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At least 19 recordsLinked to original sources
PubMed1975

Immediate-type hypersensitivity to a bean lectin source with commentary on occupational allergy in allergy-immunology laboratory and research workers.

A case of acute, severe allergic conjunctivitis is reported in a biochemist who had been grinding Bandeiraea simplicifolia, the source of an anti-B lectin. A crude extract of these beans produced immediate-type skin test reactivity, and reaginic antibodies were demonstrated in her serum. Several other examples of occupationally induced allergy in laboratory and research workers in the field of allergy-immunology are briefly cited. Exposure to potential allergens in a dry, powdered form seems particularly hazardous.

Adult↗
PubMed1978

Whither allergy or wither allergy.

The specialty of allergy appears to be at a scientific and economic crossroad. With a significant number of scientific papers questioning the value of immunotherapy, the movement of the country towards prepaid care and the necessity for demonstrating cost/benefit ratio for all therapeutic procedures, the specialty of allergy can present an enigma.

Delivery of Health Care↗
PubMed1975

Investigation of the response to some haptenic determinants in penicillin allergy by skin and in vitro allergy tests.

The role of three penicillin metabolites in human allergic reaction to penicillin has been assessed using sensitive in vitro tests in addition to skin testing. Conjugates of the benzylpenicilloyl (BPO), benzylpenicillenate (BPE) and penicillamine (PA) groups with human serum albumin (HSA) and bovine gamma globulin (BGG) have been made. In the passive haemagglutination test antibodies specific for all three determinants were found but there was no difference between allergic and non-allergic groups. However, the ratio IgG/IgM, specific for each determinant, was higher in normals than in allergics. In skin tests, histamine release from leucocytes and the lymphocyte transformation test, the BPO group was confirmed as the major determinant, but in some individuals the BPE or PA groups are more important.

Drug Hypersensitivity↗
PubMed1979

Cow's milk allergy: a critical review.

Foods which are ingested frequently, and cow's milk in particular, are a common cause of delayed-in-onset allergy. Difficulty in diagnosing milk allergy is encountered because: (1) skin tests are unreliable; (2) the symptoms of milk allergy are frequently delayed in appearing, thereby obscuring their connection with the previously ingested food; (3) when such symptoms do appear, they often fail to suggest allergy as etiologic; and (4) the offending antigen may be present in a milk product not obviously associated with milk per se such as sherbet or cheese. Contrary to common belief, most milk (and other food) allergy is not reagin (IgE) mediated. Milk allergy is not confined to infancy, but is frequently seen in children and adults, often persisting as an allergy which had supposedly been "outgrown." Since milk allergy is often a familial disorder, its presence in a patient can assist the physician in possibly discovering it in other members of the family. A two or three-week trial elimination of milk, in conjunction with written dietary instructions for the patient, is presently the only reliable diagnostic procedure.

Adolescent↗
PubMed2026

A metagenomic analysis of the gut microbiota in a mouse model of fish allergy.

BACKGROUND: Fish are among the most frequent causes of immunoglobulin E (IgE)-mediated food allergies (Type I). Currently, there is no known cure for fish allergy and individuals who are sensitized have to practice strict, lifelong avoidance of fish products in their diets. The relationship between gut microbiome and food allergies is currently a major topic of discussion; these pathologies involve the development of dysbiosis, which is a microbial imbalance resulting from immune-related mechanisms. Recent studies have provided evidence that individuals suffering from food allergies, display an intestinal microbiota with a different microbial composition compared to healthy subjects. OBJECTIVES AND METHODS: In this work, we have described for the first time the differences in microbiome composition in a mouse model of fish allergy with previous sensitization to the main allergen, beta-Parvalbumin (β-PRVB), compared to mouse individuals without allergic response. RESULTS: The metagenomic analysis has shown differences in taxonomic composition between the treatments. Regarding phyla, an increase in the relative abundance of Patescibacteria, specifically Saccharimonas genus and Candidatus_Saccharimonas group, were observed in the allergic animals (Prvb_Alum group) when compared to the other groups. In contrast, the relative abundance of the RF39 group (Bacilli), Atopobiaceae family, Erysipelotrichaceae, and the Coriobacteriaceae_UCG-002 group, was higher in the animals that did not develop an allergic response, despite being exposed to the allergen (Prvb group). Furthermore, an increase in the relative abundance of Lachnospiraceae ASF356 group was observed in the control group compared to the other treatments. This family, has been reported to be inversely associated with the progression of intestinal inflammation and anaphylactic diseases. For the first time, the gut microbiota composition of individual mice with and without fish allergies is described in detail in this work. This study may shed light on the potential contribution of gut microbiota to the onset and avoidance of food allergies.

beta-parvalbumin↗
PubMed1979

Presidential address. The advancement of the knowledge and practice of allergy.

State and local allergy societies have appeared in response to pressures created by progressive specialization, increase in knowledge, and need for cost control within the field of allergy and clinical immunology. They provide a mechanism whereby allergists and immunologists with many different interests and functions can work in an integrated and cooperative manner to provide, in a cost-effective fashion, adequate patient care, teaching, and research in allergy and immunology for the geographic area. Maximum effectiveness requires close liaison with medical schools, state medical societies, national allergy organizations, and the local chapter of the Asthma and Allergy Foundation of America. Their structure should permit frequent close communication between members in various fields of allergy and clinical immunology, and the organization of committees that can accomplish the hard work of ensuring care for the disadvantaged patient, time and money for research, cost control, identification and rehabilitation of the poorly functioning allergists, continuing education for physician and patient, and all of the other tasks that make the practice of allergy and clinical immunology such a wonderful and absorbing way of life.

