Japanese cedar pollen‐specific interleukin‐4 production develops immediately after the first exposure to pollens in infants with atopic dermatitis

Background: Although hen’s eggs are considered a cause of infantile atopic dermatitis (AD), little is known about cytokine production upon egg stimulation in infants with AD. Objective: This study aimed to characterize the production of IL-4, IL-5 and IFN-γ upon stimulation with ovalbumin (OVA), a representative allergenic protein of egg, in infants with AD. Methods: Peripheral blood mononuclear cells (PBMCs) from 68 children with AD, including 46 infants (<1 year), were stimulated with OVA and the production of IL-4, IL-5 and IFN-γ was measured with ELISA kits. Results: Upon stimulation with OVA, the production of IL-4 and IL-5, but not IFN-γ, by PBMCs was significantly higher in infants with AD than in non-atopic controls. OVA-induced IL-5 production peaked in younger infants (2–5 months) and then decreased with age increase. In contrast, OVA-induced IL-4 production peaked at the age of 1–2. This coincided with the serum level of egg white-specific IgE (EW-IgE). There was a significant positive correlation between IL-5 production and the severity of symptoms in infants with AD, while IL-4 production significantly correlated with the serum level of EW-IgE. Conclusion: These results demonstrate that OVA-induced IL-5 production fluctuates with age in a different manner than IL-4 or EW-IgE. Our results suggest that egg contributes to the development of AD in younger infants by inducing the production of IL-5, but not IL-4.

Section: Methodsmentioning

confidence: 99%

Ovalbumin-Induced IL-4, IL-5 and IFN-γProduction in Infants with Atopic Dermatitis

Kimura¹,

Obi²

2005

“…This is quite different from the changes in the serum level of JCP-specific IgE antibody with age since JCP-specific IgE antibody is insignificant in infants but rises after 1 year of age [5]. Presently, IgE antibody is almost the only routinely available laboratory parameter apart from eosinophils indicating the cause and mechanism of allergic disorders.…”

Section: Discussionmentioning

confidence: 99%

“…Sensitization to pollen allergens is thought to take more than a year because IgE antibody against pollens is not produced before 1 year of age [5, 8, 9]. Hence possible relationships between JCPs and the aggravation of infantile AD during the first spring after birth have not been considered.…”

Section: Discussionmentioning

confidence: 99%

“…Hence possible relationships between JCPs and the aggravation of infantile AD during the first spring after birth have not been considered. However, we recently demonstrated that PBMCs from infants with AD produced a large amount of IL-4 upon stimulation with JCPs immediately after the first exposure to JCPs [5], indicating that JCP-specific Th2 cells develop in infants with AD prior to the beginning of IgE synthesis.…”

Section: Discussionmentioning

confidence: 99%

“…Because serum IgE antibody against JCPs is usually negative in infants with AD [5], JCPs has never been regarded as a cause of infantile AD. However, we recently demonstrated that JCP-specific IL-4 and IFN-γ production by peripheral blood mononuclear cells (PBMCs) rose immediately after the first contact with JCPs in infants with AD [5]. Thus, JCPs may also affect the symptoms of AD in infants by inducing proinflammatory cytokines such as IL-5.…”

Section: Introductionmentioning

confidence: 99%

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Japanese Cedar-Pollen-Specific IL-5 Production in Infants with Atopic Dermatitis

Kimura

Obi²,

Saito³

2004

Background: Although food allergens and house dust mites are thought to contribute to the development of atopic dermatitis (AD) in infants, the influence of pollens has not yet been well defined. Objective: This study attempted to clarify the effect of Japanese cedar pollens (JCPs), which are scattered in Japan between February and April, on AD in infants. Methods: In the first study, seasonal changes in the number of patients who first visited our institute due to AD were analyzed by reviewing medical records of 184 infants with AD. In the second study, peripheral blood mononuclear cells from 81 children (50 infants <1 year and 31 older children) with AD were stimulated with a standardized JCP allergen. The production of IL-5 was measured and its correlation with the severity of AD in infants was analyzed. Results: The number of infants who first visited the institute due to AD peaked in spring. JCP-specific IL-5 production began to increase immediately after the first contact with JCPs in infants with AD. The production of IL-5 in infants with AD exposed to JCPs was significantly higher than in control subjects (p < 0.002) or in AD infants never exposed to JCPs (p < 0.02). There was a significant positive correlation between IL-5 production and the severity of AD in infants (p < 0.0001). Conclusion: These results suggest that JCPs play an important role in the aggravation of infantile AD in spring by inducing IL-5 production.

Organic Chemicals in Diesel Exhaust Particles Enhance Picryl Chloride-Induced Atopic Dermatitis in NC/Nga Mice

Sadakane

Ichinose²,

Takano³

et al. 2013

Background: Diesel exhaust particles (DEP) have been reported to worsen allergic airway inflammation in mice. Recently, the organic chemical components of DEP (DEP-OC) were found to be important contributors to the aggravation of allergic airway inflammation in mice. The purpose of this study was to examine the effects of DEP-OC on atopic dermatitis (AD)-like skin lesions induced by picryl chloride (PiCl) in NC/Nga mice. Methods: DEP were extracted with benzene/ethanol, and the soluble organic fraction formed the DEP-OC. NC/Nga male mice received simultaneous application of DEP-OC and/or PiCl on their ears once a week for 9 or 3 weeks. We evaluated skin lesions by noting scaling, eruption, excoriation, erosion, hemorrhage, pathologic changes, production of cytokines, and IgE level in the serum. Results: PiCl application alone produced progressively severe AD-like skin lesions. The application of PiCl plus DEP-OC resulted in a marked worsening of skin lesions in the early stages of AD. Moreover, mast cell counts significantly increased in the subcutaneous tissue. Administration of PiCl combined with DEP-OC resulted in a greater increase in the local expression of interleukin-4, keratinocyte chemoattractant, and neutrophils in subcutaneous tissue compared with PiCl treatment alone. In contrast, the combination treatment produced lower levels of IFN-γ compared with PiCl treatment alone. Conclusions: DEP-OC application to the skin aggravated PiCl-induced AD. This aggravation may be due to activation of the Th2-associated immune responses by the organic chemicals in DEP.