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Korean J Parasitol. 2014 Feb;52(1):27-33. doi: 10.3347/kjp.2014.52.1.27. Epub 2014 Feb 19.

Mucosal immune responses of mice experimentally infected with Pygidiopsis summa (Trematoda: Heterophyidae).

Author information

  • 1Department of Parasitology and Tropical Medicine, Seoul National University College of Medicine, Seoul 110-799, Korea.
  • 2Department of Parasitology and Tropical Medicine, Seoul National University College of Medicine, Seoul 110-799, Korea. ; Seoul National University Bundang Hospital, Seongnam 463-707, Korea.

Abstract

Mucosal immune responses against Pygidiopsis summa (Trematoda: Heterophyidae) infection were studied in ICR mice. Experimental groups consisted of group 1 (uninfected controls), group 2 (infection with 200 metacercariae), and group 3 (immunosuppression with Depo-Medrol and infection with 200 metacercariae). Worms were recovered in the small intestine at days 1, 3, 5, and 7 post-infection (PI). Intestinal intraepithelial lymphocytes (IEL), mast cells, and goblet cells were counted in intestinal tissue sections stained with Giemsa, astra-blue, and periodic acid-Schiff, respectively. Mucosal IgA levels were measured by ELISA. Expulsion of P. summa from the mouse intestine began to occur from days 3-5 PI which sustained until day 7 PI. The worm expulsion was positively correlated with proliferation of IEL, mast cells, goblet cells, and increase of IgA, although in the case of mast cells significant increase was seen only at day 7 PI. Immunosuppression suppressed all these immune effectors and inhibited worm reduction in the intestine until day 7 PI. The results suggested that various immune effectors which include IEL, goblet cells, mast cells, and IgA play roles in regulating the intestinal mucosal immunity of ICR mice against P. summa infection.

KEYWORDS:

IgA; Pygidiopsis summa; goblet cell; intestinal fluke; intraepithelial lymphocyte; mast cell; mucosal immunity

PMID:
24623878
PMCID:
PMC3948990
DOI:
10.3347/kjp.2014.52.1.27
[PubMed - indexed for MEDLINE]
Free PMC Article
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