Corticosteroids, IgE, and atopy

Barnes, Peter J.

doi:10.1172/jci12157

Cited by 60 publications

(47 citation statements)

References 20 publications

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“…The reason for this increase is not immediately obvious but may be related to prolonged concomitant therapy with a relatively potent topical corticosteroid. One of the paradoxical effects which have been observed for corticosteroids is an increase in IL-4-stimulated production of IgE by B lymphocytes [29]. In fact, a rise in polyclonal serum IgE was shown in asthma patients following oral administration of prednisone; however, the increase did not have a negative clinical impact and was considered to reflect the broader immunomodulatory effects of corticosteroids on T lymphocytes [30].…”

Section: Discussion/conclusionmentioning

confidence: 99%

A Randomized, Double-Blind, Placebo-Controlled Trial Assessing the Oral Administration of a Heat-Treated Lactobacillus paracasei Supplement in Infants with Atopic Dermatitis Receiving Topical Corticosteroid Therapy

Yan

Hung

et al. 2019

Skin Pharmacol Physiol

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Background/Aims: Atopic dermatitis (AD) is a common disease in infancy, for which topical steroids are the first-line therapy but have side effects. Innovative approaches are needed to reduce the burden of AD and corticosteroid usage in infants. Methods: The once-daily consumption of heat-treated probiotic Lactobacillus paracasei GM-080 or placebo for 16 weeks as supplementary approach to topical treatment with fluticasone propionate cream was compared in AD infants aged 4–30 months. Outcomes were SCORAD and its subscores, TEWL, Infants’ Dermatitis Quality of Life Index (IDQOL), corticoid “sparing effect,” CCL17/TARC, and IgE status. Results: SCORAD, objective SCORAD, itching, and IDQOL decreased significantly (p < 0.001) over the treatment period in both treatment groups. Slight decreases (ns) were noted in TEWL in lesional and unaffected skin and CCL17 levels. There were no differences between the treatment groups. Total IgE increased over the treatment period in both groups, with significantly higher increase in the heat-treated probiotic group (p = 0.038). There was no evidence of a corticoid “sparing effect” by the probiotic. Conclusions: In this design, the probiotic L. paracasei was not beneficial as a complementary approach to topical corticosteroids in infants with AD. However, slight beneficial effects may have been masked by the moderate potency corticoid.

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Section: Discussion/conclusionmentioning

confidence: 99%

A Randomized, Double-Blind, Placebo-Controlled Trial Assessing the Oral Administration of a Heat-Treated Lactobacillus paracasei Supplement in Infants with Atopic Dermatitis Receiving Topical Corticosteroid Therapy

Yan

Hung

et al. 2019

Skin Pharmacol Physiol

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“…More recently, it has been reported that GCs increase IL-4-stimulated IgE formation probably via upregulation of the costimulatory molecule CD40 ligand (CD40L) on Th cells. Binding of the CD40L to the B-cell CD40 receptor causes resting B-cell activation and IgE isotype switching [43,44] . Regarding these findings, the idea that hyperresponsiveness of the HPA axis in infants at high allergic risk may promote sensitization and subsequent IgE hyperproduction does not appear too speculative.…”

Section: Stress and Hypothalamus-pituitary-adrenal Axis Function In Amentioning

confidence: 99%

Cortisol Responses to Stress in Allergic Children: Interaction with the Immune Response

Buske‐Kirschbaum

2009

Neuroimmunomodulation

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Allergic manifestations are increasingly common in infants and children. Accumulating evidence suggests that the ‘epidemic’ increase of childhood allergy may be associated with environmental factors such as stress. Although the impact of stress on the manifestation and exacerbation of allergy has been demonstrated, the underlying mechanisms of stress-induced exacerbation are still obscure. A growing number of studies have suggested an altered hypothalamus-pituitary-adrenal (HPA) axis function to stress in allergic children. It is speculated that a dysfunctional HPA axis in response to stress may facilitate and/or consolidate immunological aberrations and thus, may increase the risk for allergic sensitization and exacerbation especially under stressful conditions. In the present review the potential impact of a hyporesponsive as well as a hyperresponsive HPA axis on the onset and chronification of childhood allergy is summarized. Moreover, potential factors that may contribute to the development of an aberrant HPA axis responsiveness in allergy are discussed.

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“…This apparent paradox between the efficacy of glucocorticoids for the treatment of allergic inflammation and the apparent increase in IgE with corticosteroids has been previously reviewed [33] . IL-4 and hydrocortisone are known to act synergistically to induce IgE isotype switching in human B cells [34] .…”

Section: Elevated Endogenous Cortisol As a Risk Factor For Allergiesmentioning

confidence: 99%

Cortisol Circadian Rhythms and Stress Responses in Infants at Risk of Allergic Disease

Ball¹

2006

Neuroimmunomodulation

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Altered hypothalamic-pituitary-adrenal function associated with allergic disease has generally been thought to be secondary to the stress of chronic disease. However, recent studies suggest that altered cortisol circadian rhythm and cortisol stress hyper-responsiveness precede the inception of allergic disease and are possible links between preventive factors associated with the hygiene hypothesis and the development of allergies. Elevated endogenous cortisol responses to stressful stimuli could predispose susceptible hosts to atopy and allergic disease by biasing the developing immune system to a T helper 2-predominant immune response, greater total and allergen-specific serum immunoglobulin E responses, and/or inhibition of peripheral immune tolerance. Because glucocorticoid receptors are present throughout the human body and many genes contain glucocorticoid response elements, variances in endogenous cortisol concentrations could have an impact on the phenotypic plasticity of a wide range of immunologically active genes during early human immune development. Here, recent findings related to hypothalamic-pituitary-adrenal function in infants predisposed to developing allergic disease are discussed along with speculation regarding the potential causal role of endogenous cortisol in the inception of allergic disease.

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Corticosteroids, IgE, and atopy

Cited by 60 publications

References 20 publications

A Randomized, Double-Blind, Placebo-Controlled Trial Assessing the Oral Administration of a Heat-Treated <b><i>Lactobacillus paracasei </i></b>Supplement in Infants with Atopic Dermatitis Receiving Topical Corticosteroid Therapy

A Randomized, Double-Blind, Placebo-Controlled Trial Assessing the Oral Administration of a Heat-Treated <b><i>Lactobacillus paracasei </i></b>Supplement in Infants with Atopic Dermatitis Receiving Topical Corticosteroid Therapy

Cortisol Responses to Stress in Allergic Children: Interaction with the Immune Response

Cortisol Circadian Rhythms and Stress Responses in Infants at Risk of Allergic Disease

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