Airway inflammation and central respiratory control: Results from in vivo and in vitro neonatal rat

Gresham, Kenneth S.; Boyer, Brooke; Mayer, Catherine; Foglyano, Ryan; Martin, Richard J.; Wilson, Christopher G.

doi:10.1016/j.resp.2011.05.008

Cited by 29 publications

(23 citation statements)

References 41 publications

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“…As IL-1β does not readily cross the blood brain barrier, a likely mechanism for the resultant apnea was thought to be IL-1β-induced activation of the cyclooxygenase-2 pathway and release of prostaglandin E2 which can cross the blood brain barrier with resultant respiratory depression (Hofstetter et al, 2007). Indeed, based upon data published from our group (Gresham et al, 2011) we have shown that both in vivo and in vitro rat models show changes in frequency of breathing rhythm in response to LPS or IL-1β. Our current data suggest that intrapulmonary or systemic infection actually stimulates IL-1β production from neurons within respiratory related regions of the brainstem.…”

Section: Discussionmentioning

confidence: 87%

Lung inflammation induces IL-1β expression in hypoglossal neurons in rat brainstem

Jafri

Belkadi

Zaidi

et al. 2013

Respiratory Physiology & Neurobiology

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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 pro-inflammatory stimulus.

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Section: Discussionmentioning

confidence: 87%

Lung inflammation induces IL-1β expression in hypoglossal neurons in rat brainstem

Jafri

Belkadi

Zaidi

et al. 2013

Respiratory Physiology & Neurobiology

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“…It is possible that microglial activation triggers the release of one or several inhibitory neuromodulators (Henry et al, 2009;Kaur et al, 2013;Lai and Todd 2006;Smith et al, 2013;Yang et al, 2013) that regulate the preB€ otC. Among the neuromodulators released by microglia are several inhibitors of respiratory rhythm generation (Aleksandrova et al, 2015;Gresham et al, 2011;Guerra et al, 1988;Kitterman et al, 1983;Olsson et al, 2003;Tai and Adamson, 2000;VanDam et al, 2008;), such as interleukins (Aleksandrova et al, 2015;Gresham et al, 2011;Henry et al, 2009;Kaur et al, 2013;Lai and Todd 2006;Olsson et al, 2003;Smith et al, 2013;Yang et al, 2013), prostaglandin E2 (Guerra et al, 1988;Kitterman et al, 1983;Tai and Adamson, 2000;Wang et al, 2011;Zhang et al, 2009), hydrogen peroxide (Garcia et al, 2011), adenosine (Lauro et al, 2010;VanDam et al, 2008;Zwicker et al, 2011) and glycine (Hayashi et al, 2006;Ren and Greer, 2006).…”

Section: Discussionmentioning

confidence: 99%

Microglia modulate respiratory rhythm generation and autoresuscitation

Lorea-Hernández

Morales

Rivera-Angulo

et al. 2015

Glia

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Inflammation has been linked to the induction of apneas and Sudden Infant Death Syndrome, whereas proinflammatory mediators inhibit breathing when applied peripherally or directly into the CNS. Considering that peripheral inflammation can activate microglia in the CNS and that this cell type can directly release all proinflammatory mediators that modulate breathing, it is likely that microglia can modulate breathing generation. It might do so also in hypoxia, since microglia are sensitive to hypoxia, and peripheral proinflammatory conditions affect gasping generation and autoresuscitation. Here, we tested whether microglial activation or inhibition affected respiratory rhythm generation. By measuring breathing as well as the activity of the respiratory rhythm generator (the preBötzinger complex), we found that several microglial activators or inhibitors, applied intracisternally in vivo or in the recording bath in vitro, affect the generation of the respiratory rhythms both in normoxia and hypoxia. Furthermore, microglial activation with lipopolysaccharide affected the ability of the animals to autoresuscitate after hypoxic conditions, an effect that is blocked when lipopolysaccharide is co-applied with the microglial inhibitor minocycline. Moreover, we found that the modulation of respiratory rhythm generation induced in vitro by microglial inhibitors was reproduced by microglial depletion. In conclusion, our data show that microglia can modulate respiratory rhythm generation and autoresuscitation.

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“…How hypoxia and inflammation interact within the CNS is an interesting and emerging area of research, with important implications for the respiratory system and the clinic (Gresham et al . ; Jafri et al . ; Lorea‐Hernandez et al .…”

Section: Introductionmentioning

confidence: 99%

“…A commonly used approach to study inflammation is the use of lipopolysaccharide (LPS; Gresham et al . ; Balan et al . ; Master et al .…”

Section: Introductionmentioning

confidence: 99%

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Advances in cellular and integrative control of oxygen homeostasis within the central nervous system

Ramírez

Severs

Ramirez

et al. 2018

The Journal of Physiology

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Mammals must continuously regulate the levels of O and CO , which is particularly important for the brain. Failure to maintain adequate O /CO homeostasis has been associated with numerous disorders including sleep apnoea, Rett syndrome and sudden infant death syndrome. But, O /CO homeostasis poses major regulatory challenges, even in the healthy brain. Neuronal activities change in a differentiated, spatially and temporally complex manner, which is reflected in equally complex changes in O demand. This raises important questions: is oxygen sensing an emergent property, locally generated within all active neuronal networks, and/or the property of specialized O -sensitive CNS regions? Increasing evidence suggests that the regulation of the brain's redox state involves properties that are intrinsic to many networks, but that specialized regions in the brainstem orchestrate the integrated control of respiratory and cardiovascular functions. Although the levels of O in arterial blood and the CNS are very different, neuro-glial interactions and purinergic signalling are critical for both peripheral and CNS chemosensation. Indeed, the specificity of neuroglial interactions seems to determine the differential responses to O , CO and the changes in pH.

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Airway inflammation and central respiratory control: Results from in vivo and in vitro neonatal rat

Cited by 29 publications

References 41 publications

Lung inflammation induces IL-1β expression in hypoglossal neurons in rat brainstem

Lung inflammation induces IL-1β expression in hypoglossal neurons in rat brainstem

Microglia modulate respiratory rhythm generation and autoresuscitation

Advances in cellular and integrative control of oxygen homeostasis within the central nervous system

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