Selenium Modulates the Allergic Response to Whey Protein in a Mouse Model for Cow's Milk Allergy.

Cow's milk allergy is a common food allergy in infants, and is associated with an increased risk of developing other allergic diseases. Dietary selenium (Se), one of the essential micronutrients for humans and animals, is an important bioelement which can influence both innate and adaptive immune responses. However, the effects of Se on food allergy are still largely unknown. In the current study it was investigated whether dietary Se supplementation can inhibit whey-induced food allergy in an animal research model. Three-week-old female C3H/HeOuJ mice were intragastrically sensitized with whey protein and cholera toxin and randomly assigned to receive a control, low, medium or high Se diet. Acute allergic symptoms, allergen specific immunoglobulin (Ig) E levels and mast cell degranulation were determined upon whey challenge. Body temperature was significantly higher in mice that received the medium Se diet 60 min after the oral challenge with whey compared to the positive control group, which is indicative of impaired anaphylaxis. This was accompanied by reductions in antigen-specific immunoglobulins and reduced levels of mouse mast cell protease-1 (mMCP-1). This study demonstrates that oral Se supplementation may modulate allergic responses to whey by decreasing specific antibody responses and mMCP-1 release.

Mechanisms of Nickel-Induced Cell Damage in Allergic Contact Dermatitis and Nutritional Intervention Strategies.

BACKGROUND: Hypersensitivity to nickel is a very common cause of allergic contact dermatitis since this metal is largely present in industrial and consumer products as well as in some commonly consumed foods, air, soil, and water. In nickel-sensitized individuals, a cell-mediated delayed hypersensitivity response results in contact to dermatitis due to mucous membranes coming in long-term contact with nickel-containing objects. This process involves the generation of reactive oxidative species and lipid peroxidation-induced oxidative damage. Immunologically, the involvement of T helper (h)-1 and Th-2 cells, as well as the reduced function of T regulatory cells, are of importance. The toxicity, mutagenicity, and carcinogenicity of nickel are attributed to the generation of reactive oxygen species and induction of oxidative damage via lipid peroxidation, which results in DNA damage. OBJECTIVE: The aim of this research is to identify nutritionally actionable interventions that can intercept nickel-induced cell damage due to their antioxidant capacities. CONCLUSION: Nutritional interventions may be used to modulate immune dysregulation, thereby intercepting nickel-induced cellular damage. Among these nutritional interventions are a low-nickel diet and an antioxidant-rich diet that is sufficient in iron needed to minimize nickel absorption. These dietary approaches not only reduce the likelihood of nickel toxicity by minimizing nickel exposure but also help prevent oxidative damage by supplying the body with antioxidants that neutralize free radicals.

Effects of short-term anti-inflammatory glucocorticoid treatment on clinicopathologic, echocardiographic, and hemodynamic variables in systemically healthy dogs.

OBJECTIVE To investigate mechanisms by which anti-inflammatory doses of orally administered intermediate-acting glucocorticoids (prednisone) could predispose dogs to progression of heart disease or congestive heart failure. ANIMALS 11 client-owned dogs with allergic dermatitis and 11 matched healthy control dogs. PROCEDURES Clinicopathologic, echocardiographic, and hemodynamic variables were measured. Dogs with allergic dermatitis then received prednisone (1 mg/kg, PO) once daily for 14 consecutive days beginning on day 0 (baseline), followed by a tapering and washout period; control dogs received no treatment. Measurements were repeated on days 7, 14, and 35. Linear mixed modeling was used to compare changes in variables across measurement points and between dog groups. RESULTS Prednisone administration caused no significant changes in serum sodium or potassium concentration, blood glucose concentration, or target echocardiographic variables. The change from baseline in systolic arterial blood pressure at day 7 was significantly greater in prednisone-treated dogs than in control dogs. Expected changes in hematologic and serum biochemical values with prednisone administration (neutrophilia, eosinopenia, isosthenuria, and high serum alkaline phosphatase and alanine aminotransferase activities) also occurred in the prednisone-treated dogs. CONCLUSIONS AND CLINICAL RELEVANCE Findings suggested that anti-inflammatory doses of orally administered glucocorticoids have the potential to adversely impact cardiac function in dogs by causing an increase in blood pressure and thus increased cardiac afterload.

The inhibitory effect of soybean and soybean isoflavone diets on 2,4-dinitrofluorobenzene-induced contact hypersensitivity in mice.

