Immunoglobulin E in Feces of Children with Intestinal &lt;i&gt;Ascaris lumbricoides&lt;/i&gt; Infestation

Nine biopsy specimens from the jejunum of patients with a clinical history of food allergy and 10 from the rectal mucosa of patients with presumed ‘allergic proctitis’ were fixed in cold ethanol and further processed for paraffin embedding. Serial tissue sections were stained for IgE by direct (polyclonal antibody) and indirect (monoclonal antibody) immunofluorescence methods. Adjacent sections were subjected to conventional mast cell staining (astra blue). In all mucosal specimens from the jejunum and in 8 rectal ones, numerous cells were found to be positive both for astra blue by transmission microscopy and for IgE by fluorescence microscopy of the same section. With the monoclonal antibody all astra-blue-positive cells were IgE-positive; however, this was not always the case with the polyclonal reagent, probably because the fluorescence was weaker with the direct technique. Detection of IgE-positive mucosal mast cells may turn out to be of diagnostic interest in patients with adverse reactions to food.

Section: Discussionmentioning

confidence: 64%

IgE-Positive Cells in Human Intestinal Mucosa Are Mainly Mast Cells

Rognum

Brandtzæg

1989

“…These responses are likely to be involved in the defence against intestinal parasites, as has been indicated from experimental animal systems [ 15] and in humans with Ascaris infections [20].…”

Section: Discussionmentioning

confidence: 91%

IgE-Positive Duodenal Mast Cells in Patients with Food-Related Diarrhea

Bengtsson¹,

Rognum

Brandtzæg

et al. 1991

Thirty-seven consecutive adult patients with a history of adverse reactions to foods, manifested mainly as diarrhea, were investigated with skin prick test (SPT), IgE levels in serum, and the presence of IgE bound to mast cells in duodenal biopsy specimens. Nineteen percent had increased serum IgE levels indicating the presence of atopic disease and in 35% positive SPTs for one or several allergens related to their gastrointestinal symptoms were found. In 92% of the patients with positive SPTs to food, IgE-positive mast cells in duodenal biopsy specimens were found, twice as many as in patients with negative SPTs (47%). Forty-two percent of normal individuals without any adverse reactions to foods had IgE-bearing mast cells in their intestinal mucosa. The results showed that ‘arming’ of mast cells with IgE locally was relatively prominent but not consistent in the gut of patients with food-related diarrhea suggested to be allergic by positive SPT. Intestinal IgE-mediated hypersensitivity reactions could be of pathogenetic significance in most of these patients. However, since also half of the normal individuals were found to have IgE-positive intestinal mast cells, this phenomenon presumably also reflects a normal physiological defence mechanism.

“…We have shown earlier that serum IgE concentra tions decrease more slowly than fecal IgE concentra tions after antiparasitic treatment had been given for intestinal A. lumbricoides infection (13). The fact that some of the individuals from the tropics/subtropics suffered from diarrhea, when the fecal samples were taken, cannot explain the high rate of occurrence of IgE-positive fecal extracts in this group.…”

Section: Discussionmentioning

confidence: 78%

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

Kolmannskog

Jansson²,

Häggblom³

et al. 1991

Self Cite

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.