کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5926195 | 1167348 | 2013 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Lung inflammation induces IL-1β expression in hypoglossal neurons in rat brainstem
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
فیزیولوژی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Lung inflammation induces IL-1β expression in hypoglossal neurons in rat brainstem Lung inflammation induces IL-1β expression in hypoglossal neurons in rat brainstem](/preview/png/5926195.png)
چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Respiratory Physiology & Neurobiology - Volume 188, Issue 1, 1 August 2013, Pages 21-28
Journal: Respiratory Physiology & Neurobiology - Volume 188, Issue 1, 1 August 2013, Pages 21-28
نویسندگان
Anjum Jafri, Abdelmadjid Belkadi, Syed I.A. Zaidi, Paulina Getsy, Christopher G. Wilson, Richard J. Martin,