Inhalative IL-10 Attenuates Pulmonary Inflammation following Hemorrhagic Shock without Major Alterations of the Systemic Inflammatory Response

Several studies report immunomodulatory effects of endogenous IL-10 after trauma. The present study investigates the effect of inhalative IL-10 administration on systemic and pulmonary inflammation in hemorrhagic shock. Male C57/BL6 mice (8 animals per group) were subjected to pressure-controlled h...

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Main Authors: Philipp Kobbe, Philipp Lichte, Helen Schreiber, Lucy Kathleen Reiss, Stefan Uhlig, Hans-Christoph Pape, Roman Pfeifer
Format: Article
Language:English
Published: Hindawi Limited 2012-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2012/512974
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spelling doaj-f0d893f5410d4c0592905573c3857c3b2020-11-24T23:29:03ZengHindawi LimitedMediators of Inflammation0962-93511466-18612012-01-01201210.1155/2012/512974512974Inhalative IL-10 Attenuates Pulmonary Inflammation following Hemorrhagic Shock without Major Alterations of the Systemic Inflammatory ResponsePhilipp Kobbe0Philipp Lichte1Helen Schreiber2Lucy Kathleen Reiss3Stefan Uhlig4Hans-Christoph Pape5Roman Pfeifer6Department of Orthopaedic Trauma Surgery, Faculty of Medicine, RWTH Aachen University, Pauwelsstraβe 30, 52074 Aachen, GermanyDepartment of Orthopaedic Trauma Surgery, Faculty of Medicine, RWTH Aachen University, Pauwelsstraβe 30, 52074 Aachen, GermanyDepartment of Orthopaedic Trauma Surgery, Faculty of Medicine, RWTH Aachen University, Pauwelsstraβe 30, 52074 Aachen, GermanyInstitute of Pharmacology and Toxicology, Faculty of Medicine, RWTH Aachen University, Pauwelsstraβe 30, 52074 Aachen, GermanyInstitute of Pharmacology and Toxicology, Faculty of Medicine, RWTH Aachen University, Pauwelsstraβe 30, 52074 Aachen, GermanyDepartment of Orthopaedic Trauma Surgery, Faculty of Medicine, RWTH Aachen University, Pauwelsstraβe 30, 52074 Aachen, GermanyDepartment of Orthopaedic Trauma Surgery, Faculty of Medicine, RWTH Aachen University, Pauwelsstraβe 30, 52074 Aachen, GermanySeveral studies report immunomodulatory effects of endogenous IL-10 after trauma. The present study investigates the effect of inhalative IL-10 administration on systemic and pulmonary inflammation in hemorrhagic shock. Male C57/BL6 mice (8 animals per group) were subjected to pressure-controlled hemorrhagic shock for 1.5 hrs followed by resuscitation and inhalative administration of either 50 μL PBS (Shock group) or 50 μg/kg recombinant mouse IL-10 dissolved in 50 μL PBS (Shock + IL-10 group). Animals were sacrificed after 4.5 hrs of recovery and serum IL-6, IL-10, KC, and MCP-1 concentrations were measured with ELISA kits. Acute pulmonary inflammation was assessed by pulmonary myeloperoxidase (MPO) activity and pulmonary H&E histopathology. Inhalative IL-10 administration decreased pulmonary inflammation without altering the systemic concentrations of IL-6, IL-10, and KC. Serum MCP-1 levels were significantly reduced following inhalative IL-10 administration. These findings suggest that inhalative IL-10 administration may modulate the pulmonary microenvironment without major alterations of the systemic inflammatory response, thus minimizing the potential susceptibility to infection and sepsis.http://dx.doi.org/10.1155/2012/512974
collection DOAJ
language English
format Article
sources DOAJ
author Philipp Kobbe
Philipp Lichte
Helen Schreiber
Lucy Kathleen Reiss
Stefan Uhlig
Hans-Christoph Pape
Roman Pfeifer
spellingShingle Philipp Kobbe
Philipp Lichte
Helen Schreiber
Lucy Kathleen Reiss
Stefan Uhlig
Hans-Christoph Pape
Roman Pfeifer
Inhalative IL-10 Attenuates Pulmonary Inflammation following Hemorrhagic Shock without Major Alterations of the Systemic Inflammatory Response
Mediators of Inflammation
author_facet Philipp Kobbe
Philipp Lichte
Helen Schreiber
Lucy Kathleen Reiss
Stefan Uhlig
Hans-Christoph Pape
Roman Pfeifer
author_sort Philipp Kobbe
title Inhalative IL-10 Attenuates Pulmonary Inflammation following Hemorrhagic Shock without Major Alterations of the Systemic Inflammatory Response
title_short Inhalative IL-10 Attenuates Pulmonary Inflammation following Hemorrhagic Shock without Major Alterations of the Systemic Inflammatory Response
title_full Inhalative IL-10 Attenuates Pulmonary Inflammation following Hemorrhagic Shock without Major Alterations of the Systemic Inflammatory Response
title_fullStr Inhalative IL-10 Attenuates Pulmonary Inflammation following Hemorrhagic Shock without Major Alterations of the Systemic Inflammatory Response
title_full_unstemmed Inhalative IL-10 Attenuates Pulmonary Inflammation following Hemorrhagic Shock without Major Alterations of the Systemic Inflammatory Response
title_sort inhalative il-10 attenuates pulmonary inflammation following hemorrhagic shock without major alterations of the systemic inflammatory response
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 2012-01-01
description Several studies report immunomodulatory effects of endogenous IL-10 after trauma. The present study investigates the effect of inhalative IL-10 administration on systemic and pulmonary inflammation in hemorrhagic shock. Male C57/BL6 mice (8 animals per group) were subjected to pressure-controlled hemorrhagic shock for 1.5 hrs followed by resuscitation and inhalative administration of either 50 μL PBS (Shock group) or 50 μg/kg recombinant mouse IL-10 dissolved in 50 μL PBS (Shock + IL-10 group). Animals were sacrificed after 4.5 hrs of recovery and serum IL-6, IL-10, KC, and MCP-1 concentrations were measured with ELISA kits. Acute pulmonary inflammation was assessed by pulmonary myeloperoxidase (MPO) activity and pulmonary H&E histopathology. Inhalative IL-10 administration decreased pulmonary inflammation without altering the systemic concentrations of IL-6, IL-10, and KC. Serum MCP-1 levels were significantly reduced following inhalative IL-10 administration. These findings suggest that inhalative IL-10 administration may modulate the pulmonary microenvironment without major alterations of the systemic inflammatory response, thus minimizing the potential susceptibility to infection and sepsis.
url http://dx.doi.org/10.1155/2012/512974
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