Group 2 innate lymphocytes protect the balance between autophagy and apoptosis in cardiomyocytes during sepsis-induced cardiac injury.

Autor: Fang K; Geriatric Medicine Center, Department of Geriatric Medicine, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), 158 Shangtang Road, Hangzhou, 310014, China.; Zhejiang University School of Medicine, Hangzhou, 310009, China., Chen H; Emergency Department, Zhejiang Hospital, Hangzhou, 310013, China., Xie J; Geriatric Medicine Center, Department of Geriatric Medicine, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), 158 Shangtang Road, Hangzhou, 310014, China., Sun D; Geriatric Medicine Center, Department of Geriatric Medicine, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), 158 Shangtang Road, Hangzhou, 310014, China., Li L; Geriatric Medicine Center, Department of Geriatric Medicine, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), 158 Shangtang Road, Hangzhou, 310014, China. lilihbch@163.com.
Jazyk: angličtina
Zdroj: Scientific reports [Sci Rep] 2024 Oct 23; Vol. 14 (1), pp. 25011. Date of Electronic Publication: 2024 Oct 23.
DOI: 10.1038/s41598-024-76606-4
Abstrakt: Group 2 innate lymphocytes (ILC2) have an important role in orchestrating sepsis-induced immune response. However, the impact of LC2 on sepsis-induced cardiac injury is still not fully understood. This study investigated the mechanisms governing ILC2 activation within the cardiac tissue after sepsis. In vivo experiments using wild-type and IL-33 deficient mice indicated that the presence of interleukin (IL)-33, which participates in expanding and activating ILC2 cells, was correlated with higher ILC2 levels (246 ± 34 vs. 66 ± 18, p < 0.01), reduced cardiac dysfunction, and lower markers of cardiac injury. Conversely, IL-33 deficiency led to exacerbated cardiac damage. Additionally, heart ILC2 significantly increased the expression and secretion of IL-5 (2.18 ± 0.34 ng/ml vs. 1.18 ± 0.24 ng/ml, p < 0.05) and IL-13 (10.55 ± 1.13 ng/ml vs. 7.59 ± 1.13 ng/ml, p < 0.05) following sepsis, with this response being mediated by IL-33. Moreover, IL-5 deficient mice exhibited increased cardiac dysfunction and myocardial apoptosis post-sepsis (20.7 ± 4.28% vs. 29.61 ± 4.28%, p < 0.05). Furthermore, in vitro experiments involving co-cultures of ILC2 with mice cardiomyocytes after lipopolysaccharide (LPS) administration suggested that IL-5 derived from ILC2 protects cardiomyocytes from autophagy and apoptosis. These findings imply that IL-33, released in response to sepsis, induces ILC2 activation and IL-5 secretion, orchestrating the equilibrium between autophagy and apoptosis in cardiomyocytes and offering potential therapeutic avenues for mitigating sepsis-induced cardiac injury.
(© 2024. The Author(s).)
Databáze: MEDLINE
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