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The effect of protein deficiency on systemic release of rat mucosal mast cell protease II during Nippostrongylus brasiliensis infection and following systemic anaphylaxis
Author(s) -
Cummins Adrian G,
Kenny Anna L,
Duncombe Victor M,
Bolin Terry D,
Davis Alan E
Publication year - 1987
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.1987.40
Subject(s) - nippostrongylus brasiliensis , mast cell , anaphylaxis , immunology , protease , systemic inflammation , systemic mastocytosis , microbiology and biotechnology , chemistry , medicine , biology , allergy , enzyme , immune system , inflammation , biochemistry
Summary Serum rat mucosal mast cell protease II (RMCPII) was measured in protein‐deficient rats to assess mucosal mast cell (MMC) activation during primary infection with the nematode, Nippostrongylus brasiliensis , and during systemic anaphylaxis produced by Nippostrongylus antigen in immune animals. In the first study, serum RMCPII increased 4‐fold by day 15 after infection. By day 20, serum RMCPII continued to rise in protein‐deficient animals, but decreased in nutritionally normal animals. This was associated with impaired worm rejection in protein‐deficient rats. During systemic anaphylaxis, serum RMCPII was elevated in three groups of protein‐deficient rats on 6%, 8% and 10% low protein diets and in nutritionally normal rats. All protein‐deficient rats exhibited 3 to 7‐fold less mucosal permeability of the small intestine to Evan's blue dye injected intravenously compared to nutritionally normal animals following anaphylactic stimulation. These results demonstrated that MMC are activated during infection in protein deficiency, and suggest that reduced MMC function does not explain delay in worm expulsion. Impaired mucosal anaphylaxis in protein deficiency could not be attributed to a failure of MMC response.