Role Of IgE-mediated Hypersensitivity Research Articles

Wild rice, hypoallergenic rice—Immunologic comparison

Rice is a cereal that is mainly produced and widely consumed in Asian countries including Korea. Several reports have suggested a role of IgE-mediated hypersensitivity in asthma and eczema associated with ingestion or inhalation of rice. In Japan, hypoallergenic rices are used for a substitute of common rice in some atopic patients. We performed this study to identify major allergens of rice and changed allergenicity in cooked and hypoallergenic rice. We purified crude extracts from a variety of rice and analyzed their protein distributions by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). Based on UniCAP test and skin-prick test, we selected sera with high sensitivity and analyzed specific IgE binding to rice by immunoblotting. In addition, the inhibition rate among some rice was determined by enzyme linked immunosorbent assay and CAP test. As the result of this study, rice with various origins and polishing levels had no difference in protein band pattern. After cooking, it was difficult to detect protein bands distributed in raw rice; and, even through IgE immunoblot analysis, it was impossible to differentiate between wild and hypoallergenic rice. In addition, both wild and hypoallergenic rice still had IgE binding activity on their remaining protein bands. In conclusion, almost all proteins of rice were excluded or weakened in the process of boiling and IgE binding activity still remained even in hypoallergenic rice.

Atopic eczema and allergy.

Although the pathomechanisms of respiratory atopy are well established, the role of IgE-mediated hypersensitivity in the elicitation and maintenance of eczematous skin lesions in atopic eczema (AE) is still controversial. There is, however, evidence for exogenous elicitation of AE by contact with aero- or food allergens (house dust mite, cat, and so forth). Recent investigations show that epidermal Langerhans' cells bind IgE via different receptors, especially the high-affinity receptor (Fc epsilon RI), which is significantly more strongly expressed in lesional skin of AE compared with other inflammatory skin diseases including allergic contact dermatitis. The clinical relevance of IgE-mediated sensitization in AE has been evaluated by the so-called atopy patch test (APT). The APT shows a much higher specificity compared with the skin prick test and radioallergosorbent test. However, allergic reactions do not play a decisive role in every case of AE. Other factors, such as nonspecific skin irritability or psychosomatic interactions, have to be considered. The concept of "extrinsic" versus "intrinsic" types of AE seems attractive. The concept of AE starting with TH2 inflammation, becoming TH1 inflammation in chronicity, and finally progressing to an autoimmune disease with IgE antibodies against autologous epidermal proteins is very attractive. Based on new knowledge, new methods in diagnosis, treatment, and prevention will develop, including more effective avoidance strategies, more potent anti-inflammatory treatment (e.g., immunomodulation or topical immunophyllins), and new ultraviolet modalities. The new findings have given rise to a possible new classification of eczema/dermatitis. The concept of "patient management," including all aspects from avoidance to therapy, has gained acceptance.

Role of IgE-mediated hypersensitivity in otitis media with effusion: pathophysiologic considerations.

A pathophysiologic model of otitis media with effusion secondary to IgE-mediated hypersensitivity is described. Specific mediators of inflammation are released by mucosal mast cells in the nasal mucosa following the interaction of antigen and specific IgE antibody. These mediators increase vascular permeability, mucosal blood flow, and, most important, mucus production. Furthermore, accessory cell types are recruited by colony-stimulating factors that in turn provide an autocrine-positive feedback for the influx of further inflammatory cells. The eustachian tube is then effectively obstructed by both intrinsic venous engorgement and extrinsic mucus plugs, isolating the middle ear space from the ambient environment. The net result is the increased exchange of nitrogen into the middle ear mucosa from the middle ear cavity. This causes the development of a significant middle ear underpressure that disrupts tight junctions and allows for transudation of fluids into the middle ear space. The prolonged obstruction of the eustachian tube with mucus results in middle ear inflammation, mucosal metaplasia, and increased glandular activities, all of which are hallmarks of chronic otitis media with effusion.

