Critical role of p38 mitogen-activated protein kinase signaling in septic lung injury.

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Asaduzzaman, Muhammad (author)

Critical role of p38 mitogen-activated protein kinase signaling in septic lung injury.

Article/chapterEnglish2008

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2008

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LIBRIS-ID:oai:lup.lub.lu.se:e0d0b744-ca9b-4571-8237-dd41dffeece4
https://lup.lub.lu.se/record/1035102URI
https://doi.org/10.1097/01.CCM.0B013E31816204FADOI

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Language:English
Summary in:English

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Subject category:ref swepub-contenttype

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OBJECTIVE: Leukocyte-mediated tissue damage is a key feature in septic lung injury, although the signaling mechanisms behind pulmonary recruitment of leukocytes remain elusive. The aim of the present study was to define the role of p38 mitogen-activated protein kinase (MAPK) signaling in septic lung injury. DESIGN: Prospective experimental study. SETTING: University hospital research unit. SUBJECTS: Male C57BL/6 mice. INTERVENTIONS: Pulmonary edema, bronchoalveolar infiltration of leukocytes, levels of myeloperoxidase, and CXC chemokines were determined 6 and 24 hrs after cecal ligation and puncture (CLP). The specific p38 MAPK inhibitors SB 239063 and SKF 86002 were given immediately before CLP induction. Phosphorylation and activity of p38 MAPK were determined by immunoprecipitation and Western blot. MEASUREMENTS AND MAIN RESULTS: CLP induced clear-cut pulmonary damage characterized by edema formation, leukocyte infiltration, and increased levels of CXC chemokines in the lung. Moreover, CLP increased phosphorylation and activity of p38 MAPK in the lung, which was markedly inhibited by SB 239063. Interestingly, inhibition of p38 MAPK signaling protected against CLP-induced lung damage and edema. Indeed, both SB 239063 and SKF 86002 decreased CLP-induced leukocyte recruitment in the bronchoalveolar space and formation of CXC chemokines in the lung. CONCLUSIONS: Our data demonstrate that p38 MAPK signaling constitutes a key role in regulating CXC chemokine production in septic lung injury and that inhibition of p38 MAPK activity abolishes pulmonary infiltration of leukocytes as well as lung edema. These novel findings suggest that targeting the p38 MAPK signaling pathway may pave the way for a new therapeutic strategy against lung injury in polymicrobial sepsis.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Anestesi och intensivvård hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Anesthesiology and Intensive Care hsv//eng
Animals Chemokines
CXC/metabolism* Chemotaxis
Leukocyte/physiology* Disease Models
Animal Male Mice Mice
Inbred C57BL Phosphorylation Pulmonary Edema/etiology* Pulmonary Edema/metabolism Pulmonary Edema/pathology Sepsis/complications* Sepsis/metabolism Sepsis/pathology Signal Transduction/physiology* p38 Mitogen-Activated Protein Kinases/physiology*

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Wang, YushengLund University,Lunds universitet,Kirurgi,Forskargrupper vid Lunds universitet,Surgery,Lund University Research Groups(Swepub:lu)yu4833wa (author)
Thorlacius, HenrikLund University,Lunds universitet,Kirurgi,Forskargrupper vid Lunds universitet,Surgery,Lund University Research Groups(Swepub:lu)kir-hth (author)
KirurgiForskargrupper vid Lunds universitet (creator_code:org_t)

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In:Critical Care Medicine36:2, s. 482-4881530-0293

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