Food allergy and atopic dermatitis

Atopic dermatitis (AD), characterized by intense pruritus, eczematous lesions, and a relapsing disease course, is a chronic inflammatory skin disease that affects both children and adults. AD often begins in infancy and is associated with atopic diseases in the personal or family history.1 Environmental factors may trigger AD by affecting the skin barrier and by triggering inflammation. The elicitation of T-helper type 2 cytokines further impairs the epidermal barrier and leads to the penetration of irritants and allergens into the epidermis and thereby perpetuating inflammation. The presence of AD and its severity has been shown to positively correlate with risk of developing food allergy (FA). Children with AD are estimated to be six times more likely to develop FA compared with their healthy peers. It has been reported that nearly 40% of children with moderate-to-severe AD have immunoglobulin E (IgE) mediated FA compared with only 6% in the general population. Although analysis of experimental data has linked skin inflammation in AD to FA, with food challenges reproducing symptoms and avoidance diets improving AD, elimination diets are not known to cure AD and may have unfavorable consequences, such as loss of tolerance, which leads to immediate-type allergy, including anaphylaxis, nutritional deficiencies, growth failure, and reduction of quality of life for the patient and family. Exacerbation of AD can be inaccurately attributed to foods. Individuals with AD are often sensitized to foods with positive testing results, however, able to tolerate the food. In light of widespread ordering and commercial availability of serum specific IgE for FA, testing for FA is recommended only if, from a detailed clinical history, immediate-type allergic symptoms occur with ingestion of food, or in infants with AD who do not improve with optimal skin care.

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Food allergy

10.1093/med/9780198759928.003.0019 ◽

2018 ◽

Author(s):

John Puntis

Keyword(s):

Food Allergy ◽

Nasal Congestion ◽

Skin Prick Testing ◽

Clinical History ◽

Specific Ige ◽

Cow Milk ◽

Severe Reaction ◽

Detailed Clinical History ◽

Food Challenges ◽

Food Specific Ige

Food allergy is an immune response to food that can be classified as immunoglobulin (Ig)-E and non-IgE mediated. Milk, egg, peanut, tree nuts, and fish are among the most prevalent causes of food allergy. Mild reactions can include itchy rash, watering eyes, and nasal congestion while a severe reaction results in anaphylaxis. A detailed clinical history is essential when making a diagnosis, and skin prick testing and quantitative measurement of food-specific IgE antibodies can be helpful. Cow milk protein allergy causes a plethora of symptoms and frequently resolves spontaneously over the first 2 years of life; diagnosis is based mainly on clinical history. Food challenges have a pivotal role in the diagnosis of food allergy. Introduction of ‘allergic’ foods at 3–6 months alongside continuing breastfeeding may prevent allergy.

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Challenge of food allergy testing and avoidance in children with atopic dermatitis

BMJ Case Reports ◽

10.1136/bcr-2021-243141 ◽

2021 ◽

Vol 14 (6) ◽

pp. e243141

Author(s):

Stephanie Ann Kubala ◽

Paula Mariam Mohyi ◽

Kristin Sokol ◽

Pamela Frischmeyer-Guerrerio

Keyword(s):

Primary Care ◽

Atopic Dermatitis ◽

Food Allergy ◽

Growth Failure ◽

Clinical History ◽

Primary Care Providers ◽

Care Providers ◽

Immediate Hypersensitivity ◽

Allergy Testing ◽

Food Avoidance

Atopic dermatitis (AD) is a common presenting complaint by children and their caretakers to their primary care providers. On testing, children with AD frequently exhibit positive food-specific IgE levels in the absence of immediate allergic reactions. Misinterpretation of these false positive tests can lead to unnecessary food avoidance, which can have tremendous psychosocial, economic and nutritional consequences and, in some cases, facilitate the development of an immediate hypersensitivity to the food. We present a child with persistent AD who underwent broad testing that led to unnecessary food avoidance resulting in Vitamin D deficiency, growth failure and the development of an IgE-mediated food allergy. This case underscores the need for caution by primary care clinicians in using food avoidance diets as a treatment for AD and the importance of limiting allergy testing to foods only when the clinical history indicates an immediate hypersensitivity reaction.

