RESUMEN
Two surface associated antigens (GLSA-82 and GLSA-56) of axenically grown G. lamblia trophozoites (PI strain) were affinity purified from its sonic extract. Both GLSA-82 and GLSA-56 were heat labile, sensitive to treatment with pronase, trypsin and were also sodium metaperiodate modifiable as assessed by micro ELISA. Lectin binding studies revealed that GLSA-82 specifically bound concanavalin A and pokeweed mitogen, and had alpha-methyl mannoside and n-acetyl-B-d-glucosamine sugar moieties. However, GLSA-56 selectively bound Ricinus communis agglutinin and phytohaemagglutinin, and had B-d-galactose and n-acetyl-B-d-galastosamine as sugar moieties. Human sera obtained during acute G. lamblia infection recognised GLSA-82 and GLSA-56 antigens. However, the antibody levels to GLSA-82 were significantly lower (P less than 0.05) during active giardiasis infection. Such surface associated antigens may be target of antiparasitic immune responses and thus, may modulate disease processes.
Asunto(s)
Animales , Anticuerpos Antiprotozoarios/biosíntesis , Antígenos de Protozoos/química , Antígenos de Superficie/química , Giardia/inmunología , Giardiasis/inmunología , Humanos , Sueros Inmunes/inmunologíaRESUMEN
Giardia lamblia, the protozoan parasite, first described by Von Leewenhoek in 1681, has come into prominence in last quarter century because of mounting awareness that it may cause significant morbidity and loss of man power. Earlier thought to be a commensal organism, it has been recognised as a true intestinal pathogen in the past three decades. Nevertheless, the mechanism of the disease caused by this protozoan parasite (in the human host's small intestine) continues to remain unexplained. The infection with G. lamblia is worldwide with an average prevalence of 12.5 per cent and is especially common in children and may cause failure of child to thrive. The G. lamblia infection has been implicated in a number of water borne epidemics and is important cause of traveller's diarrhoea all over the world. Infection with G. lamblia may be entirely asymptomatic, may produce a mild, self limiting illness or chronic diarrhoea with or without malabsorption. The reasons for such variations in severity are not clearly understood. However, interplay of virulence of parasite, nutritional status and type of the host immune responses and its effect on intestinal mucosa appear to modulate the infection.
Asunto(s)
Animales , Giardiasis/epidemiología , Humanos , Parasitosis Intestinales/epidemiología , Intestino Delgado/inmunologíaRESUMEN
Quantitation of T cell subsets in intraepithelium and lamina propria during the course of experimental G. lamblia infection in the inbred mice revealed increased influx of Thy 1.2+ (T cells) and Lyt 2.2+ (suppressor/cytotoxic T cells) during the establishment (3-5 day post-inoculation) and acute (9-11 day post-inoculation) phases of infection. The influx of these cells reduced as the parasite load declined. In contrast, no significant changes were noticed in lamina propria and intraepithelium Lyt 1.1+ (helper T cell) cells during the establishment or acute phase but such cells increased significantly in the decline (17-21 day post-inoculation) phase of infection. Further, both intraepithelium and lamina propria lymphocytes isolated from uninfected or infected animals failed to kill G. lamblia trophozoites in vitro in the absence or presence of antigiardial antibodies. Our data suggest that the clearance of G. lamblia trophozoites was not mediated by cytotoxic T cells. However, the induction of helper T cells during the declining phase of infection might be an important mechanism for the induction of parasite specific antibody response leading to the immune elimination of G. lamblia trophozoites from the gut.