Effect of intracerebroventricular injection of interleukin-1-beta on the ventilatory response to hyperoxic hypercapnia.

Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia.
European journal of medical research (Impact Factor: 1.5). 11/2010; 15 Suppl 2:3-6.
Source: PubMed


Oxidative stress developed at several disease states and strenuous resistive breathing lead to the elevation of plasma and cerebral levels of proinflammatory cytokines. We hypothesized that the elevation of the cytokine level in body fluids would modulate breathing pattern and the ventilatory response to stimulation of central chemoreceptors by hypercapnia. -
In experiments on anesthetized, tracheostomized, spontaneously breathing rats, the effects of intracerebroventricular injection of the human recombinant interleukin-1β (IL-1β) (0.5 μg/rat) on breathing were studied. -
During resting breathing IL-1β evoked a significant increase in minute ventilation and in mean inspiratory flow. Furthermore, injection of IL-1β into the cerebral-spinal fluid decreases the responses of ventilation, tidal volume, and of mean inspiratory flow to carbon dioxide. -
The elevation of a proinflammatory cytokine in cerebrospinal fluid intensifies ventilation by modulation of breathing pattern, but weakens the chemoreflex sensitivity to hypercapnia. The results suggest the participation of cytokines in the central control of breathing and in the mechanisms of central chemoreception.

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    • "At the same time little is known about the cytokine effects on the central control of visceral functions, including the respiratory function. Our previous study has demonstrated that the inflammatory cytokine IL-1␤ participates in the control of basal breathing pattern and affects the central chemoreflex sensitivity to carbon dioxide (Aleksandrova and Danilova, 2010). The current study was undertaken to elucidate the mechanism underlying the impact of IL-1␤ on the ventilatory hypercapnic response and the basal level of ventilation. "
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    ABSTRACT: At the present time very little is known about interactions between the systemic inflammatory and ventilatory control. Our previous study has demonstrated that the elevation of the major inflammatory cytokines interleukin-1β (IL-1β) in the cerebrospinal fluid (CSF) may affect the control of ventilation. The aim of the current study was to compare the respiratory effects of IL-1β before and after pretreatment with diclofenac, a nonspecific cyclooxygenase (COX) inhibitor. Using the method of rebreathing with hyperoxic gas mixture we demonstrate that the slope of the ventilatory response to carbon dioxide decreased almost twofold from 5.6±0.52 to 2.5±0.28 ml·min(-1)·mmHg(-1) (p< 0.01) 40min after cerebroventricular administration of IL-1β. In contrast, the basal level of lung ventilation increased after the elevation of IL-1β in CSF. Diclofenac pretreatment eliminated these respiratory effects of IL-1β. The data indicate that the ability of IL-1β to enhance basal ventilation and to reduce the ventilatory hypercapnic response is mediated by the COX pathway. Copyright © 2014. Published by Elsevier B.V.
    Respiratory Physiology & Neurobiology 12/2014; 209. DOI:10.1016/j.resp.2014.12.006 · 1.97 Impact Factor
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    ABSTRACT: This review summarizes and analyzes the results of the present experimental studies indicating immune system involvement in control of breathing. The hypothesis about the role of cytokines in the mechanisms of respiratory muscle fatigue and reduced ventilatory sensitivity to hypercapnia during respiration with the added resistive loading is justified. The possible ways of implementing of respiratory cytokine effects are discussed.
    Fiziologiia cheloveka 03/2012; 38(2):119-29. DOI:10.1134/S0362119712020028

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