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Wesley Burks

Publications and source records attributed to Wesley Burks.

15 recordsLinked to original sources
PubMed2006

Human subjects without peanut allergy demonstrate T cell-dependent, TH2-biased, peanut-specific cytokine and chemokine responses independent of TH1 expression.

BACKGROUND: Peanut allergy is a major cause of anaphylaxis. Regulation of immune responses to peanut allergen, particularly why sensitization does not usually progress to allergic reactions, is not well investigated. Most studies focus exclusively on serologic responses and individuals with peanut allergy. OBJECTIVE: We sought to determine the existence, prevalence, and nature of peanut-specific, T cell-dependent cytokine and chemokine responses of adults who eat peanut without having symptoms. METHODS: We developed systems to examine specific immunity in peanut-tolerant individuals who had (1) negative histories and negative peanut skin test responses, (2) negative histories and positive peanut skin test responses, and (3) clinically apparent peanut allergy. After primary culture of PBMCs restimulated with whole peanut extract, we quantified responses characteristic of TH1 (IFN-gamma and CXCL10) and TH2-like immunity (IL-5, IL-13, CCL17, and CCL22) using ultrasensitive ELISAs. Antigen-presenting cell costimulatory requirements (CD4, HLA-DR, CD80/86, and cytotoxic T lymphocyte-associated antigen 4 [CTLA4] Ig) were determined. RESULTS: T cell-dependent, peanut-specific IL-5, IL-13, and CCL22 were common in peanut-tolerant individuals, regardless of whether they had positive or negative skin test responses. These were blocked by anti-CD4 and were dependent on CD28/CD86 costimulation. None of the 70 individuals studied had demonstrable IFN-gamma or CXCL10 responses to peanut. All demonstrated TH1 and TH2 responses to the ubiquitous recall antigen streptokinase. CONCLUSIONS: Qualitatively similar and quantitatively increasing peanut-specific TH2 responses in the consistent absence of putatively protective TH1 immunity were found in both peanut-tolerant individuals and those with peanut allergy. CLINICAL IMPLICATIONS: The continuum of responses between individuals with negative and individuals with positive skin test results, rather than TH1 versus TH2 bias, might be important in peanut allergy.

Adolescent↗
PubMed2006

Food allergy.

This article reviews the classification of food allergies, their prevalence, pathophysiology, diagnosis, treatment and prognosis.

Diet Records↗
PubMed2006

Current developments in peanut allergy.

PURPOSE OF REVIEW: Peanut allergy is among the most serious, life-threatening food sensitivities, and recent studies indicate increasing prevalence, particularly among children. Our objective is to highlight recent advances in the immunology and treatment of peanut allergy. RECENT FINDINGS: Peanut sensitization may be both a Th1- and Th2-driven process, and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) may play a role in regulating the response intensity. Preliminary work shows that the food matrix is important in the immune response to peanut and that purified peanut allergens may have little intrinsic stimulatory capacity. Studies characterizing peanut allergens have revealed Ara h 1 and Ara h 2 as the most potent allergens, but Ara h 3 may be more allergenic than previously thought. There appears to be a relationship between the diversity of IgE-binding patterns and the severity of clinical symptoms. Multiple novel approaches to treatment are being investigated, which include traditional Chinese medicine, various forms of modified immunotherapy and the use of adjuvants in modified immunotherapy. SUMMARY: By understanding the immunologic response to peanut and the roles of the major peanut allergens, it may be possible to predict those at risk for severe reactions, prevent peanut sensitization and effectively treat those already sensitized.

Allergens↗
PubMed2005

Allergenic characteristics of a modified peanut allergen.

Attempts to treat peanut allergy using traditional methods of allergen desensitization are accompanied by a high risk of anaphylaxis. The aim of this study was to determine if modifications to the IgE-binding epitopes of a major peanut allergen would result in a safer immunotherapeutic agent for the treatment of peanut-allergic patients. IgE-binding epitopes on the Ara h 2 allergen were modified, and modified Ara h 2 (mAra h 2) protein was produced. Wild-type (wAra h 2) and mAra h 2 proteins were analyzed for their ability to interact with T-cells, their ability to bind IgE, and their ability to release mediators from a passively sensitized RBL-2H3 cell line. Multiple T-cell epitopes were identified on the major peanut allergen, Ara h 2. Ara h 2 amino acid regions 11-35, 86-125, and 121-155 contained the majority of peptides that interact with T-cells from most patients. The wAra h 2 and mAra h 2 proteins stimulated proliferation of T-cells from peanut-allergic patients to similar levels. In contrast, the mAra h 2 protein exhibited greatly reduced IgE-binding capacity compared to the wild-type allergen. In addition, the modified allergen released significantly lower amounts of beta-hexosaminidase, a marker for IgE-mediated RBL-2H3 degranulation, compared to the wild-type allergen.

2S Albumins, Plant↗
PubMed2005

Towards immunotherapy for peanut allergy.

