{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T07:33:29Z","timestamp":1780472009802,"version":"3.54.1"},"reference-count":48,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100005834","name":"Francis Family Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005834","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2018,8,1]]},"abstract":"<jats:p>Inflammation undermines respiratory motor plasticity, yet we are just beginning to understand the inflammatory signaling involved. Because interleukin-1 (IL-1) signaling promotes or inhibits plasticity in other central nervous system regions, we tested the following hypotheses: 1) IL-1 receptor (IL-1R) activation after systemic inflammation is necessary to undermine phrenic long-term facilitation (pLTF), a model of respiratory motor plasticity induced by acute intermittent hypoxia (AIH), and 2) spinal IL-1\u03b2 is sufficient to undermine pLTF. pLTF is significantly reduced 24 h after lipopolysaccharide (LPS; 100 \u03bcg\/kg ip, 12\u2009\u00b1\u200918%, n = 5) compared with control (57\u2009\u00b1\u200925%, n = 6) and restored by peripheral IL-1R antagonism (63\u2009\u00b1\u200913%, n = 5, AF-12198, 0.5 mg\/kg ip, 24 h). Furthermore, acute, spinal IL-1R antagonism (1 mM AF-12198, 15 \u03bcl it) restored pLTF (53\u2009\u00b1\u200915%, n = 4) compared with LPS-treated rats (11\u2009\u00b1\u200910%; n = 5), demonstrating IL-1R activation is necessary to undermine pLTF after systemic inflammation. However, in healthy animals, pLTF persisted after spinal, exogenous recombinant rat IL-1\u03b2 (rIL-1\u03b2) (1 ng\u2009\u00b1\u2009AIH; 66\u2009\u00b1\u200926%, n = 3, 10 ng\u2009\u00b1\u2009AIH; 102\u2009\u00b1\u200949%, n = 4, 100 ng + AIH; 93\u2009\u00b1\u200951%, n = 3, 300 ng\u2009\u00b1\u2009AIH; 37\u2009\u00b1\u200940%, n = 3; P &lt; 0.05 from baseline). In the absence of AIH, spinal rIL-1\u03b2 induced progressive, dose-dependent phrenic amplitude facilitation (1 ng; \u22123\u2009\u00b1\u20095%, n = 3, 10 ng; 8\u2009\u00b1\u200922%, n = 3, 100 ng; 31\u2009\u00b1\u200912%, P &lt; 0.05, n = 4, 300 ng; 51\u2009\u00b1\u200917%, P &lt; 0.01 from baseline, n = 4). In sum, IL-1R activation, both systemically and spinally, undermines pLTF after LPS-induced systemic inflammation, but IL-1R activation is not sufficient to abolish plasticity. Understanding the inflammatory signaling inhibiting respiratory plasticity is crucial to developing treatment strategies utilizing respiratory plasticity to promote breathing during ventilatory control disorders.<\/jats:p><jats:p>NEW &amp; NOTEWORTHY This study gives novel insights concerning mechanisms by which systemic inflammation undermines respiratory motor plasticity. We demonstrate that interleukin-1 signaling, both peripherally and centrally, undermines respiratory motor plasticity. However, acute, exogenous interleukin-1 signaling is not sufficient to undermine respiratory motor plasticity.<\/jats:p>","DOI":"10.1152\/japplphysiol.01051.2017","type":"journal-article","created":{"date-parts":[[2018,3,22]],"date-time":"2018-03-22T17:29:43Z","timestamp":1521739783000},"page":"504-512","source":"Crossref","is-referenced-by-count":15,"title":["IL-1 receptor activation undermines respiratory motor plasticity after systemic inflammation"],"prefix":"10.1152","volume":"125","author":[{"given":"Austin D.","family":"Hocker","sequence":"first","affiliation":[{"name":"Department of Human Physiology, University of Oregon, Eugene, Oregon"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adrianne G.","family":"Huxtable","sequence":"additional","affiliation":[{"name":"Department of Human Physiology, University of Oregon, Eugene, 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