Low Mother-to-Child CCL22 Chemokine Levels Are Inversely Related to Mite Sensitization and Asthma in Early Childhood

2018, Scientific reports

Few studies have addressed the mother-to-child transmission of Th2 immunity and the impact on the development of atopic diseases in early childhood. We investigated 186 children who were followed-up regularly for 4 years in a birth cohort study. The levels of Th2 related chemokine (C-C motif) ligand 17 (CCL17) and CCL22 were quantified in cord blood and at 1.5 years-of-age using multiplex Luminex kits. The levels of 125 pairs of CCL17 and CCL22 chemokines from birth to 1.5 years were recorded in this study. Using K-means clustering, only the declining trend of CCL22 levels was separately clustered (cluster A, n = 51; cluster B, n = 46; cluster C, n = 28). Mothers of children with higher CCL22 chemokine levels at birth were significantly more likely to display Dermatophagoides pteronyssinus sensitization. A lower CCL22 level at birth with a slight rise during infancy was associated with higher prevalence of mite sensitization and a higher risk of asthma at 3 years-of-age (P = 0.014)....

High cord blood CCL22/CXCL10 chemokine ratios precede allergic sensitization in early childhood

Oncotarget, 2017

Atopic diseases are known to be characterized by a T helper (Th) 2-skewed immunity; however, there are few studies addressing the Th1/Th2 immunity at birth related to the development of atopic diseases in early childhood. We investigated 186 children followed up regularly at the clinic for 4 years in a birth cohort study. The Th1-associated CXC chemokine ligand (CXCL)-10, CXCL11, and the Th2-associated CC chemokine ligand (CCL)-17 and CCL22 were quantified in cord blood by multiplex Luminex kits. Specific immunoglobulin E antibodies against food and inhalant allergens were measured at 6 months as well as 1, 1.5, 2, 3, and 4 years of age. Cord blood CCL22 levels were positively associated with IgE sensitization at age 2, whereas cord blood CXCL10 levels were negatively associated with mite sensitization at age 3. Furthermore, a high cord blood CCL22/CXCL10 chemokine ratio was significantly associated with a higher risk of allergic sensitization at age 3 (OR, 1.02; 95% confidence inte...

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Cytokine Responses to Rhinovirus and Development of Asthma, Allergic Sensitization and Respiratory Infections during Childhood

American journal of respiratory and critical care medicine, 2018

Immunophenotypes of anti-viral responses, and their relationship with asthma, allergy and lower respiratory tract infections (LRTIs) are poorly understood. We characterized multiple cytokine responses of peripheral-blood mononuclear cells to rhinovirus stimulation, and their relationship with clinical outcomes. In a population-based birth cohort, we measured 28 cytokines post-stimulation with rhinovirus-16 in 307 children aged 11 years. We used machine learning to identify patterns of cytokine responses, and related these patterns to clinical outcomes using longitudinal models. We also ascertained phytohaemagglutinin-induced TH2-cytokine responses [PHA-TH2]. We identified six clusters of children based on their rhinovirus-16 responses, which were differentiated by the expression of four cytokine/chemokine groups: interferon-related-(IFN); pro-inflammatory-(Inflam); TH2-chemokine-(TH2-chem); regulatory-(Reg). Clusters differed in their clinical characteristics. Children with IFNInfla...

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Scratching the Surface: Towards Understanding the Pathogenesis of Atopic Dermatitis

Critical Reviews™ in Immunology, 2008

Atopic dermatitis (AD) is a chronic inflammatory skin disease with a steadily increasing prevalence affecting 10%-20% of infants and 1%-3% of adults globally. It is often the first clinical manifestation of atopic disease preceding asthma and allergic rhinitis. At least half of the children with AD develop some other form of atopic disease later in life. The pathogenesis of AD involves a complex interplay of factors, including genetic predisposition due to altered immune or skin barrier function, interactions with the environment, and infectious triggers of inflammation. In this review, we summarize the recent advances in understanding the contribution of different factors in the pathophysiology of AD in human and animal model systems. These insights provide new therapeutic potential for the treatment of human AD.

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