Effect of dietary magnesium on Ascaris suum infections of mice

Low amounts of dietary magnesium affected the inflammatory tissue response in nonimmunized mice differently than in immunized mice. Eosinophil numbers and LPL activity in lung tissue following infection with A. suum larvae were altered by the level of magnesium in the diets of mice. Average or higher dietary levels of magnesium resulted in decreased numbers of lung larvae indicating an overall protective effect. Increases in eosinophil numbers or LPL activity were not directly related to the numbers of larvae/lungs. Larvae/livers, eosinophil numbers, and LPL activity were affected by the types of magnesium diets that mice received. Nonimmunized mice had differences in larvae/liver (at 2 days and 7 days pi) and LPL activity (at 2 days pi). Immunized mice had varying findings at 2 days pi but a direct relationship between dietary magnesium and numbers of larvae, numbers of eosinophils, and liver LPL activity at 7 days pi.     

Stimulation of leukocyte lysophospholipase activity by noninfectious agents

Mouse peritoneal leukocyte lysophospholipase (LPL) activity was studied to determine whether or not noninfectious agents cause increased enzyme activity and whether neutrophils have LPL activity. In the first study, mice infected with Ascaris suum, a known inducer of LPL activity, were given intraperitoneal injections of proteose peptone, thioglycolate, bovine albumin, paraffin, glycogen, or A. suum whole worm extract (WWE). Cell populations collected from mice injected with A. suum WWE, proteose peptone, thioglycolate, or bovine albumin contained increased numbers of neutrophils and eosinophils. These cell populations had increased LPL activity when treated, in vitro, with either A. suum WWE, zymosan-activated complement, or with the agent they were induced with. However, the LPL activity of the different cell populations did not respond to all treatments in the same way. In a second study, A. suum-infected or noninfected mice were given intraperitoneal injections of paraffin, thioglycolate, glycogen, or A. suum WWE. Enriched cell populations containing either lymphocytes or macrophages, from infected or noninfected mice, did not have increased LPL activity following in vitro stimulation with A. suum WWE, zymosan-activated complement, or with the agent they were induced with. Enriched neutrophil populations from infected or noninfected mice had increased LPL activity following in vitro treatment with A. suum WWE or zymosan-activated complement. Results demonstrate that the LPL activity of peritoneal leukocytes can be induced by noninfectious agents and that neutrophils have increased LPL activity following in vitro stimulation.     

Effects of immunoactivity on Ascaris suum infection in mice]

The immune response to sheep red blood cell (sRBC) was monitored in the mice infected with Ascaris suum or Trichinella spiralis. The effects of the infection with T. spiralis or the injection with cyclophosphamide(CY) as an immunosuppression agent prior to challenge infection with the embryonated eggs of A. suum were monitored in mice by means of the level of infection with A. suum and cellular and humoral immune response to sRBC. Following the oral administration of 1,000 eggs of A. suum to mice, delayed-type hypersensitivity (DTH) and rosette-forming rate were gradually decreased and reached to the lowest levels at the 5th week and 6th week postinfection, respectively, and then returned to normal at the 10th week. The hemagglutinin(HA) and hemolysin(HE) titers were gradually elevated and reached to peak at the 3rd week postinfection, and then returned to normal level. The appearance ratios of the eosinophils and mast cells were in peak at the 4th week and the 2nd week postinfection, respectively. Meanwhile the harvest ratio of A. suum larvae from the liver and lungs was 21.97% at the 1st week postinfection. Following the oral administration of 300 T. spiralis infective larvae, DTH and rosette-forming rate were gradually decreased with the lapse of time and reached the lowest values in the 30th and 21st day of postinfection, and then slightly increased and transiently decreased in the 70th and 80th day of postinfection, respectively. HA and HE titers were the lowest in the 21st and 90th day, whereas the ratios of eosinophils and mast cells were the highest on the 40th and 14th day postinfection, respectively. Following the intraperitoneal injection of CY, the body weight, the spleen weight, DTH, rosette-forming ratio, HA and HE titers, the number of WBC and the ratio of the mast cell were predominantly decreased in the 5th day, and then returned to the same value of the 1st day postinjection. The ratio of eosinophils was gradually decreased following to advance of days. At the 1st, 5th and 10th days after intraperitoneal injection of CY of 400 mg/kg, a dose with 1,000 eggs of A. suum was administered orally to mice, and harvest rate of the larvae at the 7th day postadministration was 7.07% in the 1st day, 14.94% in the 5th day, 10.1% in the 10th day, 8.02% in control group. The effect of prior infection with infective larvae of T. spiralis upon immunological sequelae of a challenge infection of mice with embryonated eggs of A. suum in 30 or 70 days interval was checked.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effect of egg dosage and host genotype on liver trapping in murine larval toxocariasis

