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W F Piessens

Publications and source records attributed to W F Piessens.

At least 73 records · Page 4Linked to original sources

Stage-specific and common antigens of Brugia malayi identified with monoclonal antibodies.

To identify parasite antigens that trigger protective, pathogenic, and allergic immune responses during filarial infections, we generated a series of monoclonal antibodies to infective larvae, adult worms, and microfilariae of Brugia malayi, a human pathogen. Quantitative and qualitative analysis of the reaction patterns of these monoclonal antibodies indicates the existence of stage-specific antigens of B. malayi, as well as of antigens shared by different stages of this parasite and by other related and unrelated helminths. These antibodies should provide invaluable tools for the analysis of host-parasite interactions in filariasis at the molecular level.

Animals↗

Predisposition to Brugia malayi microfilaremia in progeny of infected gerbils.

Patency of Brugia malayi infection in gerbils born of infected parents was compared to that in gerbils from noninfected parents. Following infection with third stage larvae, female progeny of infected parents generally became microfilaremic whereas those of noninfected parents rarely did so. Male progeny developed microfilaremia regardless of parentage, although descendants of infected parents tended to have higher parasitemia. We conclude that B. malayi infection in the mother predisposes the offspring to patent infection subsequent to inoculation with infective larvae.

Animals↗

Opposing effects of filariasis and chronic malaria on immunoregulatory T lymphocytes.

The effect of parasitic infections on immunoregulatory T lymphocytes was evaluated by means of quantitative determinations of total T cell and T-cell subset populations present in peripheral blood of patients with lymphatic filariasis, with the malaria-induced tropical splenomegaly syndrome (TSS), and with both infections. Total T-cell numbers were similar to control values in patients without TSS, and reduced in donors with TSS. OKT4+/OKT8+ T-cell ratios were decreased in microfilaremic donors without TSS (0.76 +/- 0.08) and elevated in patients with TSS without microfilaremia (1.97 +/- 0.16). Patients with dual infections tended to yield results similar to uninfected control donors. Thus, filariasis and chronic malaria (TSS) have opposing effects on the normal balance of immunoregulatory T lymphocytes. In patients with TSS, the imbalance appears to result from a decrease in the absolute number of circulating T cells with suppressor/cytotoxic phenotype.

Adult↗

Antigen-specific suppressor T lymphocytes in human lymphatic filariasis.

Immune responses to parasite antigens are much lower in patients with microfilaremia than in persons with other manifestations of brugian filariasis. To determine whether hyporeactivity is associated with changes in populations of lymphocytes that regulate immune responses, we quantitated helper and suppressor T cells in the blood of patients infected with Brugia malayi. Increased numbers of suppressor T cells were present in 15 of 17 patients with microfilaremia and in six of 11 patients with elephantiasis. This increase correlated with hyporeactivity to filarial antigens but not to nonparasite antigens. Removal of suppressor T cells activated in vivo or in vitro improved reactivity to filarial antigens. These results suggest that immunosuppression induced by filarial parasites is a possible mechanism of survival of these organisms in an immunocompetent host.

Adolescent↗

Brugia malayi microfilariae from the peritoneal cavity of jirds vary in their ability to penetrate the mosquito midgut.

Development in mosquitoes of Brugia malayi microfilariae obtained from the blood of jirds was compared to that of microfilariae from the peritoneal cavity. Penetration of the mosquito midgut wall as well as development into third-stage larvae was assessed. About 70% of blood-borne microfilariae penetrated the midgut wall whether ingested directly from a microfilaremic jird or from a membrane feeder containing blood from the same donor. In contrast, less than 30% of microfilariae from the peritoneal cavity penetrated the midgut wall. Microfilariae in the peritoneal cavity of jirds vary in ability to penetrate the midgut of mosquitoes; some penetrate as rapidly as do blood-borne microfilariae, others penetrate more slowly, and most fail to penetrate the midgut. Regardless of origin, microfilariae that penetrated the midgut wall developed into third-stage larvae.

Aedes↗

Complement-mediated adherence of cells to microfilariae of Brugia malayi.

Immune sera promote the adherence of human buffy coat cells to microfilariae of Brugia malayi. This effect is augmented by the simultaneous addition of fresh human or guinea pig serum. The heat-labile, adherence-promoting factor present in nonimmune sera appears to be complement. In the absence of antibody, microfilariae activate complement via the alternative pathway and C3 is deposited on the microfilarial sheath.

Animals↗

Effect of treatment with diethylcarbamazine on immune responses to filarial antigens in patients infected with Brugia malayi.

We studied the effect of treatment with diethylcarbamazine (DEC) on immune responses to parasite antigens in humans infected with Brugia malayi. In vitro lymphocyte proliferative responses to microfilarial antigens increased in patients who became amicrofilaremic after treatment with DEC. No changes in reactivity were observed in amicrofilaremic individuals who were given DEC or in a small number of patients who remained microfilaremic after treatment. Reactions to other antigens (PPD and SKSD) were not affected by drug treatment. Serum titers of antibodies to the sheath of B. malayi microfilariae did not significantly change during the period of observation. These findings indicate that DEC partially reverses the state of cellular unresponsiveness to parasite antigens associated with patient filarial infections.

Adult↗

Antigen-specific suppressor cells and suppressor factors in human filariasis with Brugia malayi.

We investigated the mechanisms of specific immune unresponsiveness to microfilarial antigens. The blood of patients with obvious Brugia malayi infections contains an adherent cell type that specifically suppresses reactions to microfilarial antigens but not to other antigens. In the absence of continued stimulation by parasite antigens, this suppressor cell loses its functional activity after overnight culture in vitro. Furthermore, serums from patients with and without microfilaremia contain factors that also suppress reactions to filarial antigens in vitro. These results suggest that immune unresponsiveness in human beings with patent filarial infections is due to active suppression of immune responses directed against the parasite and not to an intrinsic inability of infected patients to react to parasite antigens.

Adult↗

Immune responses in human infections with Brugia malayi: specific cellular unresponsiveness to filarial antigens.

We evaluated the cellular immune competence of 101 subjects living in an area of South Kalimantan (Borneo) where Malayan filariasis is endemic. All patients with elephantiasis but none with other clinical stages of filariasis reacted with adult worm antigens. The majority of subjects without clinical or parasitological evidence of filariasis and approximately one-half of those with amicrofilaremic filariasis reacted with microfilarial antigens. In contrast, most patients with patent microfilaremia did not respond to microfilarial antigens. The in vitro reactivity of all patient categories to nonparasite antigens was similar to that of the distant control group. These results indicate that patent microfilaremia is associated with a state of specific cellular immune unresponsiveness and are consistent with the current hypothesis that the various clinical manifestations of filariasis result from different types of immune responses to distinct antigens associated with different developmental stages of filarial worms.

Adolescent↗