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Expulsive immunity

Administration of Tyv-specific monoclonal antibodies to rat pups already infected with intestinal larvae causes larvae in the epithelium to be expelled (Carlisle et al, 1990). Only the LI stage is susceptible to expulsion once the larva has moulted to L2 it resists the effects of the antibodies (Carlisle et al, 1990). Expulsive immunity is transferred by three IgG isotypes, F(ab )2 fragments, as well as IgM (Carlisle et al., 1991a). These findings argue against a role for Fc-mediated effector functions and imply that antibodies against Tyv can disturb the larva s niche in a direct fashion. [Pg.115]

There is good evidence, for a number of helminth species, that different parasite lines vary in their infection characteristics in hosts, much of which is reviewed by Read and Viney (1996). For example, different isolates of Trichinella spiralis vary in the kinetics of their primary infection in the same mouse strain. Crucially, these differences are removed when mice are immunosuppressed (Bolas-Fernandez and Wakelin, 1989). Analogous observations have been made for Trichuris muris in mice. Different isolates differed in the kinetics of infection and expulsion. However, in immunosuppressed mice, all isolates had similar fecundity (Bellaby et al., 1995). Combined, these observations show immune-dependent variation between parasite lines in their infection kinetics. [Pg.102]

Taken as a whole, these observations show that parasite lines differ in an immune-dependent manner in their infection/expulsion kinetics. Furthermore, there is heritable variation in survival and fecundity in previously exposed hosts and quantitative variation in the immune response that selected parasite lines elicit. Again, taken as a whole, these observations have the necessary corollary that variation in these traits exists not only in laboratory-maintained isolates but also in helminth species in nature. The phenotypes under consideration here (infection/expulsion kinetics, survival, fecundity) are multifactorial life-history traits. Understanding the basis of variation in the components and interplay of these complex, immune-responsive phenotypes must be of crucial relevance to understanding the immunology of infections of parasitic nematodes. This is of particular relevance in view of current attempts to develop immunological methods of nematode control. [Pg.103]

In passively immunized neonatal rats, Tyv-specific antibodies exclude larvae from the epithelium (Appleton et al., 1988), where large numbers of excluded larvae become entrapped in mucus (Carlisle et al., 1991a). Similarly, when immune adult rats are challenged with larvae, many luminal parasites are observed entrapped in mucus (Lee and Ogilvie, 1982 Bell et al, 1984). Larvae are neither injured nor killed by mucus entrapment, which is reversible and is not a requirement for expulsion (Carlisle et al., 1990). Rather, mucus appears to participate in expulsion by temporarily confining larvae to the lumen, thus facilitating their elimination from the intestine by normal physiological processes. [Pg.115]

In contrast to the protection afforded to suckling rats by Tyv-specific antibodies, passive immunization of weaned rats fails to cause expulsion of T. spiralis (Otubu et al., 1993). Nevertheless, Tyv-specific antibodies do affect the behaviour of larvae in the intestines of weaned rats in the early hours following infection in that larvae are immobile in the intestinal tissue of such rats, though immobility is reversed when the larvae moult. These findings provide further evidence that antibodies specific for Tyv interfere with the LI larva s niche. [Pg.116]

Simple passive immunization with Tyv-specific antibodies does not protect adult rats against T. spiralis, however, it has been shown that prior infection with an unrelated intestinal nematode (Heligmosomoides polygyrus) in combination with passive immunization with Tyv-specific antibodies promotes expulsion of T. spiralis larvae (Bell et al, 1992). The way(s) that II. polygyrus infection synergizes with antibodies is not known. [Pg.116]

Parasitism by T. spiralis has been a subject of scientific interest for over 150 years. Recently, considerable attention has been paid to the parasite by immunologists interested in immunity to nematodes in general, and mucosal immunity in particular. It has been shown that glycan-specific antibodies are highly effective mediators of host defence against intestinal 7. spiralis infection. Protective monoclonal antibodies have been used to elucidate mechanisms of worm expulsion, as well as to identify molecules that the parasite uses to create its niche. In the future, detailed characterization of these molecules and their functions should afford additional insights into parasitism by Trichinella spiralis, and possibly also by other types of pathogen. [Pg.124]

Appleton, J.A. and McGregor, D.D. (1987) Characterization of the immune mediator of rapid expulsion of Trichinella spiralis in suckling rats. Immunology 62, 477-484. [Pg.125]

Bell, R.G., Adams, L.S. and Ogden, R.W. (1984) Intestinal mucus trapping in the rapid expulsion of Trichinella spiralis by rats induction and expression analyzed by quantitative worm recovery. Infection and Immunity 45, 267-272. [Pg.125]