In this study we examined the effect of various initial sensitizing doses of infective Toxocara canis eggs and the effect of murine host genotype on the level of trapping of larvae in the liver after larval challenge. In the initial experiments, C57BL/6J mice were infected with a sensitization dose of 5, 25, 75, 125, or 250 infective T. canis eggs on day 0 postinfection (PI). On day 28 PI all mice were challenged with 500 infective eggs. On days 7, 14, and 21 postchallenge (PC) larval numbers within individual livers were determined. Trapping of larvae was observed in mice receiving a sensitization dose of 25 or more eggs. At 7 and 14 days PC the level of trapping increased with sensitization egg dose up to a dose of 125 eggs. At 21 days PC the level of trapping reached a plateau at a sensitization dose of 75 eggs. The peak level of larval trapping was observed on day 7 and day 14 PC following sensitization doses of 125 and 250 eggs, respectively. In the subsequent experiments, mice of various strains and H-2 haplotypes were inoculated with an initial sensitization dose of 125 eggs and a challenge dose of 500 eggs on day 0 and day 28 PI, respectively. Larval trapping within the liver was determined on day 14 PC. C57BL/6J mice trapped significantly more larvae than DBA/2J mice (P less than 0.01); all other strains trapped larvae at a lower, but statistically similar, level to the C57BL6/J mice.(ABSTRACT TRUNCATED AT 250 WORDS)     

Eosinophilia in Ascaris suum-reinfected mice

The secondary response of eosinophilia has been studied in mice infected with A. suum. In mice infected orally with 1000 A. suum eggs, larvae disappeared from the body within two weeks after infection. The number of peripheral blood eosinophils decreased to the pre-infection level within eight weeks. A typical secondary response of IgG antibody production to egg antigen was found after reinfection with 1000 eggs. The number of peripheral blood eosinophils increased more rapidly after reinfection than after the primary infection. However, the peak number of eosinophils after reinfection was similar to that after primary infection, and the long-lasting characteristics of eosinophilia after reinfection did not differ from those after primary infection. These results suggest that the secondary response of eosinophilia is characterized by a rapid increase in the number of eosinophils in A. suum-reinfected mice.     

Acquired resistance to migrating larvae of Ascaris suum in young pigs by repeated drug-abbreviated infections

Cross-bred 3- and 8-wk-old pigs were used to test whether drug-abbreviated infections with Ascaris suum can stimulate acquired resistance to challenge. During the immunization period, both age groups of animals were infected with increasing numbers of A. suum eggs (500, 1,000, 2,000, 5,000, 10,000, and 20,000) at 7-day intervals while the pigs were receiving pyrantel tartrate in the feed. Two days after the last infective dose, animals were placed on unmedicated feed for 8 days and then challenged with 10,000 eggs. All pigs were killed 7 days after challenge, and milk spots on the livers and larvae recovered from the lungs were counted. Larval recoveries from lungs of the immunized animals were significantly smaller than those from the unimmunized animals in both age groups, suggesting that the pigs were capable of acquiring strong resistance to parasitic infections. In immunized animals, challenge infection did not contribute significantly to milk spot formation. The number of milk spots was significantly greater in the older animals, indicating that milk spot formation may be age related.     