PURPOSE OF REVIEW: Food allergy is a major cause of life-threatening hypersensitivity reactions. Peanut allergy is the most serious of the hypersensitivity reactions to foods due to its persistence and high risk of severe anaphylaxis. Currently, strict avoidance of the allergenic food and ready access to self-injectable epinephrine is the 'standard of care' for food allergy. Based on extensive characterization of food allergens and a better understanding of the immunological mechanisms underlying allergic disease, promising therapeutic modalities for food allergy treatment and prevention are being developed. RECENT FINDINGS: Immunotherapeutic strategies include peptide immunotherapy, mutated protein immunotherapy and DNA immunization, which all strive to decrease the deleterious Th2 response. Another approach already in clinical trials for peanut allergy is the anti-IgE therapy which prevents circulating IgE from binding to effector cells, consequently decreasing clinical symptoms after peanut ingestion. In order to be applicable, these strategies must be well tolerated, inexpensive and easily administered. Realistic treatment options would likely involve a combination of different approaches. SUMMARY: Food allergy affects approximately 4-6% of children and 3-4% of adults. Peanut allergy can be devastating as reactions range from urticaria to severe anaphylactic shock and death. The only preventive measure for peanut allergy is strict avoidance of the incriminating food. It is likely immunotherapy will be available in the near future as a well tolerated and effective therapy for treating peanut allergy. The use of the anti-IgE therapy in conjunction with other immunotherapy would possibly be the best treatment option in the future.

Allergens↗
PubMed2005

Novel treatments for food allergy.

Food allergy is a major cause of life-threatening hypersensitivity reactions. Currently, the strict avoidance of the allergenic food and ready access to self-injectable adrenaline is the standard of care for food allergy. Based on extensive characterisation of food allergens and a better understanding of the immunological mechanisms underlying allergic disease, promising therapeutic modalities for the treatment and eventual prevention of food allergy are being developed. Novel immunotherapeutic strategies include peptide immunotherapy, traditional Chinese medicine, mutated or homologous protein immunotherapy, DNA immunisation and immunisation with immunostimulatory sequences, which all strive to elicit a decreased T helper cell type 2-like response or tolerance by the immune system in response to a specific food allergen. Other approaches such as the anti-IgE therapy or the Fcgamma-Fcepsilon fusion protein aim at preventing the release of mediators by mast cells. It is the combination of these different approaches that would probably offer the best treatment option for food-allergic patients in a not too distant future.

Animals↗
PubMed2004

The pathobiology of eosinophilic gastroenteritis of childhood: is it really the eosinophil, allergic mediated, or something else?

Over the past decade clinicians have witnessed a dramatic rise in the prevalence of eosinophilic gastrointestinal diseases. Diverse symptoms, a broad range of endoscopic findings, and varying histopathologic features pose several questions: Do eosinophils represent an allergic response? What mechanisms drive eosinophils to specific mucosal targets? How do eosinophils affect the gastrointestinal tissues? Recent clinical and basic studies are investigating the pathogenesis of eosinophilic gastrointestinal diseases. This review highlights the literature concerning the mechanisms that govern these diseases, with a specific focus on diseases of gastrointestinal columnar epithelia (eosinophilic gastroenteritis and eosinophilic colitis). The roles of specific chemokines, such as eotaxin, and the data supporting the involvement of eosinophil granule proteins in disease states, are discussed.

Animals↗
PubMed2004

New approaches for treatment of peanut allergy: chances for a cure.

Food allergy is a major cause of life-threatening hypersensitive reactions. Food-induced anaphylaxis is the most common reason for a person to present to the emergency department for treatment of the anaphylactic reaction. Avoiding the allergenic food is the only currently available method for sensitized patients to prevent further reactions. Strict avoidance of specific foods is accepted treatment of food-induced allergic reactions but is often an unrealistic therapeutic strategy for the treatment and prevention of food-induced hypersensivity reactions for the many reasons. Desirable therapeutic strategies for the treatment and prevention of the food allergies must be safe, relatively inexpensive, and easily administered. Recent advances in the understanding of the immunological mechanisms underlying allergic disease and better characterization of food allergens have greatly expanded the potential therapeutic option for future use. Several different forms of immunodulatory therapies are currently under investigation: peptide immunotherapy, mutated protein immunotherapy, allergen DNA immunization, vaccination with immunostimulatory DNA sequences, and anti-immunoglobulin E-therapy.

Allergy and Immunology↗
PubMed2004

Food allergens.

Explore the source record for details and available documents.

Allergens↗
PubMed2003

Persistent protective effect of heat-killed Escherichia coli producing "engineered," recombinant peanut proteins in a murine model of peanut allergy.

