Volume 43, Issue 1
  • ISSN: 0002-9637
  • E-ISSN: 1476-1645



Tropical pulmonary eosinophilia (TPE) is believed to result from extreme immediate hypersensitivity to microfilariae localized in the pulmonary vasculature of some persons with lymphatic filariasis. Female BALB/c mice repeatedly immunized by ip injection of microfilariae become amicrofilaremic within 24 hr of iv parasite challenge, whereas non-sensitized control animals remain patent for > 72 hr. Immunized, but not control mice, develop peripheral blood and pulmonary eosinophilia (2,000 cells/mm and 65,000 cells/bronchoalveolar lavage, respectively). Serum and bronchoalveolar lavage filarial-specific IgG antibodies are greater in sensitized mice than in controls (ELISA absorbance values 20- and 10-fold higher, respectively). Serum IgE antibody levels are also greater ( < 0.01) in immunized parasite-challenged mice than in controls (mean cpm I-labeled anti-mouse IgE bound to antigen-coated Sepharose beads: 7,852 vs. 1,741, respectively). This model exhibits several of the major features of human TPE: amicrofilaremia, elevated levels of serum IgG and IgE antibodies to microfilariae, and blood and pulmonary eosinophilia. This model may be useful in the examination of the role of filarial antigen-specific lymphoid cells and antibodies in regulating the pathologic responses to microfilariae trapped in the lung.


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