T cell and cytokine regulation of enterocyte apoptosis may also be important in the expulsion of nematodes, in particular T. spiralis and T. muris, which inhabit an intracellular niche. Certainly an increase in the number of apoptotic cells within the epithelium is observed around the period of expulsion of T. muris in resistant mouse strains (D. Artis, C.S. Potten and R.K. Grencis, unpublished). Apoptosis of host enterocytes may dislodge the nematode or perhaps expose vital feeding organs to immune attack, and so enhance expulsion. Whether enterocyte apoptosis results from the burrowing action of the worms or a tissue repair mechanism, or is involved in expulsion, remains to be investigated. [Pg.364]

Ahmad, A., Wang, C.H. and Bell, R.G. (1991) A role for IgE in intestinal immunity. Expression of rapid expulsion of Trichinella spiralis in rats transfused with IgE and thoracic lymphocytes. Journal of Immunology 146, 3563-3570. [Pg.365]

In those infections that are associated with enteropathy (exemplified by T. spiralis), no experimental manipulation has, until recently, been able to separate enteropathy and immune expulsion - if one is abrogated, so is the other. This chapter illustrates how the two processes can be separated, and discusses implications of this for understanding immune expulsion of gut nematodes and the prospects for anti-nematode vaccines that cause no ill effects at either the initial induction of immunity or the expression of protective responses. The definition of that which consitututes enteropathy may vary between authors, but we take as our primary definition the most destructive and quantifiable changes in intestinal tissue that are associated with expulsion, villus atrophy and crypt hyperplasia. [Pg.382]

Immune expulsion of T. spiralis is clearly Th2- and, specifically, IL-4-dependent. However, contrary to expectations, enteropathy (as assessed by changes in villus/crypt ratios) is regulated by IL-4 and not IFN-y (Lawrence et al., 1998). Moreover, the usual severe pathology is not induced in p55 TNF receptor (TNF-R1) gene-deficient mice, which nevertheless expelled... [Pg.384]

Although it appears that severe IL-4-regulated enteropathy is not required for immune expulsion of T. spiralis, it is still possible that Th2 cytokines can act in a direct fashion to create an environment unfavourable for intestinal parasites. It remains to be shown directly whether these effects are sufficient to expel parasites. Indeed, there is considerable evidence to support a variety of pathophysiological effects of IL-4 and/or TNF on the gut. These effects may be mediated by factors including cytokines and mast-cell products (e.g. leukotrienes and 5-hydroxytryptamine). 7. spiralis infections result in increased fluid and mucus secretion into the lumen as well as increased intestinal propulsive activity and more rapid intestinal transit (Castro et al, 1979 Russell, 1986 Vermillion and Collins, 1988 Vermillion et al., 1991 Weisbrodt et al, 1994 Barbara et al, 1997). The increased contractility of radial and longitudinal muscle is greater in high-... [Pg.390]

Studies with a variety of genetically modified mice have shed new light on the complex relationship between the protective and pathological immune responses controlling parasite infections. TNF and NO are important components of the pathological response accompanying the expulsion of a gastrointestinal nematode parasite. In the absence of TNF-R1 or iNOS, mice do not develop the severe villus atrophy and mucosal mastocytosis that usually accompany infection with T. spiralis, but their ability to expel the... [Pg.395]

Lawrence, C.E., Paterson, J.C., Wei, X.Q., Liew, F.Y., Garside, P. and Kennedy, M.W. (2000) Nitric oxide mediates intestinal pathology but not immune expulsion during Trichinella spiralis infection in mice. Journal of Immunology 164, 4229-4234. [Pg.401]

Urban, J.F. Jr, Noben-Trauth, N., Donaldson, D.D., Madden, K.B., Morris, S.C., Collins, M. and Finkelman, F.D. (1998) ILrl3, ILr4R alpha, and Stat6 are required for the expulsion of the gastrointestinal nematode parasite Nippostrongylus brasiliensis. Immunity 8, 255-264. [Pg.404]

Vallance, B.A., Galeazzi, F., Collins, S.M. and Snider, D.P. (1999b) CD4 T cells and major histocompatibility complex class II expression influence worm expulsion and increased intestinal muscle contraction during Trichinella spiralis infection. Infection and Immunity 67, 6090-6097. [Pg.404]

As extracellular metazoan parasites, cestode attack and expulsion depend on a humoral immune response that will be driven principally by Th2-type cytokines. Following antigen processing and presentation and the interaction of CD4+T cells with B cells, plasma cells... [Pg.198]

In most strains of mice, worms are lost within one to two months, but the mechanism of worm expulsion remains unknown. Although early workers believed that only the tissue phase and not the lumen phase induced immunity, recent work (800) using mouse derived cysticercoids (i.e. extracted from villi) suggests that the lumen phase, too, appears to be immunogenic. [Pg.294]


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See also in sourсe #XX -- [ Pg.107 ]




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