ArticleRespiratory physiology & neurobiology2013
Lung inflammation induces IL-1β expression in hypoglossal neurons in rat brainstem.
Article in Respiratory physiology & neurobiology, 2013. 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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Who cites it
6 citing papers in PubMed, 22 citations in OpenAlex.
- Ibuprofen Does Not Prevent Inhibition of Fetal Breathing Movements Caused by Intrauterine Inflammation in Fetal Sheep.International journal of molecular sciences · 2025Article
- Time and dose-dependent impairment of neonatal respiratory motor activity after systemic inflammation.Respiratory physiology & neurobiology · 2020Article
- One bout of neonatal inflammation impairs adult respiratory motor plasticity in male and female rats.eLife · 2019Article
- Advances in cellular and integrative control of oxygen homeostasis within the central nervous system.The Journal of physiology · 2018Review
- Vagus nerve stimulation in pregnant rats and effects on inflammatory markers in the brainstem of neonates.Pediatric research · 2018Article
- Interleukin-1β and interleukin-6 enhance thermal prolongation of the LCR in decerebrate piglets.Respiratory physiology & neurobiology · 2016Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Perinatal inflammation is associated with respiratory morbidity. Immune modulation of brainstem respiratory control centers may provide a link for this pathobiology. We exposed 11-day old rats to intratracheal lipopolysaccharide (LPS, 0.5 μg/g) to test the hypothesis that intrapulmonary inflammation increases expression of the proinflammatory cytokine IL-1β within respiratory-related brainstem regions. Intratracheal LPS resulted in a 32% increase in IL-1β protein expression in the medulla oblongata. In situ hybridization showed increased intensity of IL-1β mRNA but no change in neuronal numbers. Co-localization experiments showed that hypoglossal neurons express IL-1β mRNA and immunostaining showed a 43% increase in IL-1β protein-expressing cells after LPS exposure. LPS treatment also significantly increased microglial cell numbers though they did not express IL-1β mRNA. LPS-induced brainstem expression of neuronal IL-1β mRNA and protein may have implications for our understanding of the vulnerability of neonatal respiratory control in response to a peripheral proinflammatory stimulus.
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