Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma
Identifieur interne : 003D06 ( PascalFrancis/Curation ); précédent : 003D05; suivant : 003D07Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma
Auteurs : Akram M. Zaaqoq [États-Unis] ; Rami Namas [États-Unis] ; Khalid Almahmoud [États-Unis] ; Nabil Azhar [États-Unis] ; QI MI [États-Unis] ; Ruben Zamora [États-Unis] ; David M. Brienza [États-Unis] ; Timothy R. Billiar [États-Unis] ; Yoram Vodovotz [États-Unis]Source :
- Critical care medicine [ 0090-3493 ] ; 2014.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
Abstract
Objective: Blunt trauma and traumatic spinal cord injury induce systemic inflammation that contributes to morbidity. Dysregulated neural control of systemic inflammation postinjury is likely exaggerated in patients with traumatic spinal cord injury. We used in silico methods to discern dynamic inflammatory networks that could distinguish systemic inflammation in traumatic spinal cord injury from blunt trauma. Design: Retrospective study. Settings: Tertiary care institution. Patients: Twenty-one severely injured thoracocervical traumatic spinal cord injury patients and matched 21 severely injured blunt trauma patients without spinal cord injury. Intervention: None. Measurements and Main Results: Serial blood samples were obtained from days 1 to 14 postinjury. Twenty-four plasma inflammatory mediators were quantified. Statistical significance between the two groups was determined by two-way analysis of variance. Dynamic Bayesian network inference was used to suggest dynamic connectivity and central inflammatory mediators. Circulating interleukin-10 was significantly elevated in thoracocervical traumatic spinal cord injury group versus non-spinal cord injury group, whereas interleukin-1β, soluble interleukin-2 receptor-α, interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1 a and 1β, granulocyte-macrophage colony-stimulating factor, and interferon-γ were significantly reduced in traumatic spinal cord injury group versus non-spinal cord injury group. Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal cord injury dynamic networks. In a separate validation cohorts of 356 patients without spinal cord injury and 85 traumatic spinal cord injury patients, individuals with plasma inducible protein-10 levels more than or equal to 730 pg/mL had significantly prolonged hospital and ICU stay and days on mechanical ventilator versus patients with plasma inducible protein-10 level less than 730 pg/mL. Conclusion: This is the first study to compare the dynamic systemic inflammatory responses of traumatic spinal cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible protein-10 in driving systemic interleukin-10 and morbidity and highlighting the potential utility of in silico tools to identify key inflammatory drivers.
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Inducible Protein-10, a Potential Driver of Neurally Controlled Interleukin-10 and Morbidity in Human Blunt Trauma</title>
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<author><name sortKey="Brienza, David M" sort="Brienza, David M" uniqKey="Brienza D" first="David M." last="Brienza">David M. Brienza</name>
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<author><name sortKey="Vodovotz, Yoram" sort="Vodovotz, Yoram" uniqKey="Vodovotz Y" first="Yoram" last="Vodovotz">Yoram Vodovotz</name>
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<series><title level="j" type="main">Critical care medicine</title>
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<term>Epidemiology</term>
<term>Hemorrhage</term>
<term>Human</term>
<term>Inflammation</term>
<term>Intensive care</term>
<term>Interleukin 10</term>
<term>Morbidity</term>
<term>Nervous system</term>
<term>Nervous system diseases</term>
<term>Protein A</term>
<term>Resuscitation</term>
<term>Spinal cord trauma</term>
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<term>Traumatisme de la moelle épinière</term>
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<term>Morbidité</term>
<term>Epidémiologie</term>
<term>Homme</term>
<term>Chimiokine</term>
<term>Inflammation</term>
<term>Système nerveux</term>
<term>Pathologie du système nerveux</term>
<term>Réanimation</term>
<term>Soin intensif</term>
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<front><div type="abstract" xml:lang="en">Objective: Blunt trauma and traumatic spinal cord injury induce systemic inflammation that contributes to morbidity. Dysregulated neural control of systemic inflammation postinjury is likely exaggerated in patients with traumatic spinal cord injury. We used in silico methods to discern dynamic inflammatory networks that could distinguish systemic inflammation in traumatic spinal cord injury from blunt trauma. Design: Retrospective study. Settings: Tertiary care institution. Patients: Twenty-one severely injured thoracocervical traumatic spinal cord injury patients and matched 21 severely injured blunt trauma patients without spinal cord injury. Intervention: None. Measurements and Main Results: Serial blood samples were obtained from days 1 to 14 postinjury. Twenty-four plasma inflammatory mediators were quantified. Statistical significance between the two groups was determined by two-way analysis of variance. Dynamic Bayesian network inference was used to suggest dynamic connectivity and central inflammatory mediators. Circulating interleukin-10 was significantly elevated in thoracocervical traumatic spinal cord injury group versus non-spinal cord injury group, whereas interleukin-1β, soluble interleukin-2 receptor-α, interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1 a and 1β, granulocyte-macrophage colony-stimulating factor, and interferon-γ were significantly reduced in traumatic spinal cord injury group versus non-spinal cord injury group. Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal cord injury dynamic networks. In a separate validation cohorts of 356 patients without spinal cord injury and 85 traumatic spinal cord injury patients, individuals with plasma inducible protein-10 levels more than or equal to 730 pg/mL had significantly prolonged hospital and ICU stay and days on mechanical ventilator versus patients with plasma inducible protein-10 level less than 730 pg/mL. Conclusion: This is the first study to compare the dynamic systemic inflammatory responses of traumatic spinal cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible protein-10 in driving systemic interleukin-10 and morbidity and highlighting the potential utility of in silico tools to identify key inflammatory drivers.</div>
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<fA11 i1="01" i2="1"><s1>ZAAQOQ (Akram M.)</s1>
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<fA11 i1="02" i2="1"><s1>NAMAS (Rami)</s1>
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<fA11 i1="03" i2="1"><s1>ALMAHMOUD (Khalid)</s1>
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<fA11 i1="04" i2="1"><s1>AZHAR (Nabil)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>QI MI</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>ZAMORA (Ruben)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>BRIENZA (David M.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>BILLIAR (Timothy R.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>VODOVOTZ (Yoram)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Critical Care Medicine, University of Pittsburgh</s1>
