Shorter telomeres in children with severe asthma, an indicative of accelerated aging

• Autor(a) principal: Barbé-Tuana, Florencia María
• Data de Publicação: 2021
• Outros Autores: Grun, Lucas Kich, Lima, Vinícius Pierdoná, Parisi, Mariana Migliorini, Friedrich, Frederico Orlando, Guma, Fátima Theresinha Costa Rodrigues, Pinto, Leonardo Araujo, Stein, Renato Tetelbom, Pitrez, Paulo Marcio Condessa, Jones, Marcus Herbert
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/219447
• topic: Asma; Quimiocina CCL11; Homeostase do telômero; Criança; Telomere length; CCL11; Severe asthma; Inflammaging; Senescence

Severe therapy-resistant asthma (STRA) is closely associated with distinct clinical and inflammatory pheno-endotypes, which may contribute to the development of age-related comorbidities. Evidence has demonstrated a contribution of accelerated telomere shortening on the poor prognosis of respiratory diseases in adults. Eotaxin-1 (CCL11) is an important chemokine for eosinophilic recruitment and the progression of asthma. In the last years has also been proposed as an age-promoting factor. This study aimed to investigate the association of relative telomere length (rTL) and eotaxin-1 in asthmatic children. Children aged 8-14 years (n=267) were classified as healthy control (HC, n=126), mild asthma (MA, n=124) or severe therapy-resistant asthma (STRA, n=17). rTL was performed by qPCR from peripheral blood. Eotaxin-1 was quantified by ELISA from fresh-frozen plasma. STRA had shorter telomeres compared to HC (p=0.02) and MA (p=0.006). Eotaxin-1 levels were up-regulated in STRA [median; IQR25-75)] [(1,190 pg/mL; 108–2,510)] compared to MA [(638 pg/mL; 134–1,460)] (p=0.03) or HC [(627 pg/mL; 108–1,750)] (p<0.01). Additionally, shorter telomeres were inversely correlated with eotaxin-1 levels in STRA (r=-0.6, p=0.013). Our results suggest that short telomeres and up-regulated eotaxin-1, features of accelerated aging, could prematurely contribute to a senescent phenotype increasing the risk for early development of age-related diseases in asthma.