Allergens↗
PubMedDate not supplied

Immunologic and genetic factors predisposing to allergy.

Allergy often begins with a subtle and/or transient T cell defect. This defect is first responsible for an IgA deficiency. The normal function of IgA is immune exclusion. In its absence, allergens can pass through the mucosa and stimulate the immunocompetent cells. The T cell defect may also be implied by the synthesis of IgE directed against the allergens which passed through. Clinical, biological and immunological findings (T cell defect in allergic disease, low range of IgA in the early life of atopics) are in agreement. The genetic factor for pollinosis and house dust allergy are segregated. In ragweed allergy there is an Ir gene coding for antigen-specific Ig of different classes and a group of non-linked major histocompatibility complex alleles coding for non antigen-specific IgE. There are some links with HLA. In house dust allergy the Ir gene is very common and almost everyone can produce an allergy under some conditions (T cell defect). Whatever the immunologic and genetic factors are, they need allergens and environmental factors to induce allergy. Allergy is a complex state in which several mechanisms, often associated and sometimes unclear, are involved. Some of them may be an abnormality of the autonomic nervous system, and/or an increase in the mucous membrane permeability, and/or a subtle immunodeficiency. All these mechanisms are regulated by genetic factors and modulated by environmental ones.

Environment↗
PubMed2026

Proteomic Profile Differences in Immune-Related Diseases in Pediatric Patients Under Five Years Old: Asthma and IgE-Dependent Allergies-A Pilot Study.

Asthma is a heterogeneous disease that often begins in childhood and frequently occurs alongside allergic conditions. In asthma research, it is important to focus on proteins that are the primary regulators of cellular physiology. The differences in the proteome between children with asthma and those with an atopic background remain poorly understood. The present study included 130 serum samples from four groups of pediatric patients under the age of five: (1) with asthma and IgE-dependent allergies; (2) with non-atopic asthma; (3) non-asthmatics with IgE-dependent allergy; and (4) a control group without asthma and IgE-dependent allergies. The serum samples were used for protein-peptide profiling and proteomic identification using nanoLC-MALDI-TOF/TOF MS/MS. The obtained data were analyzed using univariate statistics and the STRING tool v12.0 to identify protein-protein potential interactions. A total of seven proteins were identified as discriminative between the study groups: A2M, AACT, IgG3, C3, ITIH2, IgG3 and IGK. All of them were upregulated in patients with IgE-dependent allergy compared to other study groups. STRING analysis identified functional associations among four proteins (AACT, A2M, C3, and ITIH2) with discriminatory potential for distinguishing between non-atopic asthma and non-asthmatic patients with IgE-dependent allergy. The results suggest that the identified putative protein markers overlap in cellular pathways, including those associated with the pathophysiology of asthma and allergic disorders. These findings provide further insight into the overall proteomic profile of pediatric patients with asthma and IgE-dependent allergy, highlighting its heterogeneity across the analyzed groups.

Humans↗
PubMed1979

"Insulin" allergy due to zinc.

An investigation of two unrelated patients who had local cutaneous hypersensitivity reactions after injection of any commercially available insulin preparation has shown that the cause of the allergy was zinc. Zinc-insulin and zinc sulphate induced transformation and proliferation of peripheral-blood lymphocytes from these patients; they also induced the production of a specific leucocyte inhibitory factor. Intradermal skin-tests for zinc were positive in both patients. Similar studies carried out in a patient whose cutaneous allergy to insulin was corrected by changing from mixed beef-pork to pure pork insulin were negative. Zinc-free insulin did not produce any allergy in the first patients. The number of patients in whom zinc (which is present in all commercially available insulin preparations) is a cause of "insulin" allergy is unknown. These patients may by identified by intradermal skin-tests. This previously unrecognised allergy should be considered in all patients whose insulin allergy does not respond to conventional therapy.

Cell Migration Inhibition↗
PubMed2026

Parasites and allergies: a complex bidirectional relationship from evolutionary origins to modern therapeutics.

Parasites and allergic diseases are linked by a complex, bidirectional relationship shaped by long-term host-parasite coevolution. This review discusses how different parasites may either promote or attenuate allergic responses through immunological, epithelial, and microbiome-mediated mechanisms. IgE-mediated immunity, mast cell activation, eosinophilia, and pruritus may have evolved as protective responses against helminths and blood-feeding ectoparasites. In contrast, modern allergies may partly reflect misdirected responses to harmless environmental antigens. The effects of parasites on allergy are not uniform and depend on parasite type, infection site, exposure intensity and chronicity, host immune status, and the degree of host-parasite adaptation. Protozoa such as Giardia intestinalis may contribute to food allergy-related manifestations by disrupting the intestinal barrier, altering gut microbiota composition, and modifying mucosal immune responses, particularly in atopic individuals. In contrast, selected helminths may attenuate allergic inflammation by inducing regulatory T and B cells, anti-inflammatory cytokines, antigen-presenting cell modulation, and IgG4-associated mechanisms that can limit IgE-mediated effector responses. Molecular similarities between parasite-derived antigens and environmental allergens, including conserved protein families and carbohydrate epitopes, may contribute to cross-reactive IgE responses and complicate allergy diagnostics. Therefore, current research is shifting from live helminth therapy toward defined parasite-derived molecules and immunomodulatory pathways that may inspire safer and more controlled therapeutic strategies. A clearer understanding of parasite-allergy interactions may improve diagnostic interpretation and support the development of new approaches to the management of allergic disease.

Humans↗