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In this paper, an immune-inspired model, named innate and adaptive artificial immune system (IA-AIS) is proposed and applied to the problem of identification of unsolicited bulk e-mail messages (SPAM). It integrates entities analogous to macrophages, B and T lymphocytes, modeling both the innate and the adaptive immune systems. An implementation of the algorithm was capable of identifying more than 99% of legitimate or SPAM messages in particular parameter configurations. It was compared to an optimized version of the naive Bayes classifier, which has been attained extremely high correct classification rates. It has been concluded that IA-AIS has a greater ability to identify SPAM messages, although the identification of legitimate messages is not as high as that of the implemented naive Bayes classifier.

Oral administration of protein antigens, such as ovalbumin, may result in induction of either tolerance or immunization. To avoid oral tolerance, there are new strategies to protect the antigens from degradation within the gastrointestinal tract and to allow them to reach inductive immunological sites. One such strategy is the usage of liposomes. Different parameters may influence the stability of liposomes in the gastrointestinal tract. Herein, we studied the immunological consequences of oral administration of liposome-encapsulated ovalbumin in different strains of mice using different liposomes. Our data demonstrated that ovalbumin liposomes improved the induction of oral immunization and the degree of improvement depended on the liposome type and on the strain of mice used. The mechanism responsible for this differential effect of liposomes depended on the site of antigen release and absorption. Therefore, some liposomes might be suitable as adjuvants for oral immunization, others for oral tolerance induction.

The parotid lymph nodes of naive and previously infected Balb/c mice were studied after, respectively, infection and re-infection with cercariae of Schistosoma mansoni via the ears. Schistosomula were able to pass through the lymph node by following the lymph flow or by penetrating the veins of the medullary cords. The number of nodal mast cells was higher from day 2 to 6 of primary infection; and from day 5 to 11 of re-infection. The amount of degranulating mast cells was significantly higher at day 4 of infection and at day 1 of re-infection. Eosinophils characterized the nodal inflammatory processes observed after day 5 in both primarily-infected and re-infected mice. However, only in the latter the eosinophils were able to adhere to the larval surface. In primarily-infected mice, no intranodal larva presented signs of degeneration. In contrast, in re-infected animals, some degenerating larvae were found inside eosinophilic infiltrates. The eosinophils reached the nodal tissue by migrating through the high endothelial venules and their collecting veins.

1. Evidence is presented for the participation of mast cells in the resistance of mice to infection by Schistosoma mansoni. 2. Intravenous injection of 1 micrograms/g body weight of the ionophore 48-80, a potent mast cell degranulator, significantly reduced (42-62%) the histamine content of the ear tissue of normal mice and either increased or decreased resistance to parasite penetration and infection depending on whether the injection of the ionophore was 5 min or 2 days before cercarial penetration. 3. When 48-80 was injected 5 min before the beginning of cercarial penetration, the number of parasites recovered from ear tissue 2 days later or from the portal system 30 days later was significantly reduced (39-71% and 27-40%, respectively) in relation to untreated controls. This resistance caused by 48-80 was blocked when mice were simultaneously treated with cyproheptadine, an antagonist of vasoactive amines. 4. In contrast, when 48-80 was administered 2 days before the beginning of cercarial penetration, the number of parasites retrieved from ear tissue 2 days later or from the portal system 30 days later was 32-64% and 28-30% larger, respectively, in relation to untreated controls. 5. These findings indicate that the local inflammatory reaction mediated by mast cells is important in the resistance of mice to infection with S. mansoni.

1. In order to study local tissue anaphylactic responses to infection with Schistosoma mansoni cercariae, mice of three different strains (C57BL/10J, Balb/cJ and CBA/J) were infected by subcutaneous injection of 15 to 20 cercariae. Eleven to 16 weeks later the animals were reinfected through one ear with 250 to 350 cercariae. 2. Throughout the infection period, the histamine content of the ears increased up to 150% of control values. Upon reinfection, the penetration of cercariae through the ear reduced its histamine content to near normal values. 3. Reinfection causes inflammation as judged by a 1.5 to 2.3-fold increase in the amounts of plasma leaking through the ear vessels as measured by leakage of Evans blue dye. 4. These results suggest that the local inflammatory reaction mediated by mast cells is important in the resistance of mice to reinfection with S. mansoni.

