Linked Life Data

9217365

Source:http://linkedlifedata.com/resource/pubmed/id/9217365

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-9-8
pubmed:abstractText
Passive cutaneous anaphylaxis (PCA) reaction was developed by Ovary et al. as an animal model of mainly human type I allergic inflammation reaction. This is the most sensitive reaction for the detection of cutaneously sensitizing antibodies and provides a very effective means by which to investigate immunological reactions concerning the mechanisms of development and inhibition of allergic reactions, levels and specificity of antibodies, and the structure of antigens. These cutaneous inflammations mimic atopic dermatitis. Food ingestion has been pointed out as one of the worsened factors of atopic dermatitis. However, the body is generally protected against the invasion of high molecular substances such as non-ingested food by several barriers including digestive enzymes that break down complex food molecules into simpler substances and gastrointestinal mucosae. Accordingly, oral ingestion of food antigen seems to be physiologically and immunologically in conflict with the occurrence of dermatitis. With a view to determining whether allergic dermatitis occurs after oral ingestion of food, the present study was carried out on animals, utilizing the PCA reaction. C 57 BL/6 Ncr j mice were immunized with immunogen derived from commercially obtained eggs. Wistar rats were used as a model of PCA reaction. The results of the present investigation are summarized as follows. 1) Blue spots of 10 mm diameter were observed as a PCA reaction 50 min or more after oral administration of antigen, and the blue spots reached maximum size (20-21 mm, 1.8-1.7 micrograms) after 90-120 min. The PCA reaction was induced 20 min or more after intravenous administration of antigen. When the maximum reaction was compared between the oral and the intravenous routes after 50 min (29.5 micrograms) and 90 min (1.8 micrograms) respectively, there was about a 16-fold difference in the capacity to induce inflammations. 2) The maximum PCA reaction values were 100 and 1,600 for the oral and intravenous routes, respectively, there being a 16-fold difference between the two routes. 3) The minimum antigen concentration required to induce the PCA reaction was 10 mg/ ml for the oral route and 0.01 mg/ml for the intravenous, there being a 1,000-fold difference between the two routes. 4) Reactions with anti-egg mixture antibody and main egg constituents were specific. The PCA inhibition test results confirmed that the undigested structural portion of antigen was associated with the induction of PCA. The present investigation demonstrated that there existed a mechanism by which type I allergy is induced via the gastro-intestinal tract. This fact indicates that part of the food ingested undergoes no change in its molecular structure when transferred to the blood, thus acting as a PCA inducing antigen. This phenomenon suggests that this animal model of human type I allergic dermatitis is a useful system that strongly suggests the association of food antigen with the development of allergic dermatitis.
pubmed:language
jpn
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0048-0444
pubmed:author
pubmed:issnType
Print
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
225-31
pubmed:dateRevised
2011-7-28
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
[Induction of passive cutaneous anaphylaxis by oral administration of antigen].
pubmed:affiliation
Department of Microbiology and Immunology, Nippon Medical School, Tokyo, Japan.
pubmed:publicationType
Journal Article, English Abstract