Echinostoma caproni: Kinetics of IgM, IgA and IgG subclasses in the serum and intestine of experimentally infected rats and mice
Introduction
Echinostoma caproni (Trematoda: Echinostomatidae) is an intestinal trematode with no tissue phases in the definitive host (Fried and Huffman, 1996). After infection, metacercariae excyst in the duodenum of the definitive host, and the juvenile worms migrate to the posterior third of the small intestine where they attach to the mucosa by the ventral sucker (Fried and Huffman, 1996, Fried and Graczyk, 2004).
E. caproni has a wide range of definitive hosts, though the worm survival greatly differs between hosts. In hamsters and mice, the infections are long-lasting, while in rats the infection is expelled at 7−8 week post-infection (wpi) (Odaibo et al., 1988, Odaibo et al., 1989, Christensen et al., 1990, Hansen et al., 1991, Mahler et al., 1995, Toledo et al., 2004a). The different compatibilities to E. caproni observed in different rodent species allows these host–parasite systems to be highly suitable for elucidating aspects of the host-specific components that determine the course of infections with intestinal trematodes (Toledo and Fried, 2005).
The existing literature provides little information on the host- and parasite-related factors leading to the development of chronic E. caproni infections or, in contrast the rapid expulsion of the parasite. Earlier studies have shown that hosts in which chronic infections are developed are characterized by high inflammatory local response, high levels of seroantigens and elevated IgG levels in the serum. In contrast, the infection in rats is characterized by low levels of local inflammation, seroantigens and systemic IgG (Graczyk and Fried, 1994, Toledo et al., 2004b, Toledo et al., 2005, Toledo et al., 2006a, Toledo et al., 2006b). However, there are several aspects of the immunological response against E. caproni that remain to be studied in detail, i.e., the intestinal antibody responses, the kinetics of IgG subclasses and the potential effect of the antibodies on the course of the infection (Toledo et al., 2006b). In this sense, the only data available are those reported by Agger et al. (1993) and Brunet et al. (2000). Agger et al. (1993) analyzed the kinetics of IgM, IgA and IgG in the serum and intestinal wall of E. caproni-infected mice, during the first 70 days post-infection (dpi) and in the intestinal luminal content at 28 dpi. Elevated levels of IgM, IgA and IgG were detected in the serum and intestinal wall and only and increased level of IgA was detected in the intestinal luminal content. Regarding the IgG subclasses, Brunet et al. (2000) analyzed the profiles of IgG1 and IgG2a in the serum of mice experimentally infected with E. caproni during the first 23 dpi and a weak increasing of IgG2a was detected.
The aim of the present study was to investigate the isotype specific immune responses both at the systemic and mucosal levels in two host species of E. caproni (rats and mice) in which parasite survival differs markedly. The results obtained may be of interest to gain further insight into the host–parasite relationships in intestinal trematode infections and into the factors determining worm rejection or the development of long-lasting infections.
Section snippets
Parasite and experimental infections
The strain of E. caproni has been previously described by Hosier and Fried (1991). Encysted metacercariae of E. caproni were removed from the kidneys and pericardial cavities of experimentally infected Biomphalaria glabrata snails and used to infect mice (ICR) and albino rats (Wistar). Each of 28 male mice, weighing 32−40 g, and 28 rats, weighing 100−120 g, was infected by stomach tube with metacercariae of E. caproni. The infective doses were 75 and 100 metacercariae/animal for mice and rats,
Infection
All mice and rats experimentally exposed to metacercariae of E. caproni were infected as determined by egg examination. The duration of the pre-patent period was uniform. Egg release began 9−12 (10.1 ± 0.4) dpi in mice and 10−12 (11.34 ± 0.44) dpi in rats. All the rats reverted had reverted to negative values at the 8 wpi.
Serum antibody responses
Immunoglobulin M: The experimentally infected mice and rats developed significant IgM responses in serum against E. caproni (Fig. 1). In mice, the IgM levels rapidly increased to
Discussion
To examine the potential role of antibody responses in host-protective immunity on primary E. caproni infections, we studied the serum and intestinal antibody kinetics in two host species exhibiting different patterns of E. caproni infection. Rats develop a marked capacity to expel primary infections of E. caproni and the worms are rapidly expelled (Hansen et al., 1991, Toledo et al., 2004a). In contrast, this species of echinostome evokes long-lasting infections in mice. In this context, the
Acknowledgements
The study was supported by the projects CGL2005-02321/BOS from the Ministerio de Educación y Ciencia (Spain), GV04B/107 and GV05/039 from the Conselleria d’Empresa, Universitat I Ciència de la Generalitat Valenciana (Spain) and the Project UV-AE-20050201 de la Universitat de València (Spain). This work has been carried out while the first author (J.S.) was recipient of a pre-doctoral fellowship from the Ministerio de Educación y Ciencia, Madrid (Spain). This research complies with the current
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2012, Parasitology InternationalCitation Excerpt :Among the IgG subclasses, IgG1 increased in most of the strains, but IgG2a showed variability in production for the different strains at the 4th and 8th week of infection. In mice of C57BL/6, it seemed that IgG1 dominated IgG2a as found in rat clonorchiasis [25]; however, both IgG1 and IgG2a were elevated in other strains and suggested a mixed Th1/Th2 response [26]. Of cytokines, the level of IL-4 was higher in BALB/c and C57BL/6, moderate in ICR and DDY and lower in CBA/N and C3H/HeN at the 4th week of infection.
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2011, Experimental ParasitologyCitation Excerpt :The establishment of chronic infection has been related with the development of rapid and strong antibody responses both at local and systemic levels together with increases in local populations of mucosal neutrophils and mononuclear inflammatory cells in the mesentery. Surprisingly, the early rejection of the worms has been associated with weak antibody responses and low levels of local neutrophils and inflammatory cells (Toledo et al., 2004b, 2005, 2006b; Muñoz-Antoli et al., 2007; Sotillo et al., 2007). These results make difficult the ascertaining of the effector mechanism involved in worm rejection.