Correlation between protective antibody response and patent infection with Hymenolepis nana in mice

Correlation between protective antibody response and patent infection with Hymenolepis nana in mice. International Journal for Parasitology16: 197–203. Mice inoculated with mouse-derived cysticercoids of Hymenolepis nana, as well as with eggs, produced IgG and IgE antibodies that were detected by double diffusion (DD) and passive cutaneous anaphylaxis (PCA), respectively. When mice inoculated with eggs (day 0) were challenged with eggs (day 66), all were resistant to the challenge (assessed by the failure of cysticercoid recovery in the intestinal tissue) and produced protective antibodies evidenced by passive transfer, as well as IgG and IgE isotypes. When mice inoculated with eggs (day 0) were treated with a highly efficacious cestocide, praziquantel on day 6 at the beginning of the lumen phase, all were also resistant to the egg challenge on day 66, however, IgE, IgG, and protective antibodies were not detected. When mice treated with praziquantel before patent infection were repeatedly challenged with high doses of eggs, some of them produced IgG and IgE antibodies. From these results, it is suggested that (1) the production of protective antibody is a secondary response after patency (which may be ascribed to eggs released from mature worms), and (2) mice initially given eggs are highly resistant to egg challenge showing that an effector mechanism of acquired resistance to egg challenge may be expressed without high titres of protective antibody, at least in the serum.     

Mechanisms of protective immunity in Hymenolepis nana/mouse model.

Some immunological and parasitological aspects related to the infection of Hymenolepsis nana in mice are summarized in this review, focusing on the immune effector mechanisms involved in this host/parasite relationship. H. nana is a small cestode tapeworm of man and mice. A primary egg-infection determines within few days a strong immunity. Immunity elicited by low-level primary infection is effective as a high-level infection. The protective role of both humoral and cell-mediated immunity is summarized. The histological findings demonstrate that eosinophils and mast-cells are implicated as effector cells. This review is an attempt to re-examine, at low-level infection, the immune mechanisms in H. nana/mouse model.     

Lead and immunity: II. Suppression of humoral immune response to Hymenolepis nana in mice.

Serum protein changes in mice treated for varying durations with lead nitrate and subsequently infected with 1000 H. nana eggs were compared with their counterpart controls, only treated and only infected groups. Decreased values of beta and gamma globulins in all the experimental groups along with higher worm recoveries indicate suppression of humoral immune response by lead in association with higher worm recoveries indicate suppression of humoral immune response by lead in association with the cellular components since these globulins are known to contain antibodies. Lead treatment for a duration of 45 days proved to be most effective in suppressing the immune response.     

Hymenolepis nana: passive transfer of mouse immunity by T-cell subset of phenotype Lyt-1

Mesenteric lymph node cells obtained from donor mice (BALB/c strain) actively immunized by oral inoculation with Hymenolepis nana eggs were syngeneically transferred by intravenous injection into athymic nude mice previously uninfected. The adoptively immunized recipients were then challenged with 1000 H. nana eggs 2 days after cell transfer. The degree of immunity transferred was assessed by examining cysticercoids developed in the intestinal villi of the recipients on Day 4 of challenge infection. The criterion for success in cell transfer of immunity was the complete rejection of cysticercoids as was generally expected in mice infected previously. The transfer of 1.5 X 10(8) immune mesenteric lymph node cells obtained from donors immunized 4 days before cell collection resulted invariably in the complete rejection of cysticercoids, though not less than this cell dosage. The immunity was passively transferable to recipients by T cells, especially by T-cell subset of phenotype Lyt-1 but not those of phenotype Lyt-2.3 and Lyt-1.2.3. However, 1.5 X 10(8) immune mesenteric lymph node cells obtained from donors immunized 21 days before cell transfer and 1.5 X 10(8) immune spleen cells obtained from donors immunized 4 days before cell transfer had little or no effect on the rejection of cysticercoids.     

