The Effects of Interleukin-1β in Tumor Necrosis Factor-α-Induced Acute Pulmonary Inflammation in Mice
We determined the role of interleukin-1β (IL-1β) signaling on tumor necrosis factor alpha-induced (TNF-α) lung neutrophil influx as well as neutrophil chemoattractant macrophage inflammatory protein (MIP-2) and KC and soluble TNF-α receptor (TNFR) levels utilizing wildtype (WT), TNF receptor double...
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| Format: | Article |
| Language: | English |
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Wiley
2009-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2009/958658 |
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| _version_ | 1849692144741122048 |
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| author | Sara Saperstein Heidie Huyck Elizabeth Kimball Carl Johnston Jacob Finkelstein Gloria Pryhuber |
| author_facet | Sara Saperstein Heidie Huyck Elizabeth Kimball Carl Johnston Jacob Finkelstein Gloria Pryhuber |
| author_sort | Sara Saperstein |
| collection | DOAJ |
| description | We determined the role of interleukin-1β (IL-1β) signaling on tumor necrosis factor alpha-induced (TNF-α) lung neutrophil influx as well as neutrophil chemoattractant macrophage inflammatory protein (MIP-2) and KC and soluble TNF-α receptor (TNFR) levels utilizing wildtype (WT), TNF receptor double knockout (TNFR1/TNFR2 KO), and IL-1β KO mice after oropharyngeal instillation with TNF-α. A significant increase in neutrophil accumulation in bronchoalveolar lavage fluid (BALF) and lung interstitium was detected in the WT mice six hours after TNF-α exposure. This correlated with an increase in BALF MIP-2. In contrast, BALF neutrophil numbers were not increased by TNF-α treatment of IL-1β KOs, correlating with a failure to induce BALF MIP-2 and a trend toward increased BALF soluble TNFR1. TNF-α-instillation increased lavage and serum KC and soluble TNFR2 irrespective of IL-1β expression. These results suggest IL-1β contributes, in part, to TNF-α-mediated, chemokine release, and neutrophil recruitment to the lung, potentially associated with altered soluble TNFR1 release into the BALF. |
| format | Article |
| id | doaj-art-b15ac71eb08d484f930d9391bfb2f0a4 |
| institution | DOAJ |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2009-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-b15ac71eb08d484f930d9391bfb2f0a42025-08-20T03:20:47ZengWileyMediators of Inflammation0962-93511466-18612009-01-01200910.1155/2009/958658958658The Effects of Interleukin-1β in Tumor Necrosis Factor-α-Induced Acute Pulmonary Inflammation in MiceSara Saperstein0Heidie Huyck1Elizabeth Kimball2Carl Johnston3Jacob Finkelstein4Gloria Pryhuber5Department of Environmental Medicine, University of Rochester School of Medicine, 601 Elmwood Avenue Box 850, Rochester, NY 14642, USADepartment of Pediatrics, University of Rochester School of Medicine, 601 Elmwood Avenue Box 850, Rochester, NY 14642, USADepartment of Pediatrics, University of Rochester School of Medicine, 601 Elmwood Avenue Box 850, Rochester, NY 14642, USADepartment of Environmental Medicine, University of Rochester School of Medicine, 601 Elmwood Avenue Box 850, Rochester, NY 14642, USADepartment of Environmental Medicine, University of Rochester School of Medicine, 601 Elmwood Avenue Box 850, Rochester, NY 14642, USADepartment of Environmental Medicine, University of Rochester School of Medicine, 601 Elmwood Avenue Box 850, Rochester, NY 14642, USAWe determined the role of interleukin-1β (IL-1β) signaling on tumor necrosis factor alpha-induced (TNF-α) lung neutrophil influx as well as neutrophil chemoattractant macrophage inflammatory protein (MIP-2) and KC and soluble TNF-α receptor (TNFR) levels utilizing wildtype (WT), TNF receptor double knockout (TNFR1/TNFR2 KO), and IL-1β KO mice after oropharyngeal instillation with TNF-α. A significant increase in neutrophil accumulation in bronchoalveolar lavage fluid (BALF) and lung interstitium was detected in the WT mice six hours after TNF-α exposure. This correlated with an increase in BALF MIP-2. In contrast, BALF neutrophil numbers were not increased by TNF-α treatment of IL-1β KOs, correlating with a failure to induce BALF MIP-2 and a trend toward increased BALF soluble TNFR1. TNF-α-instillation increased lavage and serum KC and soluble TNFR2 irrespective of IL-1β expression. These results suggest IL-1β contributes, in part, to TNF-α-mediated, chemokine release, and neutrophil recruitment to the lung, potentially associated with altered soluble TNFR1 release into the BALF.http://dx.doi.org/10.1155/2009/958658 |
| spellingShingle | Sara Saperstein Heidie Huyck Elizabeth Kimball Carl Johnston Jacob Finkelstein Gloria Pryhuber The Effects of Interleukin-1β in Tumor Necrosis Factor-α-Induced Acute Pulmonary Inflammation in Mice Mediators of Inflammation |
| title | The Effects of Interleukin-1β in Tumor Necrosis Factor-α-Induced Acute Pulmonary Inflammation in Mice |
| title_full | The Effects of Interleukin-1β in Tumor Necrosis Factor-α-Induced Acute Pulmonary Inflammation in Mice |
| title_fullStr | The Effects of Interleukin-1β in Tumor Necrosis Factor-α-Induced Acute Pulmonary Inflammation in Mice |
| title_full_unstemmed | The Effects of Interleukin-1β in Tumor Necrosis Factor-α-Induced Acute Pulmonary Inflammation in Mice |
| title_short | The Effects of Interleukin-1β in Tumor Necrosis Factor-α-Induced Acute Pulmonary Inflammation in Mice |
| title_sort | effects of interleukin 1β in tumor necrosis factor α induced acute pulmonary inflammation in mice |
| url | http://dx.doi.org/10.1155/2009/958658 |
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