ArticleAmerican journal of respiratory cell and molecular biology2024
The Impact of Inflammation on Thermal Hyperpnea: Relevance for Heat Stress and Febrile Seizures.
Article in American journal of respiratory cell and molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Climate Change-Mediated Temperature Extremes: Effects on the Immune System and Associations with Immune-Related Diseases.Clinical reviews in allergy & immunology · 2026Review
- Febrile temperature-regulated TRPV1 in CD4Journal of neuroinflammation · 2025Article
- A study on the distribution of interleukin-10 gene polymorphisms and their association with febrile seizure susceptibility in children from the Wenzhou region, Zhejiang Province.Frontiers in public health · 2025Article
- Maresin 1 Alleviates Seizure Symptoms by Modulating the Crosstalk Between Inflammation and Ferroptosis.Journal of inflammation research · 2025Article
- The Role of TRPV1 in Febrile Seizure Susceptibility: Inflammation, Respiratory Alkalosis, and Seizure Threshold.American journal of respiratory cell and molecular biology · 2024Article
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6 authors at 2 institutions in 3 countries.
Funding
Abstract
Extreme heat caused by climate change is increasing the transmission of infectious diseases, resulting in a sharp rise in heat-related illness and mortality. Understanding the mechanistic link between heat, inflammation, and disease is thus important for public health. Thermal hyperpnea, and consequent respiratory alkalosis, is crucial in febrile seizures and convulsions induced by heat stress in humans. Here, we address what causes thermal hyperpnea in neonates and how it is affected by inflammation. Transient receptor potential cation channel subfamily V member 1 (TRPV1), a heat-activated channel, is sensitized by inflammation and modulates breathing and thus may play a key role. To investigate whether inflammatory sensitization of TRPV1 modifies neonatal ventilatory responses to heat stress, leading to respiratory alkalosis and an increased susceptibility to hyperthermic seizures, we treated neonatal rats with bacterial LPS, and breathing, arterial pH,
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Registered trials
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