Kinetics of liver trapping of infective larvae in murine toxocariasis

Mice sensitized by prior infection with Toxocara canis eggs trap many larvae of a challenge infection within the liver. In this study the distribution of challenge larvae in sensitized mice was examined to determine the earliest onset of liver trapping and to establish if the previously described phenomenon truly represented larval trapping. In all experiments, C57BL/6J mice were infected with a sensitization dose of 125 infective T. canis eggs on day 0 postinfection (PI) and challenged with 500 infective eggs on day 28 PI. In the initial experiments, larval numbers were determined within the intestinal contents, intestinal wall, mesenteric tissues, liver, lungs, skeletal muscle, and brain of each mouse on days 0.5, 1, 2, 3, 5, and 6 postchallenge (PC). Migration patterns were similar among the test and control groups except the peak of larval numbers in the liver, seen at 1 day PC in control mice, was delayed until 3 days PC in the test group. Larval trapping occurred within the liver of test mice at least by day 5 PC. In subsequent experiments, larval numbers were determined within the liver, skeletal muscle, brain of each mouse, and within the eyes of each mouse group at 4, 8, 12, and 16 wk PC. Larval numbers within the liver of test mice were similar both at 5 days PC and 16 wk PC, implying that larvae were trapped in this organ rather than delayed in their migration to other body sites. Liver trapping did not protect the eyes or brain of sensitized mice from larval migration, nor did it result in larval killing.     

Ascaris suum: development of intestinal immunity to infective second-stage larvae in swine

The development of protective immunity to Ascaris suum was examined in pigs naturally exposed to eggs on a contaminated dirt lot. Pigs became almost totally immune to second-stage larvae migrating from the intestines because few larvae from a challenge inoculum could be found in the lungs, and liver white-spot lesions (an immunopathologic response to migrating larvae) were absent. Blood from these pigs contained lymphocytes that responded blastogenically to larval antigens in vitro, while the serum contained antibody to larval antigens. Immunity was related to parasite exposure and not to the age of the host, and was not affected by the removal of adult A. suum from the intestines. Naturally exposed pigs responded to a variety of A. suum antigens with an immediate-type skin reactivity, and their intestinal mucosa contained relatively large numbers of mast cells and eosinophils. Other pigs were maintained on a dirt lot not contaminated with A. suum eggs and the effects of common environmental conditions on development of resistance to A. suum were studied. Resistance also developed in these pigs because 72% fewer larvae were detected in their lungs following a challenge exposure than in control pigs confined indoors on concrete floors and challenged similarly. This response was not expressed at the intestinal level, however, because their livers had numerous, intense white-spot lesions. To verify that the intestinal immunity that developed in pigs after natural exposure to A. suum was a direct result of homologous infection and not related to other stimuli encountered on a dirt lot, pigs maintained indoors on concrete floors, free from inadvertent helminthic infection, were inoculated orally with A. suum eggs daily for 16 weeks. Intestinal immunity was induced because larvae from a challenge inoculum were not detected in the lungs, and few white-spot lesions appeared on the livers of these pigs. Apparently, continual exposure of the intestinal mucosa to larvae eventually elicits the appropriate effector components necessary to prevent larval migration from the intestines.     

Alternative migration routes of Ascaris suum in the pig

Experiments were conducted to investigate possible alternative routes of extraintestinal migration of Ascaris suum larvae in the pig. Pigs were infected with A. suum via injection of newly hatched larvae into cecal veins (i.v.), into cecal lymph nodes (LN), or intraperitoneally (i.p.), and control animals were inoculated orally with infective eggs (p.o.). Two pigs per inoculation route were necropsied on days 1, 4, and 13 postinoculation. The numbers of liver lesions and the percentage of larvae recovered was considerably greater in pigs inoculated i.v. or p.o. on each necropsy day. However, irrespective of inoculation route, at least a proportion of larvae passed through the livers and were able to complete migration to the small intestine by day 13. The results indicate that larval penetration of the intestinal wall is not necessary for liver-lung migration and that passage through the liver may be favorable for migrating A. suum larvae, although a delayed arrival in the small intestine cannot be ruled out for larvae following alternative routes.     

