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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 less than 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 less than 0.001), but did not differ from that of a group of 40 allergic children (p greater than 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 less than 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.

Immunoglobulin E (IgE) was found by a double antibody radioimmunoassay technique (PRIST) in extracts of feces from 21 of 40 children with different kinds of allergy. 15 of the 22 children with gastrointestinal allergy and atopic dermatitis, but only 6 of the 17 patients with hay fever and/or bronchial asthma had detectable IgE in the extracts. The patients with gastrointestinal allergy also had the highest concentrations of fecal IgE, and the concentrations in feces did not correlate with the corresponding serum IgE levels. Furthermore, the presence of IgE in feces correlated with specific IgE antibodies in serum, measured as the sum of RAST classes to the food allergens wheat, fish, cow's milk and egg-white. IgE may therefore have been produced locally in the gut as a result of stimulation by food allergens. Since the concentrations of IgA in feces were also high in many children with allergy, and since some possibility of a positive correlation with high IgE concentration seemed to exist, the stimuli for local production of IgE and IgA may be interrelated.

The gel filtration profile of immunoglobulin E (IgE) in extracts of feces from 2 children was compared with IgE myeloma protein which had been exposed to proteolytic digestion by chymotrypsin. The peak of the chymotrypsin-digested IgE myeloma protein was found to be similar to that of fecal IgE after an elution volume between those of albumin and myoglobin, corresponding to a molecular weight of approximately 40,000 daltons. In the fractions where the peak of fecal IgE was found, no evidence for the presence of specific IgE antibodies (measured by RAST) could be detected. Fecal IgE could be purified by using an immunosorbent column to which rabbit antihuman IgE was coupled. Sufficient amounts of fecal IgE could thus be obtained and used in autoradiographic experiments. The IgE-containing fractions could also be detected with 125I-labelled second antibodies to visualize the IgE precipitates.

All concentrated human fecal extracts tested formed precipitates in double immunodiffusion with goat antiserum to IgE, as well as with normal goat sera. However, no such precipitates were formed by fecal extracts and rabbit sera. IgE precipitates obtained with both goat and rabbit antisera to IgE showed reactions of non-identity with the former precipitates which seemed to represent complexes of trypsin or chymotrypsin in feces and an alpha-protein in goat sera. This alpha-protein, which was responsible for the non-immunoglobulin precipitations, was different from human alpha 1-antitrypsin. The trypsin-like components in feces had low molecular weights, and might represent degradation products of trypsin or chymotrypsin. After using a second labelled antiserum, precipitates between rabbit antiserum to IgE and extracts of feces could be visualized by means of autoradiography. They were seen in fecal extracts in which IgE could also be determined by a double-antibody paper radioimmunoassay technique (paper radio immunosorbent test; PRIST). Since the concentrations measured by a radioactive single-radial immunodiffusion method correlated to some extent with the PRIST concentrations, the latter precipitates were likely to represent IgE in feces.

Immunoglobulin E (IgE) in human feces was characterized by radioimmunoassays with different specificities of the second antibodies, and by immunoprecipitation techniques. The fecal IgE was compared with an intact IgE myeloma protein and with Fc'' fragments of the IgE molecules, obtained after prolonged chymotrypsin-digestion of the IgE myeloma protein. The experiments showed that both the fecal IgE and Fc'' fragments shared the D epsilon 1 antigenic determinants while the intact IgE had both D epsilon 1 and D epsilon 2 determinants. They also shared thermal stability at 56 degrees C as compared to intact IgE. Fecal IgE and Fc'' fragments both showed rapid anodal migration in an electric field, different to that of intact IgE. A tandem crossed immunoelectrophoresis technique provided signs of immunological identity between the precipitates of fecal IgE and those of the Fc'' fragments. It is therefore likely that most, if not all, IgE in human feces consists of Fc" fragments.

In this study we looked for the occurrence of immunoglobulin E (IgE) in feces from healthy individuals and determined the total daily excretion and day-to-day variation in IgE in feces from patients with allergy, as well as the correlation between concentrations of IgE in small samples of feces and the total amounts of IgE in feces collected over a longer period. Concentrations of IgE in extracts of small samples of dry feces correlated well with the total daily amounts of IgE in feces collected over a 3-day period. Thus, single small samples of feces can be used to measure the excretion of IgE with feces at that time. In 3 children, studied over a 5-week period, the IgE excretion varied somewhat from one day to another, but was largely within a certain range of concentrations. Addition of trypsin inhibitor to fresh feces had no influence on the IgE concentrations of the resulting fecal extracts. Less than 10% of 88 presumably healthy infants, children, and adults had detectable IgE in their feces, while 21 of 40 children with various kinds of allergy had measurable fecal IgE. Only 3 of 13 individuals who were suffering from infectious acute gastroenteritis had IgE-positive fecal extracts. This was also the case for 6 of 25 adult patients in clinical remission of ulcerative colitis or Crohn's disease. Seven of 14 adult patients with chronic pancreatitis had measurable IgE in feces, and the concentrations were up to ten times the upper limit of IgE found in healthy individuals.(ABSTRACT TRUNCATED AT 250 WORDS)

Immunoglobulin E (IgE) was demonstrated by a double antibody radioimmunoassay technique (PRIST) in 5 of 17 unconcentrated fecal extracts from children. Four of the PRIST-positive extracts also had measurable levels of IgE determined by an enzyme-linked immunosorbent test (Enzygnost IgE). However, using a competitive antibody radioimmunoassay technique (RIST), IgE was found in all unconcentrated fecal extracts. The RIST-IgE levels of the extracts were higher and did not correlate to IgE measured by the other methods, nor to the IgE in serum from the same children or to the manifestation of allergy. On the other hand, 4 of the 5 children with measurable PRIST-IgE levels, and 3 of the 4 children with detectable Enzygnost IgE concentrations in the extracts, had elevated serum IgE as well as a history of allergy. Gel filtration studies indicated that IgE determined by the PRIST and Enzygnost IgE methods had been degraded to fragments of lower molecular weight than that of albumin. This study also suggests that the IgE in feces measured by the RIST method is overestimated due to the influence from nonspecific substances of high molecular weight.

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 Hymenolepis nana 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 less than 0.01), but not from children with different kinds of allergy (p greater than 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.