TPE has demonstrated degenerating microfiliariae within the lung parenchyma, often in association with eosinophils, alveolar macrophages, epithelioid cells, and foreign body giant cells (9,10,12,13). These microfiliariae or their products could initiate the release of chemotactic signals secondarily from inflammatory cells or inflammatory reactants or they themselves may be chemotactic for eosinophils, as has been described for some other nematode parasites (36).…”

Section: Resultsmentioning

confidence: 99%

“…This inflammation is initiated by microfilariae that have been released from lymphatic dwelling adult worms into the circulation and cleared in the pulmonary vasculature. According to this concept, these trapped microfilariae degenerate and release their antigenic constituents that trigger local inflammatory and immune processes (9)(10)(11). Consistent with this concept, very limited morphologic data has revealed evidence ofdegenerating microfilariae and diffuse inflammation in the lung parenchyma (6,9,10,12,13).…”

Section: Introductionmentioning

confidence: 91%

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

Pinkston¹,

Vk²,

Nutman³

et al. 1987

J. Clin. Invest.

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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.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 91%

See 1 more Smart Citation

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

Pinkston¹,

Vk²,

Nutman³

et al. 1987

J. Clin. Invest.

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“…This is supported by the fact that filarial complement fixation test is sometimes positive and often there is a dramatic clinical response to the administration of antifilarial drugs [5]. The condition is often thought to represent an immunopathological response to the presence of parasite and immune hypersensitivity to microfilariae, rather than direct damage by it, and is believed to be the basic underlying pathogenetic mechanism.…”

Section: Discussionmentioning

confidence: 99%

Disseminated Microfilaremia Associated with Lung Cyst and Empyema: An Autopsy Report

et al. 2009

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Clinical manifestations of extralymphatic disease caused by filariasis are varied and range from symptoms due to tropical pulmonary eosinophilia to hematuria, proteinuria, splenomegaly, and rarely arthritis. Disseminated microfilaremia in association with loculated lung cyst and empyema is of rare occurrence and to the best of our knowledge has not been documented in the literature so far. We report here a case of disseminated microfilaremia due to Wuchereria bancrofti infection accompanied by a lung cyst and empyema in a 21-year-old Indian man.

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“…In the case of TPE, however, these microfilariae appear to be trapped in the lung on their first pass through the circulation, where they are presumed to initiate an inflammatory response. The role of the filariae (and microfilariae, in particular) in the immune response of TPE has been corroborated by lung biopsy findings (37) and high levels of filaria-specific IgE and IgG found in TPE patients (15,24). In contrast to the majority of people with lymphatic filariasis, who have a downregulated response to the parasites (24), patients with TPE mount a robust systemic and localized immune response that includes elevations of both polyclonal and filaria-specific IgE and IgG (23), as well as expansion of interleukin-4 (IL-4)-and IL-5-producing T cells (19).…”

mentioning

confidence: 83%

Localized Eosinophil Degranulation Mediates Disease in Tropical Pulmonary Eosinophilia

et al. 2003

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To explore the mechanisms underlying the eosinophil-mediated inflammation of tropical pulmonary eosinophilia (TPE), bronchoalveolar lavage (BAL) fluid, serum, and supernatants from pulmonary and blood leukocytes (WBC) from patients with acute TPE (n ‫؍‬ 6) were compared with those obtained from healthy uninfected individuals (n ‫؍‬ 4) and from patients with asthma (n ‫؍‬ 4) or elephantiasis (n ‫؍‬ 5). Although there were no significant differences in the levels of interleukin-4 (IL-4), IL-5, IL-13, eotaxin, granulocyte-macrophage colony-stimulating factor, RANTES, or eosinophil cationic protein, there was a marked increase in eosinophil-derived neurotoxin (EDN) both systemically and in the lungs of individuals with TPE compared to each of the control groups (P < 0.02). Moreover, there was a compartmentalization of this response, with EDN levels being higher in the BAL fluid than in the serum (P < 0.02). Supernatants from WBC from either whole blood or BAL cells were examined for chemokines, cytokines, eosinophil degranulation products, and arachidonic acid metabolites. Of the many mediators examined-particularly those associated with eosinophil trafficking-only EDN (in BAL fluid and WBC) and MIP-1␣ (in WBC) levels were higher for TPE patients than for the non-TPE control groups (P < 0.02). These data suggest it is the eosinophilic granular protein EDN, an RNase capable of damaging the lung epithelium, that plays the most important role in the pathogenesis of TPE.Tropical pulmonary eosinophilia (TPE), an unusual manifestation of human lymphatic filarial infection, is characterized by an eosinophilic pulmonary inflammatory infiltrate and marked elevations of immunoglobulin E (IgE) and circulating eosinophils in the serum, all felt to be mediated by immunologic hyperreactivity to filarial parasites or their antigens. Although 129 million people worldwide are infected with lymphatic filariasis, Ͻ0.01% develop TPE (20). It is unclear what factors predispose patients to the rare, localized, and profound immune dysregulation associated with TPE.

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Tropical Eosinophilia Demonstration of Microfilariæ in Lung, Liver, and Lymph-Nodes

Cited by 104 publications

References 11 publications

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

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

Disseminated Microfilaremia Associated with Lung Cyst and Empyema: An Autopsy Report

Localized Eosinophil Degranulation Mediates Disease in Tropical Pulmonary Eosinophilia

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