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Food Allergy: Unproven diagnostics and therapeutics

Journal of Food Allergy ◽

10.2500/jfa.2020.2.200013 ◽

2020 ◽

Vol 2 (1) ◽

pp. 91-94

Author(s):

Megan F. Patterson ◽

Stacy L. Dorris

Keyword(s):

Food Allergy ◽

Adverse Reactions ◽

Immunoglobulin E ◽

Skin Prick Testing ◽

Scientific Evidence ◽

Food Challenge ◽

Clinical History ◽

Specific Ige ◽

Therapeutic Modalities ◽

Diagnostic Modalities

Food allergy or intolerance is often attributed by patients as the cause of many symptoms unknown to be directly related to food ingestion. For immunoglobulin E (IgE) mediated food allergy, diagnostic modalities are currently limited to the combination of clinical history, evidence of sensitization with food-specific IgE testing and skin-prick testing, and oral food challenge. Many patients find an appeal in the promise of identification of the etiology of their symptoms through alternative food allergy or intolerance diagnostic modalities. These patients may seek guidance from allergists or their general providers as to the legitimacy of these tests or interpretation of results. These tests include food-specific serum IgG or IgG4 testing, flow cytometry to measure the change in leukocyte volume after exposure to food, intradermal or sublingual provocation-neutralization, electrodermal testing, applied kinesiology, hair analysis, and iridology. In addition, there are some unconventional therapeutic modalities for adverse reactions to foods, including rotary diets. None of these have been supported by scientific evidence, and some even carry the risk of severe adverse reactions. It is important that we offer our patients evidence-based, accurate counseling of these unproven modalities by understanding their methods, their paucity of credible scientific support, and their associated risks.

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Effects of mineral complex material treatment on 2,4- dinitrochlorobenzene-induced atopic dermatitis like-skin lesions in mice model

BMC Complementary Medicine and Therapies ◽

10.1186/s12906-021-03259-5 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Johny Bajgai ◽

Jing Xingyu ◽

Ailyn Fadriquela ◽

Rahima Begum ◽

Dong Heui Kim ◽

...

Keyword(s):

Atopic Dermatitis ◽

Water Loss ◽

Immunoglobulin E ◽

Skin Barrier ◽

Skin Lesions ◽

Total Serum ◽

Skin Barrier Function ◽

Barrier Dysfunction ◽

Complex Material ◽

Mineral Complex

Abstract Background Atopic dermatitis (AD) is a chronic allergic inflammatory skin disease characterized by complex pathogenesis including skin barrier dysfunction, immune-redox disturbances, and pruritus. Prolonged topical treatment with medications such as corticosteroids, calcineurin inhibitors, and T-cell inhibitors may have some potential side-effects. To this end, many researchers have explored numerous alternative therapies using natural products and mineral compounds with antioxidant or immunomodulatory effects to minimize toxicity and adverse-effects. In the current study, we investigated the effects of mineral complex material (MCM) treatment on 2, 4-dinitrochlorobenzene (DNCB)-induced AD-like skin lesions in SKH-1 hairless mice. Methods Animals were divided into four groups; normal control (NC), negative control treated with DNCB only (DNCB only), positive control treated with DNCB and tacrolimus ointment (PC) and experimental group treated with DNCB and MCM patch (MCM). Skin inflammation and lesion severity were investigated through analyses of skin parameters (barrier score and strength, moisture and trans-epidermal water loss level), histopathology, immunoglobulin E, and cytokines. In addition, reactive oxygen species (ROS), nitric oxide (NO), glutathione peroxidase (GPx), and catalase (CAT) levels were measured in both serum and skin lysate. Results Our results demonstrates that MCM patch improved the progression of AD-like skin lesions by significantly increasing skin barrier strength and decreasing trans-epidermal water loss. Additionally, dermal administration of MCM patch significantly reduced epidermal thickness, ROS, and NO levels in skin lysate. Furthermore, we found that MCM suppressed the levels of AD-involved (Th1 and Th2) cytokines such as IL-2, IFN-γ, and IL-4 in blood. In addition, the levels of other Th1, and Th2 and inflammatory cytokines such as IL-1β, TNF-α, IL-6, IL-12(p70) and IL-10 were found lowest in the MCM group than in the DNCB only and PC groups. Moreover, we found total serum IgE level significantly increased after DNCB treatment, but decreased in the PC and MCM groups. Conclusion Taken together, our findings suggest that MCM application may have beneficial effects either systemic or regional on DNCB-induced AD lesional skin via regulation of the skin barrier function and immune-redox response.