Taenia taeniaeformis: early inflammatory response around developing metacestodes in the liver of resistant and susceptible mice II. Histochemistry and cytochemistry

Female BALB/cJ (resistant), C3H/HeJ (intermediate resistant), and C3H/HeDub (susceptible) inbred mice, 4-5 wk old, were infected with Taenia taeniaeformis. Liver sections were stained for the enzymes acid phosphatase, beta-glucuronidase, and peroxidase. Eosinophils present around the parasite were identified by the ethanolic Congo red method. Possible gross changes in lipid metabolism in the hepatocytes surrounding the parasite were investigated with the Sudan black B method. The results of observations made by light microscopy were: (1) beta-glucuronidase activity above background levels was observed only in the hepatocytes around the parasite in BALB/cJ mice at 4, 5, and 6 days postinfection (PI); no reaction was observed in the other 2 strains of mice studied; (2) acid phosphatase activity was very strong at 2, 3, and 4 in the 3 strains of mice while this reactivity was weak at 5 and 6 days PI; (3) the cytoplasm of the hepatocytes around the metacestode stained more heavily with Sudan black B than other hepatocytes; and (4) the presence of eosinophils appearing at 3 days PI around the parasite in all 3 strains of mice was demonstrated by staining with Sudan black B, the substrate of peroxidase, and Congo red. Infected C3H/HeJ and BALB/cJ mice had higher numbers of liver eosinophils than infected C3H/HeDub mice throughout the observation time. The present results suggest 2 conclusions: (1) a parasite-liver interaction occurs as is evident by hepatocyte changes in beta-glucuronidase activity and Sudan black B staining, and (2) resistance to the early stages of T. taeniaeformis is associated with the appearance of eosinophils.     

Studies on the abomasal pathology of immunized and non-immunized sheep infected with Haemonchus contortus

Five adult ewes and five lambs were repeatedly immunized with weekly doses of 10,000 irradiated Haemonchus contortus L3 before challenge with 100,000 and 10,000 normal larvae respectively. Two groups of non-immunized ewes and lambs were similarly challenged and one animal from each of the four groups killed on days 3, 5, 7, 10 and 24 post-challenge. The cellular changes in the abomasal mucosa were less marked in the non-immunized groups than in the immunized animals and appeared later in the lambs than in the ewes. Thus, in the immunized ewes increases in the numbers of mast cells and eosinophils were evident within five days of challenge whereas similar changes appeared later in the immunized lambs. Also marked lymphoid aggregates at the base of the mucosa and in the submucosa were detected only in the immunized ewes. However, both immunized and non-immunized ewes showed rises in the numbers of IgA plasma cells after challenge which were not evident in either group of lambs.     

Depletion of eosinophils by anti-IL-5 monoclonal antibody treatment of mice infected with Trichinella spiralis does not alter parasite burden or immunologic resistance to reinfection.