<s2>Pittsburgh, PA</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Surgery, University of Pittsburgh</s1>
<s2>Pittsburgh, PA</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Center for Inflammation and Regenerative Modeling, McGowan Institute for Regenerative Medicine, University of Pittsburgh</s1>
<s2>Pittsburgh, PA</s2>
<s3>USA</s3>
<sZ>2 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Sports Medicine and Nutrition, University of Pittsburgh</s1>
<s2>Pittsburgh, PA</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Rehabilitation Science and Technology, University of Pittsburgh</s1>
<s2>Pittsburgh, PA</s2>
<s3>USA</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Department of Bioengineering, University of Pittsburgh</s1>
<s2>Pittsburgh, PA</s2>
<s3>USA</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA20><s1>1487-1497</s1>
</fA20>
<fA21><s1>2014</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>17751</s2>
<s5>354000501831030210</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2014 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>42 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>14-0168428</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Critical care medicine</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Objective: Blunt trauma and traumatic spinal cord injury induce systemic inflammation that contributes to morbidity. Dysregulated neural control of systemic inflammation postinjury is likely exaggerated in patients with traumatic spinal cord injury. We used in silico methods to discern dynamic inflammatory networks that could distinguish systemic inflammation in traumatic spinal cord injury from blunt trauma. Design: Retrospective study. Settings: Tertiary care institution. Patients: Twenty-one severely injured thoracocervical traumatic spinal cord injury patients and matched 21 severely injured blunt trauma patients without spinal cord injury. Intervention: None. Measurements and Main Results: Serial blood samples were obtained from days 1 to 14 postinjury. Twenty-four plasma inflammatory mediators were quantified. Statistical significance between the two groups was determined by two-way analysis of variance. Dynamic Bayesian network inference was used to suggest dynamic connectivity and central inflammatory mediators. Circulating interleukin-10 was significantly elevated in thoracocervical traumatic spinal cord injury group versus non-spinal cord injury group, whereas interleukin-1β, soluble interleukin-2 receptor-α, interleukin-4, interleukin-5, interleukin-7, interleukin-13, interleukin-17, macrophage inflammatory protein 1 a and 1β, granulocyte-macrophage colony-stimulating factor, and interferon-γ were significantly reduced in traumatic spinal cord injury group versus non-spinal cord injury group. Dynamic Bayesian network suggested that post-spinal cord injury interleukin-10 is driven by inducible protein-10, whereas monocyte chemotactic protein-1 was central in non-spinal cord injury dynamic networks. In a separate validation cohorts of 356 patients without spinal cord injury and 85 traumatic spinal cord injury patients, individuals with plasma inducible protein-10 levels more than or equal to 730 pg/mL had significantly prolonged hospital and ICU stay and days on mechanical ventilator versus patients with plasma inducible protein-10 level less than 730 pg/mL. Conclusion: This is the first study to compare the dynamic systemic inflammatory responses of traumatic spinal cord injury patients versus patients without spinal cord injury, suggesting a key role for inducible protein-10 in driving systemic interleukin-10 and morbidity and highlighting the potential utility of in silico tools to identify key inflammatory drivers.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B27B</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17A07</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Hémorragie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Hemorrhage</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Hemorragia</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Traumatisme de la moelle épinière</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Spinal cord trauma</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Traumatismo de médula espinal</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Protéine A</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Protein A</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Proteína A</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Interleukine 10</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Interleukin 10</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Interleuquina 10</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Morbidité</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Morbidity</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Morbilidad</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Epidémiologie</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Epidemiology</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Epidemiología</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Homme</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Human</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Hombre</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Chimiokine</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Chemokine</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Quimioquina</s0>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Inflammation</s0>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Inflammation</s0>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Inflamación</s0>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Système nerveux</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Nervous system</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Sistema nervioso</s0>
<s5>16</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Réanimation</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Resuscitation</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Reanimación</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Soin intensif</s0>
<s5>19</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Intensive care</s0>
<s5>19</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Cuidado intensivo</s0>
<s5>19</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Cytokine</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cytokine</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Citoquina</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Pathologie de la moelle épinière</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Spinal cord disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Médula espinal patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>39</s5>
</fC07>
<fN21><s1>209</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>
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