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Siraitia grosvenorii Residual Extract Attenuates Atopic Dermatitis by Regulating Immune Dysfunction and Skin Barrier Abnormality

Nutrients ◽

10.3390/nu12123638 ◽

2020 ◽

Vol 12 (12) ◽

pp. 3638

Author(s):

Yoon-Young Sung ◽

Heung-Joo Yuk ◽

Won-Kyung Yang ◽

Seung-Hyung Kim ◽

Dong-Seon Kim

Keyword(s):

Atopic Dermatitis ◽

Immunoglobulin E ◽

Allergic Inflammation ◽

Skin Barrier ◽

Human Keratinocytes ◽

Skin Lesions ◽

Protein Levels ◽

Siraitia Grosvenorii ◽

Ifn Γ

Atopic dermatitis is a persistent inflammatory skin disorder. Siraitia grosvenorii fruits (monk fruit or nahangwa in Korean, NHG) are used as a natural sweetener and as a traditional medicine for the treatment of asthma and bronchitis. We evaluated the activity of S. grosvenorii residual extract (NHGR) on allergic inflammation of atopic dermatitis in a Dermatophagoides farinae mite antigen extract (DfE)-treated NC/Nga murine model and in vitro. Oral administration of NHGR significantly reduced epidermal hyperplasia and inflammatory cell infiltration in the skin lesions of DfE-induced atopic dermatitis, as well as the dermatitis severity score. NHGR reduced serum immunoglobulin E levels. Splenic concentrations of IFN-γ, interleukin (IL)-4, IL-5, and IL-13 were reduced by NHGR administration. Immunohistofluorescence staining showed that NHGR administration increased the protein levels of claudin-1, SIRT1, and filaggrin in atopic dermatitis skin lesions. In addition, NHGR inhibited the phosphorylation of mitogen-activated protein kinases and decreased filaggrin and chemokine protein expression in TNF-α/IFN-γ-induced human keratinocytes. Moreover, NHGR also inhibited histamine in mast cells. The quantitative analysis of NHGR revealed the presence of grosvenorine, kaempferitrin, and mogrosides. These results demonstrate that NHGR may be an efficient therapeutic agent for the treatment of atopic dermatitis.

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Diagnostic and Therapeutic Principles In Allergy

10.2310/im.1067 ◽

2018 ◽

Author(s):

Mitchell H. Grayson ◽

Peter Mustillo

Keyword(s):

Food Allergy ◽

Immunoglobulin E ◽

Skin Testing ◽

Allergic Sensitization ◽

Allergic Diseases ◽

Specific Ige ◽

Severe Form ◽

Therapeutic Principles ◽

Anticytokine Therapy ◽

Release Assay

The incidence of allergic diseases, like asthma, allergic rhinitis, and food allergy, is increasing in Westernized countries. This chapter discusses the importance of taking a careful and focused history and physical examination, as well as the laboratory studies that can be used to demonstrate the presence of allergic sensitization. Treatment for allergic disease is discussed, with an emphasis on new biologic therapies that have been developed. Finally, the chapter explores relatively new studies on the potential for interventions to prevent food allergy. Allergy is defined as an untoward physiologic event mediated by immune mechanisms, usually involving the interaction between an allergen and the allergic antibody, immunoglobulin E (IgE). Allergic reactions typically occur due to exposure to either airborne allergens, foods, drugs, chemicals, or Hymenoptera (such as wasps, bees and fire ants). Allergies manifest in numerous ways, including allergic asthma, allergic rhinoconjunctivitis, urticaria, eczema, and in its most severe form, anaphylaxis. This review contains 4 videos, 5 figures, 4 tables and 42 references Key Words: Delayed allergic reaction (Alpha-gal), Allergy diagnosis, Measurement of specific IgE, Allergy and asthma therapies, Anticytokine therapy (dupilumab, mepolizumab, reslizumab), AntiIgE therapy (omalizumab), Allergy skin testing, Basophil histamine release assay

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Chamaejasmine Isolated from Wikstroemia dolichantha Diels Suppresses 2,4-Dinitrofluoro-benzene-Induced Atopic Dermatitis in SKH-1 Hairless Mice

Biomolecules ◽

10.3390/biom9110697 ◽

2019 ◽

Vol 9 (11) ◽

pp. 697 ◽

Cited By ~ 2

Author(s):

Tae-Young Kim ◽

No-June Park ◽

Jonghwan Jegal ◽

Sangho Choi ◽

Sang Woo Lee ◽

...