The role of IgE-mediated hypersensitivity in otitis media with effusion

Introduction: The role of immunoglobin (Ig) E-mediated hypersensitivity in otitis media with effusion (OME) has been the subject of much controversy and personal bias. Uncontrolled studies report the incidence of respiratory allergy in children with OME to range from 4% to over 90%. Materials and Methods: Children 1 to 18 years old who had OME requiring a myringotomy and tubes from January 1, 1987, through July 1, 1988, were the subjects of this study. The history of allergic and radioallergosorbent test (RAST) analysis of specific serum IgE levels was undertaken for 26 allergens on 89 children in the study group and 59 children in the control group. Result: The incidence of allergen as diagnosed by RAST score was higher in children with OME than children in the control group ( P > f .05). There was no correlation between positive RAST scores and the number of polyethylene-ventilating (PE) tubes previously placed, history of tonsillectomy, history of adenoidectomy, or the character of the effusion (mucous v serous). Conclusion: Respiratory allergy is a factor involved in the pathogenesis of OME.

The Role Of IgE-Mediated Hypersensitivity in the Development of Otitis Media with Effusion

The potential mechanisms of IgE-mediated hypersensitivity in OME have been reviewed. Two important questions were addressed at the beginning of this manuscript: (1) is OME an allergic disease, or (2) is OME a complication of an allergic disease in another part of the respiratory system? In regard to the first question, recurrent OME is associated with allergic rhinitis in about one-third of the studied population. However, of the patients who do have allergic rhinitis, in the great majority of children the middle ear mucosa is not the target organ. Rather, there appears to be increasing evidence that with both nasal provocation and natural antigen provocation in children during a normal allergen season, eustachian tube function is altered by nasal allergy. Whether this is truly physiologic or an artificial phenomenon cannot be determined at this time, as it is not absolutely clear whether the nine-step eustachian tube function test currently performed is really a measure of eustachian tube dysfunction, despite its forming the basis of all studies published so far, although one must conclude from current data that allergic rhinitis can produce eustachian tube dysfunction; there have been no cases in these studies in which allergic rhinitis produced otitis media. However, eustachian tube dysfunction is one of the major precursors in the development of OME. We believe that the anatomic part of the upper respiratory tract involved in the IgE-mediated hypersensitivity is most likely the mucosa of the nasopharyngeal portion of the eustachian tube. Inasmuch as total nasal obstruction, at least in adults, does not produce eustachian tube dysfunction in the great majority of cases, it is proposed that eustachian tube dysfunction that follows nasal provocation and occurs during the normal allergy season does so as a result of the transport of mediators of inflammation from inflammatory cells in the nasal mucosa via the nasal mucociliary system to the nasopharyngeal orifice of the eustachian tube. The role of food allergy is still problematic, but this author suggests that there is some supportive evidence that food immune complexes, particularly with dairy products, may play a role, especially in the otitis-prone child under the age of 2 years.(ABSTRACT TRUNCATED AT 400 WORDS)

Atopic Eczema, Langerhans Cells and Allergy

While the pathomechanisms of respiratory atopy are rather well established, the role of IgE-mediated hypersensitivity in the elicitation and maintenance of eczematous skin lesions in atopic eczema is still controversial. Few diseases are characterized by an equally elevated production of IgE antibodies as atopic eczema. Many authors, however, regard this only as epiphenomenon. On the other hand, there is clearcut clinical evidence for exogenous elicitation of atopic eczema by contact with aero or food allergens. A variety of hypotheses may help to explain the participation of IgE antibodies in the induction of eczema: vasoactive mediators secreted by skin mast cells or basophils after allergen contact may produce itch, contact urticaria or a 'late-phase-reaction' with consequent eczematous skin changes further maintained by scratch responses. Recent investigations stress a possible role of Langerhans cells in the epidermis with a low affinity receptor for IgE with possible function for antigen presentation, mediator release or regulatory interactions. Certain cytokines such as interleukin-4 or gamma-interferon are able to enhance the expression of the IgE-receptor on the surface of Langerhans cells. IL-4 and gamma-interferon act synergistically in this respect on Langerhans cells, contrary to B cells. Furthermore lymphocytes may act directly via certain cytokines (e.g. histamine releasing factor, chemotactic factors etc.) on mast cells or eosinophil granulocytes in a proinflammatory sense. Eosinophils seem also to be involved in the inflammatory response in atopic eczema by releasing products such as major basic protein (MBP) or eosinophil cationic protein (ECP) which has been found to be elevated in severe atopic eczema.(ABSTRACT TRUNCATED AT 250 WORDS)

