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Molecular and Cellular Pediatrics
Fig. 1 | Molecular and Cellular Pediatrics

Fig. 1

From: Perinatal origins of chronic lung disease: mechanisms–prevention–therapy—sphingolipid metabolism and the genetic and perinatal origins of childhood asthma

Fig. 1

Expanding landscape of pediatric asthma investigation. Clinical features of wheeze, breathlessness, and cough were first related to the triad of airway inflammation, bronchoconstriction, and mucus production, followed by increased understanding of T-helper (Th) cell-associated pathways linking allergen exposure and Th2 cell cytokines to airway eosinophilia and mast cell degranulation. Neutrophil dominant airway inflammation was also identified and related Th1 and Th17 pathways, mediated by interferon γ and IL-17, respectively. Applied to samples from large pediatric asthma cohorts, technologies based on high throughput sequencing and mass spectrometry have revealed surprising, but correlative, genomic, and metabolic disturbances in connection with constitutive elements of the multiple inflammatory pathways. This includes the association of 17q21 SNPs with alterations to sphingolipid gene expression and metabolism in children with non-atopic asthma.

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