Keyword(s):

Atopic Dermatitis ◽

Clinical Symptoms ◽

Skin Barrier ◽

Topical Administration ◽

Skin Lesions ◽

Specific Ige ◽

Transepidermal Water Loss ◽

Skin Barrier Function ◽

Enzyme Linked Immunosorbent Assay ◽

Dermal Thickness

Plants of the genus Wikstroemia have long been used as traditional medicines to treat diseases like pneumonia, rheumatism, and bronchitis. This study was designed to determine the effect of chamaejasmine, a biflavonoid present in W. dolichantha, on atopic dermatitis (AD)-like skin lesions in a 2,4-dinitrochlorobenzene (DNCB)-induced murine model of AD. Initially, we examined the anti-allergic activities of ten flavonoids from W. dolichantha by measuring β-hexosaminidase release from RBL-2H3 cells. Subsequently, an SKH-1 hairless mouse model of AD was developed based on the topical application of DNCB. Chamaejasmine (0.5%) or pimecrolimus (1%, positive control) were applied to dorsal skins of DNCB-sensitized AD mice for two weeks. Serum IL-4 and IgE levels were determined using enzyme-linked immunosorbent assay kits and transepidermal water loss (TEWL) and skin hydration were measured using a Tewameter TM210 and a SKIN-O-MAT, respectively. Of the ten flavonoids isolated from W. dolichantha, chamaejasmine most potently inhibited DNP-specific IgE-induced degranulation in RBL-2H3 cells. Topical administration of chamaejasmine attenuated the clinical symptoms of DNCB-induced dermatitis (i.e., itching, dryness, erythema, and edema). Histological analyses demonstrated that dermal thickness and mast cell infiltration in dermis were significantly reduced by chamaejasmine. In addition, 0.5% chamaejasmine inhibited DNCB-induced increases in total IL-4 and IgE levels in serum, improved skin barrier function, and increased epidermis moisture. Our findings suggest chamaejasmine might be an effective therapeutic agent for the treatment of atopic diseases.

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Influence of Atopic Dermatitis on Cow’s Milk Allergy in Children

Medicina ◽

10.3390/medicina55080460 ◽

2019 ◽

Vol 55 (8) ◽

pp. 460 ◽

Cited By ~ 1

Author(s):

Arianna Giannetti ◽

Francesca Cipriani ◽

Valentina Indio ◽

Marcella Gallucci ◽

Carlo Caffarelli ◽

...

Keyword(s):

Atopic Dermatitis ◽

Complex Disease ◽

Allergic Sensitization ◽

Skin Barrier ◽

Specific Ige ◽

Point Of View ◽

Cow’S Milk ◽

Skin Barrier Function ◽

Cow's Milk ◽

Significant Difference

Background and Objectives: Cow’s milk protein allergy (CMA) is the most common allergy in children. The natural history of CMA is generally favorable and the majority of children reach tolerance during childhood, even if studies show variable results. Atopic dermatitis (AD) is a complex disease from an immunological point of view. It is characterized by an impaired skin barrier function and is often the first clinical manifestation of the so-called “atopic march”. The aim of our study is to evaluate, in a cohort of children with CMA, if the presence of AD in the first months of life can influence the atopic status of patients, the tolerance acquisition to cow’s milk, the level of specific IgE (sIgE), and the sensitization towards food and/or inhalant allergens. Materials and Methods: We enrolled 100 children with a diagnosis of CMA referred to our Pediatric Allergology Unit, aged 1–24 months at the time of the first visit. Results: 71 children had AD and 29 did not. The mean follow-up was 5.28 years. The CMA manifestations were mainly cutaneous, especially in children with AD (91.6% vs. 51.7%; P < 0.001). Patients with AD showed higher rates of polysensitization to foods and higher levels of both total IgE and sIgE for milk, casein, wheat, peanuts, and cat dander at different ages when compared to patients without AD. We analyzed the presence of IgE sensitization for the main foods and inhalants at various ages in the two groups of patients: a statistically significant difference emerged in the two groups of patients for milk, yolk and egg white, hazelnut, peanuts, soybean, grass pollen and cat dander. Meanwhile, we did not find significant differences in terms of tolerance acquisition toward cow’s milk, which was nonetheless reached around 5 years of age in 61% of patients. The level of cow’s milk sIgE at the age of 5 years was significantly higher in the group of patients who did not acquire tolerance (38.38 vs. 5.22 kU/L; P < 0.0001). Conclusions: An early barrier deficiency appears to promote the development of allergic sensitization, but does not seem to influence the acquisition of tolerance.