Recent advances in immunologic reactivity in otitis media with effusion

The role of IgE-mediated hypersensitivity in the development of middle ear disease has not been completely resolved. However, on the basis of our investigations and those of other laboratories, we suggest that approximately two thirds of patients with chronic recurrent otitis media do not have allergies. The other third may have allergic rhinitis, and this allergic rhinitis could play a direct role in producing eustachian tube dysfunction in recurrent otitis media. However, viral infections of the upper respiratory tract may also induce IgE-mediated release of mast cell inflammatory mediators, and could cause otitis media on the basis of viral infection alone. Subtle immunologic deficiencies involving the IgG 2 subclass and other immunoglobulin subclasses may also be lower in otitis-prone children, and this may be a genetically inheri ed disorder. Finally, the possibility of food allergy in otitis media must be considered, particularly in the young otitis-prone child with chronic recurrent otitis media.

The Role of IgE-Mediated Hypersensitivity in Otitis Media with Effusion: A 1987 Update

The role of IgE-mediated hypersensitivity in the development of middle ear disease has not been completely resolved. However, on the basis of our investigations and those of other laboratories, we would suggest that approximately two-thirds of patients with chronic recurrent otitis media (OM) are not allergic. The other third may have allergic rhinitis, and this allergic rhinitis may play a direct role in producing eustachian tube dysfunction in recurrent OM. However, viral infections of the upper respiratory tract may also induce IgE-mediated release of mast cell inflammatory mediators and could cause OM on the basis of viral infection alone. The role of allergic rhinitis on eustachian tube dysfunction is now well documented, and finally, the possible role of food allergy and OM must be seriously considered, particularly in the young OM-prone child with chronic recurrent rhinitis and OM.

Further observations on the role of IgE-mediated hypersensitivity in recurrent otitis media with effusion.

One hundred young patients with recurrent otitis media with effusion (OME) were evaluated for IgE-mediated hypersensitivity by critical analysis of history, physical findings, skin testing for selected antigen, laboratory determination of total IgE, and radioallergosorbent testing (RAST) for six inhalant and two food allergens. The patients could be divided into allergic rhinitis and nonallergic groups. Allergic rhinitis patients had higher total IgE in their serum, and middle ear effusion (MEE). IgE was elevated in 16 of 35 allergic patients. In 8 of these 16 (23% of the allergic group), the IgE/mg protein was higher in the MEE than in the corresponding serum, suggesting local production of IgE. Nasal IgE was substantially increased in the allergic patients; however, in many patients there was no correlation between the corresponding MEE IgE and elevated nasal IgE, suggesting that local production of nasal and middle ear IgE is independent. We conclude that IgE-mediated allergic reactions may play a role in the pathogenesis of OME in about 23% of young allergic patients.

The Role of IgE Mediated Hypersensitivity in Otitis Media with Effusion

The Role of IgE Mediated Hypersensitivity in Otitis Media with Effusion

The role of IgE-mediated hypersensitivity in otitis media with effusion.

Forty-one children with recurrent otitis media with effusion (OME) were evaluated for IgE mediated allergy by critical analysis of history, physical findings, skin testing for selected antigens, and laboratory determination of total IgE and radioallergosorbent testing (RAST) for six inhalant and two food allergens. The children were divided into an allergic and nonallergic group. The allergic group clearly had higher total IgE in their serum. There was an elevation of middle ear effusion (MEE) IgE in 5 of 20 allergic cases. In three of these five patients or 15% of the allergic group, the IgE/mg protein was higher in the MEE than in the corresponding serum, suggesting the possibility of local production of IgE. Specific IgE antibody as measured by RAST was noted in 9 of 20 MEE and 5 of 20 nasal washings in the allergic group and in only 2 of 21 MEE and in 10 nasal washings of the nonallergic group. Nasal IgE was substantially increased in three patients of the allergic group; however, the corresponding MEE IgE was not increased in proportion to the nasal IgE. The MEE RAST was positive in 22% of the allergic group and in less than 1% of the nonallergic group. Nasal RAST was positive in 20% of the allergic group and in none of the nonallergic group. We conclude that IgE-mediated allergic reactions may play a role in the pathogenesis of OME in only about 15% of children defined as allergic on the basis of clinical and laboratory evidence. Allergy investigation as a diagnostic procedure in children with recurrent OME, but without a history of allergy on the basis of history, family history, or laboratory testing is likely to be nonproductive.