Immunological memory and lymphoblast-migration in mice infected with Hymenolepis nana

The presence of small cells carrying memory and lymphoblast migration in C57 Bl/6N inbred mice with the intestinal parasite Hymenolepis nana were investigated. Hymenolepis nana egg-infection stimulated an enhanced accumulation of mesenteric lymphoblasts at days 3, 6 and 9 after infection; lymphoblasts accumulated selectively in the mesenteric nodes (MLN) of mice suggesting a cell-trapping effect. The migration was studied using lymphoblasts from non-infected donors. Spleen cells and MLNC collected from donor mice 30 days after a primary infection and enriched for T cells were able to transfer an adoptive immunity, by contrast unseparated cells were uneffective. This result provides preliminary evidence for the existence of T memory cells in the spleen and in the mesenteric nodes.     

Lumen phase specific cross immunity between Hymenolepis microstoma and H. nana in mice

, and 1988. Lumen phase specific cross immunity between Hymenolepis microstoma and H. nana in mice. International Journal for Parasitology 18: 1019–1027. When mice inoculated with five cysticercoids of Hymenolepis microstoma were challenged with H. nana, they showed strong resistance to challenges with both eggs and cysticercoids of H. nana from day 20. The immunity became complete from day 30 onward: no tissue cysticercoids or lumenal adults of H. nana were established in these mice. However, when mice were challenged with H. nana 10 or 20 days after 10-day old immature H. microstoma were removed by an anthelmintic, the immunity evoked was directed exclusively against the lumenal phase of the cysticercoid challenge but not the tissue cysticercoids of the egg challenge. When mice experienced the prepatent infection with H. microstoma twice, the immunity evoked was also against the lumenal phase of the egg challenge: the oncospheres developed into tissue cysticercoids but thereafter completely failed to develop into lumenal adult tapeworms. Infection with a single cysticercoid of H. microstoma was shown to be sufficient to evoke immunity against H. nana cysticercoid infections in two strains of mice. Sera from mice which experienced a patent infection with H. microstoma revealed that IgG, IgA, IgM isotypes reacted against oncospheres and cysticercoids of both species, while sera from mice which experienced two prepatent infections reacted with cysticercoids only. Sera from H. microstoma infected mice resistant to H. nana caused precipitations on 4-day-old H. nana in vitro. A correlation exists between the presence of stage specific antibodies and resistance to the different stages.     

Circulating immunoglobulins and complement in mice with Hymenolepis nana infection

Changes in the circulating immunoglobulins and complement in ddY mice were assayed at various times after immunizing and challenge infections with Hymenolepis nana eggs. The levels of IgG1 and IgG2a consistently increased during 3–4 weeks after immunizing infection. The increase of these immunoglobulins after challenge infection was quicker and more intense than that following immunization. It was not possible to correlate increased levels of IgG1 and IgG2a with the onset of destruction of challenge larvae in immunized mice. IgM concentrations increased slightly during 4 days after immunization but challenge infection did not further increase IgM levels. IgA and IgG2b levels showed no significant change during the course of the infection. Serum C3 levels showed no discernible change after either immunizing or challenge infections. An attempt to specifically suppress the acquisition of resistance by administration of the complement-depleting agent, cobra venom factor (CoF), before immunization failed and depletion of complement activity with CoF that was administered just before challenge infection also failed to affect resistance. These results suggest that complement has no critical role in either induction of the response nor in the anamnestic response to H. nana infection in mice.     

Primary antibody and delayed type hypersensitivity response of mice to ovalbumin

The control of the ability to respond to three doses of ovalbumin has been studied in an attempt to find the minimum dose of antigen necessary for activation of primary antibody response and delayed type hypersensitivity response. In seven of the ten mouse strains studied, concordance of the minimum dose needed to elicit the two responses was observed. Discordance is found in the other strains, suggesting that the ability to respond to ovalbumin is independently controlled in several cells. The antibody and delayed type hypersensitivity responses to ovalbumin are controlled by at least two genes, one localized in the major histocompatibility complex.     

