Abstract
Neonatal inflammation is common and has lasting consequences for adult health. We investigated the lasting effects of a single bout of neonatal inflammation on adult respiratory control in the form of respiratory motor plasticity induced by acute intermittent hypoxia, which likely compensates and stabilizes breathing during injury or disease and has significant therapeutic potential. Lipopolysaccharide-induced inflammation at postnatal day four induced lasting impairments in two distinct pathways to adult respiratory plasticity in male and female rats. Despite a lack of adult pro-inflammatory gene expression or alterations in glial morphology, one mechanistic pathway to plasticity was restored by acute, adult anti-inflammatory treatment, suggesting ongoing inflammatory signaling after neonatal inflammation. An alternative pathway to plasticity was not restored by anti-inflammatory treatment, but was evoked by exogenous adenosine receptor agonism, suggesting upstream impairment, likely astrocytic-dependent. Thus, the respiratory control network is vulnerable to early-life inflammation, limiting respiratory compensation to adult disease or injury.
Highlights
At birth, neonates transition from a sterile maternal environment into an environment filled with pathogens, microbes, and toxins and must simultaneously begin robust, rhythmic breathing
Because the lasting impairment of Q-pathway-evoked Phrenic long-term facilitation (pLTF) was inflammation-dependent, we examined whether neonatal inflammation had lasting effects on adult neuroinflammation in regions involved in respiratory neural control and motor plasticity
We investigated the longterm consequences of neonatal systemic inflammation on adult respiratory motor plasticity, a key feature of the neural control of breathing providing adaptability to respiratory system challenges (Mitchell and Johnson, 2003)
Summary
Neonates transition from a sterile maternal environment into an environment filled with pathogens, microbes, and toxins and must simultaneously begin robust, rhythmic breathing. Inflammation appears to augment respiratory dysfunction in neonates, whereby inflammation depresses hypoxic responses (Olsson et al, 2003; Rourke et al, 2016) and induces recurrent apneas (Hofstetter et al, 2007). Despite the prevalence of early life inflammation, little is known about the long-lasting consequences of neonatal inflammation on adult neurorespiratory control. We are beginning to understand the potential for long-term consequences of early life inflammation in other physiological systems. We know very little about the long-term effects of neonatal inflammation on adult neurorespiratory control
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