Murine contact hypersensitivity (CHS) is one of the most frequently used animal models of human allergic contact dermatitis. We investigated the inhibitory effects of soybean and soy isoflavone (SI) diets on 2,4-dinitrofluorobenzene- (DNFB) induced CHS in mice. The DNFB-induced ear swelling was inhibited in the soy- and SI-treated groups. Histopathological investigations revealed that oral feeding of soybean and SI attenuated ear tissue edema and reduced the number of Gr-1(+) cell infiltrations into ear tissues. DNA microarray analysis showed that the expression of Ccl24, Xcl1, Ifng, and Ccl17 in the ear tissues was lower in the soy-treated mice than in the positive controls. In addition, CCL24 mRNA and protein expression in the ear tissues were more highly suppressed in the soy- and SI-treated groups. These results suggest that soybean and SI consumption downregulated the gene and protein expression of CCL24, thereby affording protection against CHS in mice.

[Dietetic interventions in allergic contact dermatitis--when are they reasonable?]. / Interwencje dietetyczne w alergicznym wyprysku kontaktowym--kiedy maja uzasadnienie?

This paper focuses on three questions of dietetic interventions in allergic contact dermatitis: 1) in which cases it is justified to suspect that an ingested hapten causes allergic reaction, 2) how to verify the causal relationship between the hapten and current disease, and 3) in which cases dietary interventions are justified? Clinical studies, cases, and reasoning collated in this article indicate that contact allergy to food haptens should be suspected when symptoms are consistent with the clinical picture of systemic reactivation of allergic contact dermatitis or systemic photoallergy. Positive patch test result is not sufficient as confirmation of causality--the clinical relevance should be judged by means of double-blind placebo-controlled provocation with hapten in question. If such challenge appears not feasible, the relevance may be confirmed indirectly by the clearance of symptoms after introducing a low-hapten diet with remission lasting for at least 4 weeks after withdrawal of pharmacotherapy, and the recurrence of symptoms following the return to the old diet. In the majority of cases, "nickel-free" or "low nickel" diets are burdensome and with no real benefit. Nickel is the fifth most abundant element on Earth and even most restrictive diets could reduce nickel load by 50% at best. In the EU alone, 65 million people are allergic to nickel, while only 1-11% of patients with clinical nickel allergy will experience benefits from "nickel-free" diets. Indiscriminate introduction of such dietary regimens based merely on positive patch test results poses a considerable burden to individuals and society, therefore, it is not recommended.

Systemic contact dermatitis to foods: nickel, BOP, and more.

Systemic contact dermatitis (SCD), a cutaneous reaction that is a direct manifestation of systemic exposure to a known allergen in a sensitized individual, has been increasingly recognized as a cause of persistent cutaneous contact dermatitis that is refractory to conventional therapies. While SCD in response to drugs has been described well in the literature, SCD to allergens in common foodstuffs is a less well-articulated phenomenon. Several foods that are universally consumed throughout the world contain potent allergens including nickel, balsam of Peru, trace metals, urushiol, and sesquiterpene lactones as well as a host of others that may cause a distinctive clinical picture. In this review article, the authors review the typical presentation and prevalence of SCD to foods, pathophysiology, the most common offensive ingestible food allergens, several appropriate diets, and effectiveness of dietary avoidance for situations in which SCD is suspected.

Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis.

Systemic (gastrointestinal and skin) reactions to ingestion of nickel rich foods in patients with nickel allergic contact dermatitis characterize Systemic Nickel Allergy Syndrome (SNAS). The objective of the study was to describe the nosologic framework of the syndrome and to compare sensibility and specificity for SNAS diagnosis between two different low nickel diets - BraMa-Ni and the usually prescribed list of forbidden foods - along with patient adherence to diet. One hundred forty-five patients with suspected SNAS (by history and benefit from nickel dietary restrictions) were selected and orally challenged with nickel for a definite diagnosis. Specificity and sensibility of the diets were calculated in relation to the results of nickel challenges. The nosologic framework of SNAS was deduced from the clinical pictures of 98 patients with positive nickel challenge and characterized essentially by skin and gastrointestinal symptoms, whereas all other symptoms (dizziness, headache etc.) were never elicited by the oral nickel challenge. The specificity and sensibility of BraMa-Ni in detecting SNAS were significantly higher than the forbidden food list diet, with an excellent patient adherence. Therefore, BraMa-Ni diet can be prescribed for the treatment of the syndrome other than for the diagnosis, the gold standard of which remains the oral nickel challenge.

