Abstract
Neuroinflammation is produced by local or systemic alterations and mediated mainly
by glia, affecting the activity of various neural circuits including those involved
in breathing rhythm generation and control. Several pathological conditions, such
as sudden infant death syndrome, obstructive sleep apnea and asthma exert an inflammatory
influence on breathing-related circuits. Consequently breathing (both resting and
ventilatory responses to physiological challenges), is affected; e.g., responses to
hypoxia and hypercapnia are compromised. Moreover, inflammation can induce long-lasting
changes in breathing and affect adaptive plasticity; e.g., hypoxic acclimatization
or long-term facilitation. Mediators of the influences of inflammation on breathing
are most likely proinflammatory molecules such as cytokines and prostaglandins. The
focus of this review is to summarize the available information concerning the modulation
of the breathing function by inflammation and the cellular and molecular aspects of
this process. I will consider: 1) some clinical and experimental conditions in which
inflammation influences breathing; 2) the variety of experimental approaches used
to understand this inflammatory modulation; 3) the likely cellular and molecular mechanisms.
Abbreviations:
DTP (diphtheria/tetanus/whole-cell pertussis), EP3 (E-prostanoid receptor subtype 3), HIF-1α (hypoxia-inducible factor 1-alpha), iNOS (inducible NO synthase), IgG (immunoglobulin M), IgM (immunoglobulin M), IL-1β (interleukin-1 beta), IL-6 (interleukin-6), ICV (intracerebroventricular), LPS (lipopolysaccharide), LTF (long-term facilitation), L-NAME (N(G)-nitro-l-arginine methyl ester), NADPH (nicotinamide adenine dinucleotide phosphate), NSAID (nonsteroidal anti-inflammatory drug), NF-kB (nuclear factor kappa B), nTS (nucleus of the solitary tract), OSA (obstructive sleep apnea), Pico (post-inspiratory complex), preBötC (preBötzinger complex), PGE2 (prostaglandin E2), PGE-M (prostaglandin E metabolite), ROS (reactive oxygen species), RSV (respiratory syncytial virus), RTN/pFN (retrotrapezoid nucleus/parafacial nucleus), RVLM (rostral ventrolateral medulla), SIDS (sudden infant death syndrome), TRIF (TIR domain containing adaptor inducing interferon-beta protein), TLR (Toll-like receptor), TNFα (tumor necrosis factor alpha)To read this article in full you will need to make a payment
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Article info
Publication history
Published online: November 11, 2018
Accepted:
November 7,
2018
Received in revised form:
November 6,
2018
Received:
June 26,
2018
Identification
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© 2018 Elsevier B.V. All rights reserved.
