The immune response and immunity from infection with this parasite are poorly understood. Limited evidence exists in humans for acquired immunity to invasive infection with E. histolytica. De Leon (1970), working in Mexico, followed 1021 patients recovered from amebic liver abscess for the 5 year period 1963-1968 and found that only three individuals relapsed with a second episode of liver abscess; unfortunately this study lacked case-controls. It is also unclear whether immunity is acquired against colonization, since E. dispar and E. histolytica can colonize individuals who have serum anti-amebic antibodies, albeit at a lower frequency than seronegative individuals (Gathiram and Jackson, 1987; Choudhuri et al., 1991). In Colombia, it was demonstrated that individuals with serum anti-amebic antibodies were less frequently colonized: 3.5% of individuals who were not infected with E. histolytica-E. dispar had an indirect hemag-glutination inhibition titer of anti-amebic antibodies of ^1/320, compared to 2.0% of colonized individuals. Titers of anti-amebic antibodies < 1/320 were not associated with a lower incidence of colonization, suggesting that the quantity of anti-amebic antibodies was a predictor of protection (Krupp, 1970).

Spontaneous resolution of asymptomatically colonized individuals over a period of weeks to months also suggests that the immune system is able to protect against colonization (Gathiram and Jackson, 1987). However, immunity to colonization, if it exists, is not complete, as individuals can remain colonized with E. histoly-tica for months, despite the presence of serum anti-amebic antibodies (Choudhuri et al., 1991). Evidence against immunity to colonization exists, such as the observation that the incidence of E. histolygica-E. dispar infection increased with age in the Gambia, West Africa, from 1.9% of children < 1 year of age to 35% of individuals aged >40 (Bray and Harris, 1977). In contrast, surveys of patients with diarrhea in Natal, South Africa, and amebic colitis in Dhaka, South Africa (Wanke et al., 1988) have demonstrated a decline in the incidence of E. histolytica-E. dispar infection after age 14, with a second peak of infection in adults aged >40. In Dhaka, Bangladesh, E. histolytica-E. dispar is less frequently observed in the stools of individuals aged >14 with diarrhea, which could be interpreted as supporting the existence of immunity to intestinal colonization or invasion. Additional studies are needed to determine whether protective immunity is acquired after infection with E. histolytica, and whether immunity, if it exists, protects against both colonization and invasion. The current literature can be summarized as supporting the existence of acquired, albeit incomplete, immunity against colonization.

Evidence for both humoral and cell-mediated immunity has been detected in patients recovering from invasive disease. The relative contributions of different anti-E. histolytica immune responses to protective immunity observed have not been conclusively established. Support for a role for protective antibodies has been demonstrated, using a severe combined immunodeficient (SCID) mouse model. SCID mice lack functional B and T cells and, unlike immunocompetent mice, are susceptible to ame-bic liver abscess. Passive transfer of rabbit anti-amebic sera to SCID mice resulted in complete protection against amebic liver abscess in 58% of the mice (Cieslak et al., 1992)

A secretory immune response has also been observed, with anti-amebic and anti-adherence lectin IgA antibodies detected in the stool, saliva and colostrum of patients with clinical amebiasis (Aceti et al., 1991; Agarwal et al., 1992; Kelsall et al., 1994). Anti-adherence lectin antibodies directed against epitopes 1 and 2 have been shown to increase the adherence of amebae to human colonic mucins by directly activating the lectin's carbohydrate binding activity (Petri et al., 1991).

Cell-mediated immunity has an important role in protection against E. histolytica infection via cytokine activation of macrophages and neutrophils. In animal models, decreased cellular immunity, such as neonatal thymectomy, sple-nectomy, steroid treatment, radiation, silica therapy and anti-macrophage or anti-lymphocyte globulin enhanced the formation of amebic liver abscesses. Lymphocytes from patients recovered from invasive amebic disease demonstrated cellmediated immune responses, such as T cell proliferation, amebicidal activity and interleu-kin-2 (IL-2) and interferon gamma (IFNy) production (Salata et al., 1985, 1986) in vitro against total E. histolytica extracts. IFNy- and TNFa-stimulated human macrophages and neutrophils are capable of killing E. histolytica trophozoites, while in the absence of IFNy these effector cells were killed by the amebae (Denis and Chadee, 1989; Salata et al., 1985, 1986; Lin and Chadee, 1992). In murine macrophages, TNFa was shown to play a central role in activating macrophages for nitric oxide-dependent cytotoxicity against E. histolytica (Denis and Chadee, 1989; Lin and Chadee, 1992; Lin et al., 1994).

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