Cross-reactions of sera from Ascaris suum, Toxocara canis, and Angiostrongylus cantonensis infected mice with Ascaris suum antigens

TMUIR > College of Medicine > Department of Medicine > Department of Molecular Parasitology and Tropical Diseases > Periodical Article > Item 987654321/16534

Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/16534

Title:	Cross-reactions of sera from Ascaris suum, Toxocara canis, and Angiostrongylus cantonensis infected mice with Ascaris suum antigens
Authors:	范家? Fan CK;Su KE;;;
Contributors:	醫學系寄生蟲科
Date:	2004
Issue Date:	2009-11-13 09:48:35 (UTC+8)
Abstract:	Ascaris suum larval excretory-secretory (AsES) antigen and larval (AsLA) as well as adult somatic antigen (AsAA) which were thought to be possibly helpful in the diagnosis of visceral larva migrans (VLM) due to A. suum infection were investigated in the present study. Serum taken from mice orally inoculated with approximately 250 embryonated eggs of A. suum or Toxocara canis, or 40 third-stage larvae of Angiostrongylus cantonensis were assessed by enzyme-linked immunosorbent assay (ELISA) using the AsES antigen, AsLA or AsAA at 1, 2, 3, 4, 6 and 8 weeks post infection (WPI). The titer of serum IgG from mice infected with A. suum increased from 1 WPI and a peak at 4 WPI was observed when it reached approximately three times the level of uninfected control mice. Thereafter, it decreased gradually but remained high as found from 6 to 8 WPI. No cross-reactions of heterologous serum IgG against AsES antigen was observed, whereas heterologous serum IgM exhibited significant cross-reactions to AsES antigen. Cross-reactivities to AsLA and AsAA by heterologous serum IgG as well as IgM antibodies were also observed in the trial. Altogether, the AsES antigen apparently seemed to be superior to the other two somatic antigens when used in the diagnosis of A. suum-induced VLM with serum IgG as tested by ELISA. Moreover, it was the first report to test the possibly antigenic cross-reactivity between A. suum and A. cantonensis.
Relation:	Parasitology International
Note:	Although toxocaral granulomatous hepatitis (TGH) characterized with a dominant-Th2 type immune response is a self-limiting disease, little is known concerning the role of fibrosis-related cytokine transforming growth factor-beta 1 (TGF-β1) in pathogenesis of TGH. A detailed histological and quantitatively immunohistochemical analysis of TGF-β1, α-smooth muscle actins (α-SMA), and collagen was performed on the liver tissues from mice infected with Toxocara canis as assessed between day 1 and 42 weeks post-infection (DPI or WPI). TGF-β1 was detected mainly in infiltrating leukocytes in lesions with strong expressions from 4 to 16 WPI. Larvae per se also exhibited strong TGF-β1-like molecule expressions in the trial. Alpha-SMA was detected predominantly in hepatic stellate cells (HSC) which surrounded the lesions with moderate expressions largely throughout the period of the entire experiment. Collagen was observed to accumulate in inflammatory lesions and biliary basement with moderate to strong expressions from 1 WPI onwards in the trial. Since many evidences have indicated that leukocytes have the potential to influence HSC by producing TGF-β1 which can affect HSC to increase collagen synthesis in various liver diseases, we may propose that persistently elevated TGF-β1 expression in infiltrating leukocytes and active HSC with marked α-SMA expressions may contribute to healing of injured sites through up-stimulation of collagen deposition; in contrast, abnormally persistent collagen accumulation may cause irreversible fibrotic injury in the TGH. Keywords: Immunohistochemistry; Granulomatous hepatitis; Toxocara canis; Transforming growth factor-β1; Stellate cells; α-Smooth muscle actins; Collagen; Mice
Data Type:	article
Appears in Collections:	[Department of Molecular Parasitology and Tropical Diseases] Periodical Article

Files in This Item:

File	Description	Size	Format
20-4.pdf		212Kb	Adobe PDF	367	View/Open
摘要.pdf		39Kb	Adobe PDF	135	View/Open

Loading...