Mechanisms of parasite killing by eosinophils are widely studied and are often implicated in mediating resistance to parasitic infection, especially in conjunction with specific antibodies. Evidence for the eosinophil as an anti-parasite killer cell in vivo is limited and may not justify the belief that eosinophils engage and/or kill infective helminths. We reexamined this question in a mouse model of trichinosis in which antisera to eosinophils were previously used to show the requirement for eosinophils in resistance to this nematode. The current studies used mAb to IL-5 to suppress eosinophil levels in CF1 mice infected with Trichinella spiralis. In mice given a primary infection and injected with an isotype control mAb or left untreated, the medullary and peripheral blood eosinophil numbers peaked at 3 wk postinfection (PI) and returned to baseline levels by 4 wk PI. Peripheral blood eosinophil numbers in infected mice injected with anti-IL-5 were maintained at levels below those of uninfected normal mice through 4 wk of infection. Histologically, there was a prominent eosinophil accumulation in infected, untreated, or control-mAb-treated mice associated with nurse cell complexes containing infective juveniles in skeletal muscle at 3 and 4 wk PI. This was largely eliminated in mice treated with anti-IL-5 mAb. However, the number of muscle stage juvenile worms recovered 3 and 4 wk PI after acid pepsin digestion was unaffected by eosinophil depletion. Challenge infections, in which mice were infected at day 0 with 125 muscle stage worms and challenged at day 28 PI with 350 muscle stage worms, developed peak eosinophil numbers in bone marrow and peripheral blood 3 wk after primary infection and 2 wk after challenge infection in mice receiving either no treatment or control mAb. In challenged mice receiving anti-IL-5 mAb, medullary and peripheral blood eosinophil numbers remained at or below those of uninfected animals. Although all groups exhibited significant resistance measured as muscle stage worm burdens 56 days PI, eosinophil depletion did not affect resistance of muscle worm recovery. These results suggest that eosinophils are not essential in the control of T. spiralis in either primary or challenge infections of CF1 mice. This in vivo study illustrates the questionable value of in vitro killing assays to assign effector function to any single inflammatory cell type.     

Vaccination with recombinant Ascaris suum 24-kilodalton antigen induces a Th1/Th2-mixed type immune response and confers high levels of protection against challenged Ascaris suum lung-stage infection in BALB/c mice

Previous studies have shown that antigens from various life-cycle stages of Ascaris suum can induce host-protective immunity against challenge infections with infective eggs of A. suum. This study evaluated whether Escherichia coli-expressed recombinant 24-kDa antigen from A. suum (rAs24) was a suitable vaccine candidate for the control of Ascaris infections by examining its performance in a mouse model. Immunization of BALB/c mice in three consecutive doses with rAs24 in Freund's Complete Adjuvant (FCA) results in protection against challenge infections as manifested by a 58% reduction (P<0.001) in recovery and stunted development of A. suum lung-stage larvae at day 7 post-challenge. Sera obtained from immune protected mice had a significantly increased level of immunoglobulin G (IgG) (P<0.0001) but had no IgE response. Analysis of IgG-subclass profiles revealed that IgG1 (P<0.0001) showed the greatest increase followed by IgG2b (P<0.005), IgG2a (P<0.006) and IgG3 (P<0.04). Splenic T cells from rAs24-FCA immunized mice secreted significantly high levels of both Th1 cytokine gamma-interferon (P<0.005) and Th2 cytokine interleukin-10 (P<0.001) after stimulation with rAs24 in vitro. Interestingly, affinity purified anti-rAs24 IgG was shown to inhibit moulting of A. suum lung-stage L3 to L4 in vitro by 26%, indicating an in vivo function of the endogenous As24 in the moulting processes. An intense expression of endogenous As24 in the hypodermis and gut epithelium of A. suum lung-stage L3 by immunofluorescence supports a function for endogenous As24. These findings may contribute to the understanding of rAs24-induced Th1/Th2-mediated effector mechanisms required for the protection of A. suum lung-stage larval infection.     

Adrenal and liver in normal and cld/cld mice synthesize and secrete hepatic lipase, but the lipase is inactive in cld/cld mice

