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Biomedical subjects

K S Warren

Publications and source records attributed to K S Warren.

At least 145 records · Page 8Linked to original sources
PubMed1975

Antieosinophil serum and the kinetics of eosinophilia in Schistosomiasis mansoni.

Mice were exposed to different intensities of infection with Schistosoma mansoni (10, 50, or 200 cercariae) and the kinetics of peripheral and bone marrow eosinophilia was followed for as long as 20 wk. When the schistosomula (immature worms) were migrating from the lungs to the liver there was a mild, transient eosinophilia, but soon after the onset of egg laying by the schistosomes, a major and prolonged increase in eosinophils occurred. This was terminated in the heavier infections by the death of the animals, but showed a spontaneous decline beginning at 18 wk in the lightly infected mice. The effect of S. mansoni eggs on eosinophilia in the blood, bone marrow, and granulomatous lesions was then examined by injecting schistosome eggs into mice intraperitoneally, subcutaneously, and intravenously. While the host response was dependent on the route by which eggs were administered, primary peripheral and bone marrow responses were seen on intravenous injection, and secondary responses occurred on intravenous and subcutaneous injection. In unsensitized and egg-sensitized mice, eosinophils were first seen around eggs injected into the pulmonary microvasculature at 96 and 24 h respectively. When the granulomas were maximal in size eosinophils made up at least 50% of the lesions. Administration of antieosinophil serum profoundly suppressed eosinophils in the peripheral blood, eliminated mature eosinophils and markedly increased eosinophil precursors in the bone marrow, and ablated eosinophils from the tissue lesions, considerably reducing their area.

Animals↗
PubMed1975

Suppression of delayed hypersensitivity in schistosome-infected patients by niridazole.

Niridazole, an anti-parasitic drug, suppresses manifestations of delayed hypersensitivity and retards allograft rejection in laboratory animals. We investigated the immunosuppressive effects of the standard antihelminthic regimen of niridazole (25 mg/kg/day for seven days) in five patients with schistosomiasis. Although 15-minute skin reactions to schistosomal antigens remained unchanged, niridazole reduced or ablated positive 48-hour skin reactions to tuberculin (PPD), mumps and schistosome antigens in all patients tested six and 15 days after therapy began. Complete recovery of delayed dermal hypersensitivity was observed by 114 days. PPD-induced lymphocyte transformation was severely depressed in three and partially depressed in two of the five patients. Suppression was observed at either six or 15 days (or both) after beginning of treatment, and complete recovery at 114 days. It is concluded that therapeutic doses of niridazole suppress delayed hypersensitivity and antigen-induced lymphocyte transformation in man.

Adolescent↗
PubMed1975

Streptozotocin-induced diabetes mellitus and the host-parasite relation in murine schistosomiasis mansoni.

The effect of streptozotocin-induced diabetes mellitus on both the host and the parasite was studied in mice infected with Schistosoma mansoni. Neither the drug nor the marked rise in concentration of blood glucose had any effect on penetration of the skin by the cercariae, their subsequent maturation into adult worms, or their output of eggs. During the acute stages of the infection (at eight weeks), the diabetic animals showed marked suppression of the host granulomatous reaction to schistosome eggs trapped in the liver, accompanied by an alleviation of hepatosplenic disease. During the chronic stages of infection (at 16 weeks), there was a pronounced megalocytosis of the hepatocytes only in the infected animals with streptozotocin-induced diabetes; these animals also had an exacerbation of hepatosplenic disease.

Animals↗
PubMed1975

Calorie and protein malnutrition in chronic murine schistosomiasis mansoni: effect on the parasite and the host.