BACKGROUND: Peanut allergy (PNA) is a life-threatening food allergy for which there is no definitive treatment. OBJECTIVE: We investigated the long-term immunomodulatory effect of heat-killed Escherichia coli producing engineered (mutated) Ara h1, 2, and 3 (HKE-MP123) administered rectally (pr) in a murine model of PNA. METHODS: Peanut-allergic C3H/HeJ mice received 0.9 (low dose), 9 (medium dose), or 90 (high dose) microg HKE-MP123 pr, HKE-containing vector (HKE-V) alone, or vehicle alone (sham) weekly for 3 weeks. Mice were challenged 2 weeks later. A second and third challenge were performed at 4-week intervals. RESULTS: After the first challenge, all 3 HKE-MP123 and HKE-V-treated groups exhibited reduced symptom scores (P <.01,.01,.05,.05, respectively) compared with the sham-treated group. Interestingly, only the medium- and high-dose HKE-MP123-treated mice remained protected for up to 10 weeks after treatment accompanied by a significant reduction of plasma histamine levels compared with sham-treated mice (P <.05 and.01, respectively). IgE levels were significantly lower in all HKE-MP123-treated groups (P <.001), being most reduced in the high-dose HKE-MP123-treated group at the time of each challenge. IL-4, IL-13, IL-5, and IL-10 production by splenocytes of high-dose HKE-MP123-treated mice were significantly decreased (P <.01;.001,.001, and.001, respectively), and IFN-gamma and TGF-beta production were significantly increased (P <.001 and.01, respectively) compared with sham-treated mice at the time of the last challenge. CONCLUSIONS: Treatment with pr HKE-MP123 can induce long-term "downregulation" of peanut hypersensitivity, which might be secondary to decreased antigen-specific T(H)2 and increased T(H)1 and T regulatory cytokine production.

2S Albumins, Plant↗
PubMed2003

Skin manifestations of food allergy.

The pediatrician is faced with evaluating a panoply of skin rashes, a subset of which may be induced by food allergy. Acute urticaria is a common manifestation of an allergic skin response to food, but food is rarely a cause of chronic urticaria. Approximately one third of infants/children with moderate to severe atopic dermatitis have food allergy. Although diagnosis of acute urticaria provoked by a food may be evident from a straightforward history and confirmed by diagnostic tests to detect food-specific IgE antibody, determination of the role of food allergy in patients with atopic dermatitis is more difficult and may require additional diagnostic maneuvers, including elimination diets and oral food challenges. The immunopathologic basis of food-allergic disorders that affect the skin and a rational approach to diagnosis and treatment are discussed. Additional disorders that are caused by or mimic ones caused by food allergy are reviewed.

Animals↗
PubMed2002

Food allergies in children affect nutrient intake and growth.

OBJECTIVES: To identify if specific food allergies, elimination diets, or other variables associated with food allergies have an impact on the growth and nutrient intake of children with food allergies. DESIGN: Measurements of height, weight, and body mass index were used to determine potential growth problems. Estimates of energy and nutrient intakes were based on 3-day diet records. A questionnaire was used to determine number of food allergies and other variables. SUBJECTS: Ninety-eight children with food allergies (subjects, mean age 3.7 +/- 2.3 years) and 99 children without food allergies (controls, mean age 4.1 +/- 2.4 years) participated in this age-matched, consecutive sampling, cross-sectional study. STATISTICAL ANALYSIS PERFORMED: Cochran-Mantel-Haenszel statistics using general association and Fisher Exact Test, with 2-sided probability, were conducted. RESULTS: Children with two or more food allergies were shorter, based on height-for-age percentiles, than those with one food allergy (P<.05). More than 25% of children in both groups consumed less than 67% of the DRI (RDA or AI) for calcium, vitamin D, and vitamin E. More children with cow's milk allergy or multiple food allergies consumed dietary calcium less than age- and gender-specific recommendations compared with children without cow's milk allergy and/or one food allergy. The possibility of consuming a less than recommended intake of calcium and vitamin D in children with food allergy was less if the child received nutrition counseling (P<.05) or consumed a safe infant/toddler formula or fortified soy beverage. APPLICATIONS/CONCLUSIONS: Children diagnosed with food allergies need an annual nutrition assessment to prevent growth problems or inadequate nutrient intake. Children with milk allergies or multiple food allergies are at greater risk. Nutrition education needs to address how to avoid all forms of the allergen and incorporate alternative nutrient-dense foods. This population would benefit from the development and validation of a medical nutrition therapy protocol.

Arachis↗
PubMed2002

Current understanding of food allergy.

IgE-mediated hypersensitivity reactions account for the majority of well-documented food allergy reactions, but non-IgE-mediated immune mechanisms do cause some hypersensitivity disorders. A variety of gastrointestinal, cutaneous, respiratory, and generalized symptoms and syndromes have been associated with IgE-mediated food allergy. The diagnostic approach to adverse food reactions begins with a careful medical history and physical examination. Laboratory studies may then be used appropriately in the evaluation. Once the diagnosis of food allergy is established, the only proven therapy is the strict elimination of the food from the patient's diet. Studies in both children and adults indicate that symptomatic reactivity to food allergens is often lost over time, except possibly reactions to peanuts, tree nuts, and seafood.

Adolescent↗