Taenia crassiceps in the rat: transfer of immunity and immunocompetence with lymph node cells.

Using T. crassiceps infections of young AS₂ rats as a model system, it was shown that immunity can be transferred adoptively with lymph node cells, whereas serum from the same donors was ineffective. Normal adult rat lymph node cells also conferred immunocompetence on neonatal recipients. There was no correlation between antibody and elimination or persistence of metacestodes in infected rats. It is suggested that susceptibility of neonates to infection with this parasite is the result of functional immaturity of thymus-derived cells involved in cell-mediated immune responses rather than T-cell facilitation of antibody production.     

Hymenolepis diminuta and H. nana: cross immunity against the lumen phase in BALB/c mice

When BALB/c mice initially given cysticercoids of Hymenolepis diminuta orally (Day 0) were challenged with eggs or cysticercoids of H. nana, almost all the mice became completely resistant to H. nana challenges from Day 30 onward, and no luminal adults of H. nana were established. There was a tendency for the number of tissue cysticercoids recovered 4 days after egg challenge in immunized mice to be much less than that in control mice (P less than 0.001, Student's t test). However, when these cysticercoids recovered from immune group mice were inoculated into uninfected mice, they matured in the lumen. Thus, the cross immunity to H. nana challenge evoked by an initial prepatent infection with H. diminuta appeared to be directed not against the tissue phase but against the lumen phase of H. nana. When BALB/c mice initially given eggs of H. nana were challenged with H. diminuta, they became resistant to H. diminuta from Day 15 onward. When the mice given eggs of H. nana were treated with a cestocide, praziquantel, at the beginning of the expected luminal development of H. nana and experienced a tissue phase only before challenge with H. diminuta, they showed no resistance to H. diminuta. Thus, the cross immunity to H. diminuta challenge evoked by an initial patent infection with H. nana appeared to be due to the immunogens of the lumen phase of H. nana but not those of the tissue phase. The cross immunity may be, therefore, essentially evoked by the lumen phase of these two phylogenetically closely related species and not by or against the tissue phase of H. nana.(ABSTRACT TRUNCATED AT 250 WORDS)     

The passive transfer of protective immunity against Angiostrongylus cantonensis with immune lymph node cells from different lymphoid tissues in rats

-Yong W. K. and Dobson C. 1982. The passive transfer of proctective immunity against Angiostrongylus cantonensis with immune lymph node cells from different lymphoid tissues in rats. International Journal for Parasitology12: 423–425. Lymph node cells from the posterior cervical and mesenteric lymph nodes of immune rats passively protected syngeneic recipient rats against Angiostrongylus cantonensis better than cells from the spleen, thymic and inguinal lymph nodes either as reduced worms burdens and/or stunted growth. No antibody was detected in the sera of recipient rats after transfer of the cells and before infection which suggested that the protection was cell- rather than antibody-mediated.     

Antigen specific lymphocyte transformation, delayed hypersensitivity and protective immunity. I. Kinetics of the response

The association between protective immunity, delayed hypersensitivity (DTH) and in vitro antigen specific lymphocyte transformation (ASLT) has been studied during the course of BCG infection in mice. The peak ASLT response was obtained 2 weeks after a subcutaneous footpad infection using lymph node cells draining the immunization site. This response decreased to a low but statistically significant level by week 4 and persisted indefinitely thereafter. A similar course of events was observed in splenic cell cultures, but the size of the response was smaller. The reactive cells were shown to be T-lymphocytes. The ability to express DTH to tuberculin purified protein derivative coincided with the emergence of cells capable of responding in ASLT assays. In contrast, there was a poor association between ASLT and protective immunity: lymphocytes from lymph nodes that did not drain the immunization site conferred substantial protective immunity but nonetheless failed to respond significantly in ASLT assays. The latter failure could not be attributed to insufficiency of sensitized lymphocytes and was independent of the antigen concentration and the culture incubation time. It was concluded that the ASLT reactive cells were either immunoblasts or recent progeny of these cells.