The effects of diets containing 8% and 4% protein and of 50% calorie-deficient diets on the host, the parasite, and the parameters of disease in chronic hepatosplenic schistosomiasis were studied in mice that were infected for 20 weeks with Schistosoma mansoni. Controls consisted of uninfected mice of the same size and age maintained on a balanced 20% protein diet. Each of four corresponding dietary groups of infected and uninfected animals was fed on its assigned diet from the 20th to the 24th week of infection. Between the 24th and the 28th week of infection, all groups were nutritionally repleted by being returned to the standard control diet. Changes in body weight and deaths were recorded throughout the experiment (20-28 weeks). Parasite and host responses were measured at 24 weeks and again at 28 weeks. Severe protein and calorie deficiencies were associated with diminished egg output, an effect that appeared to be residual in the most severely malnourished animals for some time after malnutrition has been corrected. In general, the parameters of hepatosplenic disease were less severe in the more severely malnourished animals; 50% calorie deficiency was the cause of greater amelioration than marked protein depletion. During the period of malnutrition the mortality rate in mice given the 4% protein diet was not significantly different from that in controls (approximately 30%), while that in the calorie-restricted animals was only 9%.

Animals↗
PubMed1975

The lymphokine eosinophil stimulation promoter and human schistosomiasis mansoni.

An in vitro assay for the new lymphokine eosinophil stimulation promoter has been adapted for use with human material. Peripheral eosinophils from patients with schistosomiasis mansoni were specifically induced to migrate on incubation with egg antigen. Furthermore, the peripheral lymphocytes of these patients on incubation with the egg antigen secreted the lymphokine eosinophil stimulation promoter, which enhanced the migration of purified eosinophils from patients with or without schistosomiasis. The test can be easily performed with human target cells and may be helpful for diagnostic or investigative purposes.

Antigens↗
PubMed1975

Regulation of spleen growth and portal pressure in hepatic shcistosomiasis.

Growth rate and histology of splenic autotransplants in subcutaneous pockets were compared with those of autotransplants in the extrahepatic portal bed in splenectomized mice infected with cercariae of Schistosoma mansoni and in splenectomized uninfected controls. By the fifteenth week after transplantation (and tenth week after injection of cercariae) subcutaneous transplants gained 6.5 times and omental transplants 8.2 times more weight in infected animals than corresponding transplants in uninfected animals. Portal pressures averaged 11 to 13 cm of water in infected animals with transplants and 17 cm in those with intact spleens (compared to that of 6 to 7 cm in controls). Hyperplasia of white pulp with increase in germinal center activity characterized transplants as well as intact spleens of infected animals. The results suggest that a) During the first 10 weeks of experimentally induced infection, portal congestion is not the predominant mechanism regulating increased spleen growth; and b) An intact enlarged spleen appears to contribute to elevated portal pressure.

Animals↗
PubMed1975

The Schistosoma japonicum egg granuloma.

Although Schistosoma japonicum egg granulomas are generally considered to be similar to those of S. mansoni (which are largely immunologic reactions of the delayed hypersensitivity type) there are suggestions that the histopathology and perhaps the etiology of the lesions are different. In mice with light S. japonicum infections, at 5 weeks after infection (2 weeks after egg production began), the livers contained 36,000 eggs each, but there was no reaction to the eggs, nor any evidence of hepatosplenic disease. By 6 weeks, large abscesses replete with cosinophils occurred around some of the eggs, and there was periportal inflammation consisting predominantly of plasma cells. From this time on, major lesions occurred mainly around large aggregates of eggs, and there was hepatosplenomegaly and portal hypertension. Living S. japonicum eggs injected into the pulmonary microvasculature of mice did not evoke significant granulomatous reactions on either primary or secondary exposure. Even when the eggs were injected into the lungs of infected animals, which had large granulomas around egg aggregates in the liver, little or no inflammatory reaction was seen around the eggs distributed singly throughout the pulmonary vessels. When the priming dose of eggs or soluble egg antigens was injected subcutaneously with or without complete Freund's adjuvant, significant granuloma formation occurred around eggs subsequently injected into the lungs. On the basis, therefore, of differences in the parasite factor (eggs) and host factors (histopathology and responses to routes of injection) it is suggested that the immunologic factors responsible for granuloma formation around S. mansoni and S. japonicum eggs may differ significantly.

Animals↗