Risk factors for and expression of immune and inflammatory factors in atopic dermatitis in Chinese population: A birth cohort study

Jin, Jing-Ji; Zou, Yingxue; Zeng, Sanwu

doi:10.1016/j.mcp.2016.03.006

Cited by 10 publications

(7 citation statements)

References 22 publications

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“…Increased levels of IL‐4 were detected in cell culture supernatants of CBMC of newborns of allergic mothers in comparison to infants of healthy mothers. This observation is in line with the work reported previously confirming that the immune system of newborns of allergic mothers is altered and thus predisposing children to later allergy development.…”

Section: Discussionsupporting

confidence: 93%

Decreased allergy incidence in children supplemented with E. coli O83:K24:H31 and its possible modes of action

et al. 2018

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The growing knowledge of the key role of microbiota in the maturation of neonatal immune system suggests that manipulation of microbiota could be exploited in hampering allergy development. In this study, Escherichia coli O83:K24:H31 (EcO83) was administered to newborns that were followed prospectively. Several immunological characteristics (cytokines, specific IgE, total T regulatory cells (Treg) and subpopulation of natural Treg (nTreg) and induced Treg (iTreg)) were tested in peripheral blood of 8-year-old children. Incidence of allergic disease was decreased in EcO83 supplemented children and significantly elevated levels of IL-10 and IFN-ɣ were detected in serum of EcO83 supplemented children. Probiotic supplementation did not influence the numbers of the total Treg population but their functional capacity (intracellular expression of IL-10) was significantly increased in children supplemented with EcO83 in comparison to nonsupplemented children. Morover, decreased proportion of iTreg was present in peripheral blood of non-supplemented in comparison to EcO83 supplemented children. Finally, stimulation of cord blood cells with EcO83 promoted both gene expression and secretion of IL-10 and IFN-ɣ suggesting that beneficial effect of EcO83 in prevention of allergy development could be mediated by promotion of regulatory responses (by IL-10) and Th1 immune response (by IFN-ɣ). Keywords: allergy r cord blood r E. coli r probiotics r Treg Additional supporting information may be found online in the Supporting Information section at the end of the article. , L. et al., Guidelines for the use of flow cytometry and cell sorting in immunological studies. Eur. J. Immunol. 2017. 47: 1584-1797. Abbreviations: CBMC: cord blood mononuclear cells · CFU: colony forming units · EcO83: Escherichia coli O83:K24:H31 · IQR: interquartile range · nTreg: natural Treg · Treg: T regulatory cells · iTreg: induced Treg

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Section: Discussionsupporting

confidence: 93%

Decreased allergy incidence in children supplemented with E. coli O83:K24:H31 and its possible modes of action

et al. 2018

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“…A majority of the AD subjects reacted to house dust mite (88.2%, 30 of 34) (>17.5 kUA/L), thereby indicating the AD subjects were mainly allergic to house dust mite in the present study cohort (Table S1), in concordance with a previous AD study with Chinese cohort. 15…”

Section: The Clinical Characteristics Of Subjects With Admentioning

confidence: 99%

Skewed inflammation is associated with aberrant interleukin‐37 signaling pathway in atopic dermatitis

Hou

Tsang

Chu

et al. 2021

Allergy

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Background Atopic dermatitis (AD) is a severe global burden on physical, physiological, and mental health. The role of IL‐37, a fundamental inhibitor of immunity, in AD was herein explored. Method Serum levels of IL‐37 and T helper (Th) 2‐related inflammatory mediators were quantified in subjects with or without AD. The expression of IL‐37 receptors was determined by flow cytometry. Proteomics was employed to explore the serum protein profile and novel biomarkers. In vitro cell model, 3D‐keratinocytes mimicking skin model, and the serum of subjects with or without AD were investigated to verify the proteomic results. Results AD patients were found to present with higher levels of total and specific IgE as well as Th2 inflammatory mediators compared with healthy controls (HC). IL‐37 level and its receptor IL18Rɑ expression in AD patients were significantly decreased, together with increased population of eosinophils, indicating that the signaling of IL37/IL18Rɑ was dampened. In addition, proteomic analysis revealed a significantly differential protein profile of AD patients compared with HC. IL‐37 showed the strongest negative correlation with involucrin, a keratinizing epithelia protein. IL‐37 was verified to suppress induced involucrin expression in in vitro skin cell models. AD patients show a significantly higher serum concentration of involucrin compared with HC. Together, our results demonstrated that IL‐37 plays a regulatory role in AD. Its deficiency may lead to the aberrant involucrin expression in AD. Conclusions The dysregulation of serum protein and skin disruption in AD is related to the insufficiency of IL‐37 and its attenuated anti‐inflammatory signaling.

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“…Recently, IL-18 levels in the maternal serum and cord blood were found to be a predisposing factor of childhood AD [152]. Elevated levels of serum IL-18 and IL-18 receptors have been suggested as biomarkers of AD severity [146,153], but additional research is required to confirm this suggestion [154,155].…”

Section: Immunological Abnormalitiesmentioning

confidence: 99%

Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis

Kim

Cho

et al. 2016

IJMS

110

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Atopic dermatitis (AD) is a multifactorial inflammatory skin disease resulting from interactions between genetic susceptibility and environmental factors. The pathogenesis of AD is poorly understood, and the treatment of recalcitrant AD is still challenging. There is accumulating evidence for new gene polymorphisms related to the epidermal barrier function and innate and adaptive immunity in patients with AD. Newly-found T cells and dendritic cell subsets, cytokines, chemokines and signaling pathways have extended our understanding of the molecular pathomechanism underlying AD. Genetic changes caused by environmental factors have been shown to contribute to the pathogenesis of AD. We herein present a review of the genetics, epigenetics, barrier dysfunction and immunological abnormalities in AD with a focus on updated molecular biology.

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Risk factors for and expression of immune and inflammatory factors in atopic dermatitis in Chinese population: A birth cohort study

Cited by 10 publications

References 22 publications

Decreased allergy incidence in children supplemented with E. coli O83:K24:H31 and its possible modes of action

Decreased allergy incidence in children supplemented with E. coli O83:K24:H31 and its possible modes of action

Skewed inflammation is associated with aberrant interleukin‐37 signaling pathway in atopic dermatitis

Molecular Mechanisms of Cutaneous Inflammatory Disorder: Atopic Dermatitis

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