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Published on: August 7, 2017
Contribution of systemic and airway immune responses to pediatric obesity-related asthma
Laura Chen1, Kayla Collado1, Deepa Rastogi2
1Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, United States.
Insights
Childhood obesity is linked to asthma, with immune responses differing in obese children. Novel pathways, like CDC42, show promise for targeted obesity-related asthma therapies.
Area of Science:
- Immunology
- Pediatrics
- Genetics
Background:
- Childhood obesity is a significant risk factor for asthma development.
- Immune responses in obese children with asthma differ from normal-weight children.
- Both allergic and non-allergic (non-T2) asthma phenotypes are observed in obesity-related asthma.
Purpose of the Study:
- To investigate the underlying immune mechanisms in childhood obesity-related asthma.
- To explore potential genetic and epigenetic factors influencing these immune responses.
- To identify novel therapeutic targets for obesity-related asthma.
Main Methods:
- Review of existing literature on immune responses in childhood asthma and obesity.
- Analysis of preliminary data on gene expression in non-T2 immune responses.
- Focus on the CDC42 pathway and its role in T helper cell physiology.
Main Results:
- Obese children with asthma exhibit distinct innate and adaptive immune profiles.
- Non-T2 asthma phenotypes show T helper (Th)1 polarization.
- Upregulation of CDC42 pathway genes was identified in non-T2 immune responses.
Conclusions:
- The CDC42 pathway plays a crucial role in Th cell differentiation and function, relevant to obesity-related asthma.
- Understanding these novel pathways offers opportunities for targeted therapeutic interventions.
- Further research into genetic and epigenetic mechanisms is warranted to address the burden of childhood obesity-related asthma.
Abstract:
Childhood obesity contributes to many diseases, including asthma. Although the precise mechanism by which obesity causes asthma is not known, there is literature to suggest that innate and adaptive systemic and airway immune responses in obese children with asthma differ from those in normal-weight children with asthma. Both non-allergic or non-T2 phenotype with systemic T helper (Th)1 polarization and allergic Th cell responses have been reported in childhood obesity-related asthma. There is preliminary evidence to suggest that genetic and epigenetic mechanisms contribute to these immune responses. Initial investigations into the biology of non-T2 immune responses have identified upregulation of genes in the CDC42 pathway. CDC42 is a RhoGTPase that plays a key role in Th cell physiology, including preferential naïve Th cell differentiation to Th1 cells, as well as cytokine production and exocytosis. These novel pathways are promising findings to direct targeted therapy development for obesity-related asthma to address the disease burden.
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