Mechanically transformed schistosomula of Schistosoma mansoni exposed to mouse, rat or human inactivated immune sera (coated schistosomula) and then injected intravenously into CBA mice were recovered from their lungs in smaller numbers than were schistosomula exposed to normal sera, immune sera absorbed with S. mansoni tegument, or sera from mice bearing unisexual cercarial infections and displaying moderate titers of lethal antibodies. The reduction of the number of coated schistosomula recovered from the lungs, as well as the lethal effect in vitro, were mediated by 7S fraction of the immune sera. Decomplementation (by Cobra Venom Factor) or irradiation (650 R, 1, 3, and 5 days before injection) of recipient mice, increased the number of coated schistosomula recovered from their lungs.

The ability of Schistosoma mansoni schistosomula to evade in vitro cytotoxic activity of antibodies plus complement is shown to be increased by incubation with Concanavalin A (Con A) or with non-immune inactivated human serum. This effect was not observed if S-adenosyl-homocysteine (SAH) a methyltransferase inhibitor was added to the incubation medium. Methyl group incorporation occurs in schistosomulum phospholipids if parasites are incubated in Earle's balanced salt solution. This incorporation is increased by Con A addition and this increase is inhibited by SAH. Supernatants of schistosomula incubated in culture media containing Con A were able to promote phospholipid methylation, showing that methyltransferases were liberated into the culture media. The possible roles played by these phenomena in host-parasite interactions are discussed.

A marked reduction in the number of plaque-forming cells from spleens of mice infected with Schistosoma mansoni to sheep erythrocytes (SRBC) and lipopolysaccharide from Escherichia coli was observed. This reduction coincided with the late stages of the infection and was also observed in unisexual infection with male worms. Treatment of the animals with a schistosomicidal compound (oxamniquine) almost completely abolished the immunosuppression. The suppression could be induced by administration of 60 microgramg protein from worm membrane preparations (24 h before SRBC injection), but not by egg-extract injection. When the crude membrane preparation was injected 48 h before or 0 to 24 h after the SRBC challenge, the immunosuppression was not observed. Significant reduction of footpad swelling was also noted in infected mice when injected with SRBC.

Incorporation of labelled amino acid into tegumental proteins and acquisition of protection by schistosomula against antibody-mediated killing in vitro were simultaneously stimulated by serum factors and inhibited by puromycin. Comparison of polyacrylamide gel electrophoresis patterns with fluorographic autoradiography indicates that the majority of proteins in the parasite tegument were labelled with the isotope after incubation for 3 h. No new, clearly defined band was observed in the autoradiography pattern. During this period a decreasing susceptibility of the schistosomula to antibody plus complement was observed. Quantitative fluorescence assay shows that schistosomula insensitive to antibody plus complement were still able to bind the same amount of antibody as the unprotected parasites. Pre-culture of schistosomula in the presence of inactivated normal rabbit serum also decreased the susceptibility of the parasites to the in vivo killing mechanism.

Acquired immunity to Schistosoma mansoni induced by a primary infection with cercariae of one or both sexes was assessed in mice by the recovery of parasites of a challenge infection from the lungs or the liver. In addition, the antibody-dependent complement-mediated cytotoxicity against schistosomula in vitro was titrated in sera obtained from both groups of animals. The degree of immunity as detected by the lung recovery technique in mice infected with a mixture of male and female cercariae was variable and lower than 50%. In contrast, no immunity was observed in the group of animals infected with 40 'single-sex' cerariae. The titre of lethal antibody in a pool of sera firm these animals was about 10, whereas it was about 640 in a pool of sera from bisexually infected animals. Lethal antibody titres ranged from 20 to 120 for unisexual infection and 240 to 1920 for bisexually infected mice. In some cases a significant degree of immunity was detected by liver perfusion in mice with a primary unisexual infection. However, the lethal antibody titre of sera from mice with a 'single-sex' infection remained low, even when the immunity was apparent.

Normal and S. mansoni-infected mice were exposed to the penetration of 250-350 cercariae through one ear. Two days later, when the ear was removed and chopped, 30 to 50% more schistosomula were recovered from the ears of normal mice than from the ears of infected (immune) mice. Administration of cyproheptadine, a histamine-serotonin antagonist (2 mg/kg), 30 min before challenge infection rendered immune mice indistinguishable from normal mice. Partial depletion of histamine by pretreatment with compound 48-80, a histamine releaser (1 mg/kg) 2 days before challenge infection increased the numbers of schistosomula recovered from the ears of both normal and immune mice. These results are interpreted to mean that vasoactive amines released by skin mast cells play an important role in hindering the viable passage of schistosomula through the skin of normal and immune mice.