Vagal afferents modulate cytokine-mediated respiratory control at the neonatal medulla oblongata

Balan, Kannan V.; Kc, Prabha; Hoxha, Zana; Mayer, Catherine; Wilson, Christopher G.; Martin, Richard J.

doi:10.1016/j.resp.2011.03.003

Cited by 78 publications

(50 citation statements)

References 45 publications

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“…A study in rat pups demonstrated that systemic exposure to lL-1β decreased respiratory activity in response to hypoxia while another study showed similar hypoxic respiratory depression in the context of intra-tracheal administration of LPS (Balan et al 2011; Olsson et al 2003). Maternal and fetal pro-inflammatory stimuli can also initiate signaling cascades through HIF-1α.…”

Section: Intersection Of Hypoxia and Hyperoxia With Systemic Inflammamentioning

confidence: 97%

Perinatal oxygen in the developing lung

Vogel

Britt

Trinidad

et al. 2015

Can. J. Physiol. Pharmacol.

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Lung diseases, such as bronchopulmonary dysplasia (BPD), wheezing, and asthma, remain significant causes of morbidity and mortality in the pediatric population, particularly in the setting of premature birth. Pulmonary outcomes in these infants are highly influenced by perinatal exposures including prenatal inflammation, postnatal intensive care unit interventions, and environmental agents. Here, there is strong evidence that perinatal supplemental oxygen administration has significant effects on pulmonary development and health. This is of particular importance in the preterm lung, where premature exposure to room air represents a hyperoxic insult that may cause harm to a lung primed to develop in a hypoxic environment. Preterm infants are also subject to increased episodes of hypoxia, which may also result in pulmonary damage and disease. Here, we summarize current understanding of the effects of oxygen on the developing lung and how low vs. high oxygen may predispose to pulmonary disease that may extend even into adulthood. Better understanding of the underlying mechanisms will help lead to improved care and outcomes in this vulnerable population.

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Section: Intersection Of Hypoxia and Hyperoxia With Systemic Inflammamentioning

confidence: 97%

Perinatal oxygen in the developing lung

Vogel

Britt

Trinidad

et al. 2015

Can. J. Physiol. Pharmacol.

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“…We have recently shown that rat pups exposed to intratracheal lipopolysaccharide demonstrate increased expression of mRNA for the proinflammatory cytokines IL-1 ␤ and IL-6 in the brainstem. This is associated with an attenuated ventilatory response to hypoxia, both before and after carotid sinus nerve transection [17] . This is consistent with prior data that endotoxemia impairs the ventilatory response to hypoxia in rat pups [18] , and that prostaglandin-mediated respiratory inhibition may be implicated [19] .…”

Section: Intermittent Hypoxia As a Proinflammatory Stressmentioning

confidence: 99%

Intermittent Hypoxic Episodes in Preterm Infants: Do They Matter?

et al. 2011

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Intermittent hypoxic episodes are typically a consequence of immature respiratory control and remain a troublesome challenge for the neonatologist. Furthermore, their frequency and magnitude are underestimated by clinically employed pulse oximeter settings. In extremely low birth weight infants the incidence of intermittent hypoxia progressively increases over the first 4 weeks of postnatal life, with a subsequent plateau followed by a slow decline beginning at weeks 6–8. Such episodic hypoxia/reoxygenation has the potential to sustain a proinflammatory cascade with resultant multisystem morbidity. This morbidity includes retinopathy of prematurity and impaired growth, as well as possible longer-term cardiorespiratory instability and poor neurodevelopmental outcome. Therapeutic approaches for intermittent hypoxic episodes comprise determination of optimal baseline saturation and careful titration of supplemental inspired oxygen, as well as xanthine therapy to prevent apnea of prematurity. In conclusion, characterization of the pathophysiologic basis for such intermittent hypoxic episodes and their consequences during early life is necessary to provide an evidence-based approach to their management.

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“…Since the capacity for LPS penetration across the BBB is low (Banks and Robinson, 2010), recent research has highlighted multiple alternative transmission mechanisms. Even low-dose LPS (intraperitoneal or intratracheal) is sufficient to induce inflammatory gene and protein expression in the CNS without significant levels of LPS crossing the BBB (Balan et al, 2011; Banks and Robinson, 2010; Laye et al, 1995). Vagal afferents moderate communication of low-level systemic inflammation to the CNS, since vagotomy eliminates the febrile response associated with sickness and inflammation after very low doses of LPS (1ug/kg), but not higher doses.…”

Section: Models Of Inflammationmentioning

confidence: 99%

The impact of inflammation on respiratory plasticity

Hocker

Stokes

Powell

et al. 2017

Experimental Neurology

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Breathing is a vital homeostatic behavior and must be precisely regulated throughout life. Clinical conditions commonly associated with inflammation, undermine respiratory function may involve plasticity in respiratory control circuits to compensate and maintain adequate ventilation. Alternatively, other clinical conditions may evoke maladaptive plasticity. Yet, we have only recently begun to understand the effects of inflammation on respiratory plasticity. Here we review some of common models used to investigate the effects of inflammation and discuss the impact of inflammation on nociception, chemosensory plasticity, medullary respiratory centers, motor plasticity in motor neurons and respiratory frequency, and adaptation to high altitude. We provide new data suggesting glial cells contribute to CNS inflammatory gene expression after 24 hours of sustained hypoxia and inflammation induced by 8 hours of intermittent hypoxia inhibits long-term facilitation of respiratory frequency. We also discuss how inflammation can have opposite effects on the capacity for plasticity, whereby it is necessary for increases in the hypoxic ventilatory response with sustained hypoxia but inhibits phrenic long term facilitation after intermittent hypoxia. This review highlights gaps in our knowledge about the effects of inflammation on respiratory control (development, age, and sex differences). In summary, data to date suggest plasticity can be either adaptive or maladaptive and understanding how inflammation alters the respiratory system is crucial for development of better therapeutic interventions to promote breathing and for utilization of plasticity as a clinical treatment.

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Vagal afferents modulate cytokine-mediated respiratory control at the neonatal medulla oblongata

Cited by 78 publications

References 45 publications

Perinatal oxygen in the developing lung

Perinatal oxygen in the developing lung

Intermittent Hypoxic Episodes in Preterm Infants: Do They Matter?

The impact of inflammation on respiratory plasticity

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