Severe dermatitis with loss of epidermal Langerhans cells in human and mouse zinc deficiency.

Zinc deficiency can be an inherited disorder, in which case it is known as acrodermatitis enteropathica (AE), or an acquired disorder caused by low dietary intake of zinc. Even though zinc deficiency diminishes cellular and humoral immunity, patients develop immunostimulating skin inflammation. Here, we have demonstrated that despite diminished allergic contact dermatitis in mice fed a zinc-deficient (ZD) diet, irritant contact dermatitis (ICD) in these mice was more severe and prolonged than that in controls. Further, histological examination of ICD lesions in ZD mice revealed subcorneal vacuolization and epidermal pallor, histological features of AE. Consistent with the fact that ATP release from chemically injured keratinocytes serves as a causative mediator of ICD, we found that the severe ICD response in ZD mice was attenuated by local injection of soluble nucleoside triphosphate diphosphohydrolase. In addition, skin tissue from ZD mice with ICD showed increased levels of ATP, as did cultured wild-type keratinocytes treated with chemical irritants and the zinc-chelating reagent TPEN. Interestingly, numbers of epidermal Langerhans cells (LCs), which play a protective role against ATP-mediated inflammatory signals, were decreased in ZD mice as well as samples from ZD patients. These findings suggest that upon exposure to irritants, aberrant ATP release from keratinocytes and impaired LC-dependent hydrolysis of nucleotides may be important in the pathogenesis of AE.

Bovine milk fat enriched in conjugated linoleic and vaccenic acids attenuates allergic dermatitis in mice.

BACKGROUND: Orally administered milk fat enriched in conjugated linoleic acid (CLA) and trans-vaccenic acid (VA) ('enriched milk fat'), produced by supplementing the diet of pasture-fed cows with fish and sunflower oil, has been shown previously to suppress the development of allergic airway disease in mice. OBJECTIVE: To investigate whether topical or oral application of enriched milk fat and its two major fatty acids cis-9, trans-11 CLA (c9,t11-CLA) and VA inhibit allergic dermatitis in mice. METHODS: Allergic dermatitis was induced in C57BL/6 mice by epicutaneous sensitization of tape-stripped skin with ovalbumin (OVA). Enriched milk fat and its two major fatty acids were either topically applied to the OVA-sensitized skin, or orally fed to mice by supplementation of the diet. Blood and skin tissues were collected for analysis after the third skin sensitization. RESULTS: Both topical and oral administration of enriched milk fat and its two major fatty acids led to significant suppression of allergic dermatitis as evidenced by reduced clinical and histological scores of affected skins, infiltration of inflammatory cells, and circulating allergen-specific IgE levels, compared with treatment with normal milk fat or the base control diet. C9,t11-CLA and VA individually inhibited multiple facets of allergic dermatitis when topically applied, and their combination produced a strong additive effect. CONCLUSION AND CLINICAL RELEVANCE: Enriched milk fat, and its two major fatty acids c9,t11-CLA and vaccenic acid attenuate allergic dermatitis in mice.

Role of contact sensitization in chronic urticaria.

We tested the hypothesis that contact allergy plays a role in chronic urticaria, and included the Italian series of patch tests in the diagnostic workup. Of 121 patients with chronic urticaria, 50 (41%) tested positive to contact allergens. In all patients, avoidance measures led to a complete remission within 1 month. We suggest that testing for contact sensitization can be helpful in the management of chronic urticaria.

A intervenção precoce nas doenças alérgicas em pediatria: como e quando intervir / Early intervention in allergic diseases in pediatrics: how and when

Objetivo: avaliar os fatores intervenientes na evolução das principais doenças alérgicas em pediatria: dermatite atópica, rinite e asma. Identificar a eficácia de medidas dietéticas, medicamentosas e da imunoterapia nesta evolução. Fontes Pesquisadas: a base de dados MEDLINE, referente aos fatores de risco a hereditariedade e fatores ambientais que têm início durante a gestação e estendem-se à primeira infância...

Balsam-related systemic contact dermatitis.