Combined lipase deficiency (cld) is a recessive mutation in mice that causes a severe lack of lipoprotein lipase (LPL) and hepatic lipase (HL) activities, hyperlipemia, and death within 3 days after birth. Earlier studies showed that inactive LPL and HL were synthesized by cld/cld tissues and that LPL synthesized by cld/cld brown adipocytes was retained in their ER. We report here a study of HL in liver, adrenal, and plasma of normal newborn and cld/cld mice. Immunofluorescence studies showed HL was present in extracellular space, but not in cells, in liver and adrenal of both normal and cld/cld mice. When protein secretion was blocked with monensin, HL was retained intracellularly in liver cell cultures and in incubated adrenal tissues of both groups of mice. These findings demonstrated that HL was synthesized and secreted by liver and adrenal cells in normal newborn and cld/cld mice. HL activities in liver, adrenal, and plasma in cld/cld mice were very low, <8% of that in normal newborn mice, indicating that HL synthesized and secreted by cld/cld cells was inactive. Livers of both normal newborn and cld/cld mice synthesized LPL, but the level of LPL activity in cld/cld liver was very low, <9% of that in normal liver. Immunofluorescence studies showed that LPL was present intracellularly in liver of cld/cld mice, indicating that LPL was synthesized but not secreted by cld/cld liver cells. Immunofluorescent LPL was not found in normal newborn liver cells unless the cells were treated with monensin, thus demonstrating that normal liver cells synthesized and secreted LPL. Livers of both groups of mice contained an unidentified alkaline lipase activity which accounted for 34-54% of alkaline lipase activity in normal and 65% of that in cld/cld livers. Our findings indicate that liver and adrenal cells synthesized and secreted HL in both normal newborn and cld/cld mice, but the lipase was inactive in cld/cld mice. That cld/cld liver cells secreted inactive HL while retaining inactive LPL indicates that these closely related lipases were processed differently.     

Experimental lagochilascariosis: histopathological study of inflammatory response to larval migration in the Murine model

The goal of this study was to investigate the pattern of inflammatory response induced by Lagochilascaris minor in murine experimental model. For this purpose 115 mice were given 1000-3000 L. minor infective eggs "per os" and 51 uninfected mice were considered as controls. Four hours post-inoculation (PI), 3rd stage larvae were seen passing through the mucosa of terminal ends of small intestine. Six hours PI larvae were observed as an embolus inside the portal vein and also migrating through the liver parenchyma. During the first 24 h larvae-containing eggs of L. minor were observed in the lumen of intestinal tract. Two days PI larvae were seen migrating through lung parenchyma associated with an initial neutrophilic perivasculitis. From the 13th day of this experimental study, L. minor larvae were found mainly in skeletal muscles, in the center of granulomas. Concentric fibrosis with mixed inflammatory infiltrate involved the larvae after the 47th day PI, persistently. This experimental murine study with L. minor indicated that the 3rd stage larvae penetrated via ileum-cecal mucosa reaching the liver and probably other tissues through the hematogenic via. Throughout its pathway the larvae induced a granulomatous reaction, with abundant polimorphonuclear cells.     

Strongyloides ratti: the role of interleukin-5 in protection against tissue migrating larvae and intestinal adult worms

To determine the role of interleukin-5 (IL-5) and eosinophils in protection against Strongyloides ratti, mice treated with anti-IL-5 monoclonal antibody (mAb) were infected with S. ratti larvae. Strongyloides ratti egg numbers in faeces (EPG) in mAb treated mice were higher than those in control mice on days 6 and 7 after inoculation. The numbers of migrating worms in mAb treated mice 36 h after inoculation were higher than those observed in control mice. Intestinal worm numbers in mAb treated mice 5 days after inoculation were higher than those in control mice. These results show that eosinophils effectively protected the host against S. ratti infection by mainly the larval stage in primary infections. The involvement of eosinophils in protection against secondary infection was also examined. Before secondary infection, mice were treated with anti-IL-5 mAb and infected with S. ratti. Patent infections were not observed in either mAb treated or control Ab treated mice. The numbers of migrating worms in the head and lungs of mAb treated mice increased to 60% of that in primary infected mice. Intestinal worms were not found in mAb treated mice or in control mice after oral implantation of adult worms. Eosinophils were therefore mainly involved in protection against tissue migrating worms in secondary infections.     

