Serum IgE Levels in Protozoal and Helminthic Infections

Eighteen of 27 individuals, aged from 6 months to 19 years (mean 5 years, 7 months), from countries in the tropics or the subtropics had either intestinal parasitic infestations or intestinal enteropathogenic bacterial infections or both. Fourteen of those with intestinal pathogens had detectable concentrations of IgE in their fecal extracts, ranging from <0.5 to 420 IU/ml extract (mean 33 IU/ml). This rate of occurrence was significantly higher than the number of IgE-positive fecal extracts in a group of 54 healthy nonallergic Norwegian children (p <0.001), but did not differ from that of a group of 40 allergic children (p >0.20). The individuals with intestinal helminthic infection had the highest fecal IgE concentrations. Of the 9 individuals who did not have any demonstrable intestinal pathogen, low concentrations of IgE could be detected in feces from only 2, which did not differ from the rate in the healthy Norwegian controls. The concentrations of IgE in the feces of the subjects from tropical/subtropical regions correlated linearly with the corresponding serum concentrations of IgE (r = 0.69; p <0.001). The results indicate that the combined load of intestinal pathogens, including helminths, protozoa, and enteropathogenic bacteria, may stimulate IgE production in the gut.

Section: Discussionmentioning

confidence: 99%

Immunoglobulin E in the Feces of Children and Adolescents from Some Tropical and Subtropical Countries

Kolmannskog

Jansson²,

Häggblom³

et al. 1991

“…Parasites contain and can release a variety of po tent allergens [2], and they can stimulate increased IgE production, as measured by raised serum IgE levels [21]. However, it has been found that specific IgE antibodies to parasites usually account for only 5-10% of the total serum IgE [2], It has therefore been suggested that the parasites may potentiate a non specific IgE response [23], which has been thought to provide protection against allergic diseases [3].…”

Section: Discussionmentioning

confidence: 99%

“…Clinical hypersensitiv ity reactions [1] and increased immunoglobulin pro duction [2] have been known to follow infections with parasites which tend to cross the intestinal mucosa lining. On the other hand, protozoan parasites which remain in the intestinal lumen rarely induce such a response [21].…”

Section: Introductionmentioning

confidence: 99%

Immunoglobulin E in Feces of Children with Intestinal <i>Ascaris lumbricoides</i> Infestation

Kolmannskog¹

1986

Five of 6 fecal extracts from small children with intestinal Ascaris lumbricoides infection were IgE-positive before antiparasitic treatment with mebendazole was given. After treatment one patient still showed high fecal IgE level, but the samples from the remaining children showed either undetectable IgE values, or values just above the limit of detection. The serum IgE concentrations, however, decreased more slowly than the fecal IgE levels did. In the child with persistent high fecal IgE level after therapy, ova from Hymenolepisnana could still be found in feces, although the A. lumbricoides infection had been successfully treated. Gel filtration studies showed that fecal IgE from a patient with the parasitic infection was degraded to fragments corresponding to a molecular weight of approximately 40,000 daltons, similar to that of fecal IgE from a patient with gastrointestinal allergy. The number of IgE-positive fecal extracts in those patients before antiparasitic treatment was given differed significantly from the number of positive fecal IgE extracts from healthy nonallergic children (p <0.01), but not from children with different kinds of allergy (p >0.20). The fecal IgA concentrations were not different before and after antiparasitic therapy. The finding of IgE in feces from individuals with intestinal ascaris infection and nearly complete disappearance of IgE in feces after successful therapy is further evidence of local production of IgE in the gut mucosa.

“…Infections in experimental animals with various nematodes, including the pig worm Ascaris suum, often result in two wellknown accompaniments of metazoan parasi tic (and allergic) diseases -IgE antibody production and increased numbers of circu lating and tissue eosinophils [Zolov and Levine, 1969;Dobson, 1972;Ezeoke et al, 1973;Jarrett, 1973;Radermecker et al, 1974;Ogilvie and Love, 1974;Bradbury et al, 1974;Zucker-Franklin, 1974]. Al though nothing can be learnt about hostparasite relationships with a system such as A. suum infections in mice, useful informa tion can be obtained on fundamental ques tions such as the nature of allergens and the mechanisms of induction, and possible rela tionship, of IgE antibody production and eosinophilia.…”

Section: Introductionmentioning

confidence: 99%

Studies on Immune Responses to Parasite Antigens in Mice

Hogarth-Scott

et al. 1976

In terms of day 7 lung larvae numbers, mice vary markedly in their susceptibility to a first infection with the nematode worms, Ascaris suum, and the highly susceptible strain, C57B1, is resistant to second infection. Time course studies suggested that the period of residence in the liver or migration to, or into, the lungs are stages of the life cycle in which natural or acquired resistance of the host is expressed. The traits, susceptibility and resistance to first infection, were under poly genie control and no linkage of susceptibility to the major histocompatibility complex of C57B1 mice (H-2^b) was observed. Acquired resistance (to second infection) has not been dissected because of our inability to show adoptive transfer of resistance to naive recipients. Studies in hypothymic BALB/c. nu/nu mice indicate that natural resistance (to first infection) is not affected by a lack of T cells. The T cell dependence of acquired resistance in C57B1 mice remains in doubt although in the relatively resistant strain BALB/c, hypothymic nu/nu mice after second infection contain as many larvae in their lungs and liver as are present after first infection. An eosinophilia is observed in infected intact mice but not in infected T cell-deficient mice. Partially T cell-dependent serum antibodies and plaque-forming cells to phosphorylcholine (PC) were present in mice infected with A. suum but no evidence was obtained that this anti-PC antibody response was in any way protective for the host. The cell membrane-active properties of PC and related molecules suggest that PC-containing parasite antigens may be tolerogens for certain of the B cells with specificity for parasite antigens. A state of partial tolerance involving high affinity antibody production may be one means whereby parasites survive in natural or unnatural hosts.