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Bacterial skin colonization and infections in patients with atopic dermatitis

Anais Brasileiros de Dermatologia ◽

10.1590/s0365-05962012000500010 ◽

2012 ◽

Vol 87 (5) ◽

pp. 729-734 ◽

Cited By ~ 20

Author(s):

Vanessa Petry ◽

Giancarlo Resende Bessa ◽

Claudia Schermann Poziomczyck ◽

Caio Fernando de Oliveira ◽

Magda Blessmann Weber ◽

...

Keyword(s):

Atopic Dermatitis ◽

Bacterial Resistance ◽

Antimicrobial Agents ◽

Secondary Infection ◽

Skin Barrier ◽

Skin Inflammation ◽

Skin Surface ◽

Number Of Children ◽

Chronic Skin ◽

Systemic Antibiotics

Atopic Dermatitis is a chronic inflammatory skin disease that affects a large number of children and adults. The disease results from an interaction between genetic predisposition, host environment, skin barrier defects, and immunological factors. A major aggravating factor associated with Atopic Dermatitis is the presence of microorganisms on the patient's skin surface. Staphylococcus aureus and Streptococcus pyogenes, for instance, can exacerbate chronic skin inflammation. As a result, antimicrobials have often been prescribed to control the acute phase of the disease. However, increased bacterial resistance to antimicrobial agents has made it difficult for dermatologists to prescribe appropriate medication. In the presence of disseminated dermatitis with secondary infection, systemic antibiotics need to be prescribed; however, treatment should be individualized, in an attempt to find the most effective antibiotic with fewer side effects. Also, the medication should be used for as short as possible in order to minimize bacterial resistance.

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Ex-Vivo Skin Explant Culture Is a Model for TSLP-Mediated Skin Barrier Immunity

Life ◽

10.3390/life11111237 ◽

2021 ◽

Vol 11 (11) ◽

pp. 1237

Author(s):

Thomas Bauer ◽

Daniela Gubi ◽

Jörg Klufa ◽

Philipp Novoszel ◽

Martin Holcmann ◽

...

Keyword(s):

Atopic Dermatitis ◽

Ex Vivo ◽

Skin Barrier ◽

Skin Inflammation ◽

The Body ◽

Suitable Model ◽

Ex Vivo Model ◽

Egfr Inhibition ◽

Explant Cultures ◽

Barrier Immunity

The skin is the outermost barrier protecting the body from pathogenic invasion and environmental insults. Its breakdown initiates the start of skin inflammation. The epidermal growth factor (EGFR) on keratinocytes protects this barrier, and its dysfunction leads to atopic dermatitis-like skin disease. One of the initial cytokines expressed upon skin barrier breach and during atopic dermatitis is TSLP. Here, we describe the expression and secretion of TSLP during EGFR inhibition and present an ex-vivo model, which mimics the early events after barrier insult. Skin explants floated on culture medium at 32 °C released TSLP in parallel to the activation of the resident Langerhans cell network. We could further show the up-regulation and activation of the AP-1 family of transcription factors during atopic-like skin inflammation and its involvement in TSLP production from the skin explant cultures. Inhibition of the c-Jun N-terminal kinase pathway led to a dose-dependent blunting of TSLP release. These data indicate the involvement of AP-1 during the early stages of atopic-like skin inflammation and highlight a novel therapeutic approach by targeting it. Therefore, skin explant cultures mimic the early events during skin barrier immunity and provide a suitable model to test therapeutic intervention.

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