Observations on Toxocara pteropodis infections in mice

Infection in mice with Toxocara pteropodis was investigated. In mice fed infective eggs, third-stage larvae hatched out and penetrated the mucosa, predominantly that of the lower intestine. They travelled via the portal vein to the liver, where they remained at least 14 months. They grew in length from 430 +/- 15 micron, at three days post infection (p.i.), to 600 +/- 50 micron, at six to nine weeks p.i., after which time growth ceased. Blood eosinophilia appeared at 28 days p.i., and eosinophil levels continued to rise gradually beyond this time. In female mice the larvae did not migrate from the liver in response to pregnancy or lactation. When infective eggs were inoculated subcutaneously or intra-peritoneally, larvae hatched out and ultimately appeared in the liver in larger numbers than seen with oral infections.     

The IgM and IgG antibody responses in iron-deficient and iron-loaded mice

The humoral immune response was evaluated in male CD-1 mice fed the iron deficient (7 ppm Fe), iron sufficient (120 ppm Fe), and high-iron diets (3000 or 5000 ppm Fe) for 54 d. The IgM and IgG antibody responses against sheep erythrocytes (SRBC) determined by hemolytic plaque assay were suppressed by 65.4 and 51.2%, respectively, in the iron deficient mice. Subclinical iron deficiency was manifested by a marked reduction in hepatic iron concentration without any changes in hematocrit or body weight gain. In contrast, consumption of high-iron diets caused a marked accumulation of iron in the liver and a twofold reduction in the IgM antibody response without alteration in the IgG response. The suppression of the IgG antibody response in the iron deficient mice, however, did not result in a compensatory increase in delayed type hypersensitivity response.     

Radiolabeling and autoradiographic tracing of Toxocara canis larvae in male mice

Artificially hatched infective larvae of Toxocara canis were labeled with 75Se in Medium 199 (Gibco) containing 75Se-methionine. Male CD-1 mice were infected with radiolabeled larvae by intragastric intubation or by intraperitoneal injection. At intervals of 3-56 days mice were killed and the organs prepared for compressed organ autoradiography. Radioactivity of parasitic larvae showed an exponential decrease with time, reflecting catabolism of label with a biological half life of 26 days (effective half life of 21 days) making possible experiments lasting several months. Total body larva counts, estimated by total body autoradiography, displayed an overall downward trend, but the rate of reduction was probably not constant because no significant positive or negative trends were noted from day 14 onward in the numbers of larvae. The carcass accumulated the greatest number of larvae followed by the central nervous system, liver, and lung in that order. When the numbers of larvae were considered in relationship to the mass of tissue, there were 4 groupings: central nervous system, liver, lung, carcass, and kidney, and genito-urinary organ, pelt, and intestine. No significant difference between intragastric and intraperitoneal administration was observed in the larval distribution after the larvae had left the initial site of deposition.     

Eosinophil and IgE responses of IL-5 transgenic mice experimentally infected with Nippostrongylus brasiliensis.

Eosinophil and IgE responses of interleukin (IL)-5 transgenic and normal C3H/HeN mice were studied after experimental infection with Nippostrongylus brasiliensis (Nb). Intestinal worms were recovered at day 5 post-infection (PI), and numbers of total white blood cells (WBC) and eosinophils, and total serum IgE and anti-hapten (dinitrophenyl) (DNP) specific IgE titers, were measured at days 0, 14 and 21 PI. IL-5 mice appeared resistant to Nb infection showing a significantly lower worm recovery rate than normal mice (P < 0.05). Total WBC and eosinophil counts (/mm3) were significantly increased in Nb infected normal mice (P < 0.05), but unchanged (total WBC) or decreased (eosinophils) in IL-5 mice at day 21 PI. The total serum IgE level remarkably increased in normal mice, but only a little in IL-5 mice at days 14 and 21 PI. Priming with DNP brought about more remarkable increases of the total and anti-DNP specific IgE in normal mice than in IL-5 mice. The results show that IL-5 mice are resistant to Nb infection, and that eosinophil and IgE responses in these mice are not augmented by Nb infection.