BACKGROUND: Positive patch tests to balsam of Peru (BOP) or fragrance mix (FM) suggest the possibility of systemic contact dermatitis from balsam-related foods and spices. OBJECTIVE: This was a retrospective study to determine whether avoidance of balsam-related foods results in an improvement of dermatitis in these patients. METHODS: A review of the records of all patients seen from July 1 to Dec 31, 1998 with positive patch tests to BOP, FM, cinnamic aldehyde, and balsam of tolu was performed 9 to 14 months after their evaluation in a tertiary dermatology center. All patients were contacted via telephone to assess the status of their dermatitis and whether they were able to note any specific balsam-related food allergies. RESULTS: A total of 75 patients were identified, and 71 could be contacted. Fourteen were only allergic to BOP or FM on testing; 31 were positive to BOP/FM and other allergens with presumed relevance to BOP/FM; 26 were positive to BOP/FM and others with other allergens felt to be responsible for the dermatitis and were not placed on a BOP diet. Excluding this last group, 21 of 45 (47%) had complete or significant improvement that they related to dietary modification. Ten did not modify their diet, with 8 reporting no improvement. Eight improved with fragrance or other allergen avoidance only, and 6 modified their diet unsuccessfully. Most commonly implicated foods included tomatoes, citrus, and spices. CONCLUSION: Almost half of the subjects with positive patch tests to BOP or FM who followed a BOP reduction diet reported significant to complete improvement of their dermatitis.

Chronic allergic-like dermatopathies in nickel-sensitive patients. Results of dietary restrictions and challenge with nickel salts.

Nickel frequently contaminates foods. In sensitized patients, dietary nickel can cause a relapse of contact eczema and also widespread chronic dermatopathies quite similar to those triggered by authentic food allergy (IgE-mediated), from atopic dermatitis to chronic urticaria with angioedema. The present study was intended to evaluate the the results of an elimination diet and of the oral challenge test with nickel salts in a population of adults suffering from chronic urticaria or angioedema, pruritus or atopic dermatitis, and concomitant contract sensitization to nickel salts. The study involved a population of adult patients (112 subjects, 106 women and 6 men, aged from 16 to 58, mean age 29 +/- 10) with widespread allergic-like dermatopathies and contact sensitization to nickel salts (positive patch test). All of these subjects were prescribed a low nickel diet for four weeks. The patients who recovered or whose clinical manifestations greatly improved underwent an oral double-blind, placebo-controlled challenge: they were administered two successive, noncumulative doses of 10 and 20 mg nickel sulphate hexahydrate, respectively equal to 2.23 and 4.47 mg of elemental nickel. A search for specific IgE and the check on skin reactivity by skin-prick test against nickel were carried out in the patients who had shown particularly severe reactions after the oral challenge. A low nickel diet was effective in controlling the symptoms in 44 patients (39.28%, among whom there was one man). The oral double-blind, placebo-controlled challenge test was positive in all the patients who had favourably responded to the elimination diet, except one. In the patients with anaphylactoid reactions on the oral challenge, skin-prick tests were negative and no serum-specific IgE antibodies against nickel were found. Such findings appear to demonstrate that, in some patients with concomitant contact allergy, intolerance to ingested nickel salts might be the real cause of the onset and perpetuation of widespread, chronic, allergic-type dermatopathies.

Contact hypersensitivity in patients with orofacial granulomatosis.

BACKGROUND: Orofacial granulomatosis is a clinical entity presenting with chronic swelling of the oral or facial tissues in association with histological evidence of noncaseating granulomatous inflammation. Its cause remains unclear, but a possible role of contact sensitivity to dietary components has been proposed. OBJECTIVES: This study was performed to document the prevalence of contact sensitivity to food additives in patients with orofacial granulomatosis and assess the role of elimination diets in management. METHODS: Successive patients with a clinical diagnosis of orofacial granulomatosis were patch tested to the European Standard series and an Oral Battery containing common food additives. In addition, testing for immediate contact reactions to components of the Oral Battery was performed. In selected cases, appropriate elimination diets were implemented. RESULTS: Forty-eight patients were investigated. Ten showed positive reactions to components of the Oral Battery on standard patch testing and, of these, seven showed improvement on an elimination diet. CONCLUSIONS: Orofacial granulomatosis is a heterogenous clinical entity. Patch testing permits identification of a subgroup of patients likely to benefit from dietary manipulation and allows more appropriate targeting of such treatment.