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Endogenous IL-17 as...
Endogenous IL-17 as a mediator of neutrophil recruitment caused by endotoxin exposure in mouse airways
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Miyamoto, M. (author)
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Prause, O. (author)
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- Sjöstrand, Margareta, 1947 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för lungmedicin och allergologi,Institute of Internal Medicine, Dept of Respiratory Medicine/Allergology
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Laan, Martti, 1971 (author)
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- Lötvall, Jan, 1956 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för lungmedicin och allergologi,Institute of Internal Medicine, Dept of Respiratory Medicine/Allergology
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- Lindén, Anders, 1961 (author)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för lungmedicin och allergologi,Institute of Internal Medicine, Dept of Respiratory Medicine/Allergology
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(creator_code:org_t)
- 2003
- 2003
- English.
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In: Journal of immunology (Baltimore, Md.. - 0022-1767. ; 170:9, s. 4665-72
- Related links:
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https://gup.ub.gu.se...
Abstract
Subject headings
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- We have previously demonstrated that administration of the recently described cytokine IL-17 in rat airways in vivo recruits and activates neutrophils locally. In the current study, we examined whether endogenous IL-17 is involved in mediating neutrophil recruitment caused by endotoxin exposure in mouse airways. Our in vivo data show that local endotoxin exposure causes the release of free, soluble IL-17 protein 6 h later. Systemic pretreatment with a neutralizing anti-IL-17 Ab almost completely inhibits neutrophil recruitment 24 h, but not 6 h, after endotoxin exposure in the airways. Pretreatment with neutralizing anti-IL-6 and anti-macrophage inflammatory protein (MIP)-2 Abs inhibits neutrophil recruitment caused by local endotoxin exposure and IL-17, respectively. Our in vitro data show that endotoxin exposure stimulates the release of soluble IL-17 protein in T lymphocytes harvested from lung and spleen, respectively, and that this cytokine release requires coculture with airway macrophages. Intracellular IL-17 protein is detected in T lymphocytes from spleen but not in airway macrophages after coculture and stimulation of these two cell types. Finally, anti-IL-17 does not alter endotoxin-induced release of IL-6 and MIP-2 from T lymphocytes and airway macrophages in coculture. In conclusion, our results indicate that endotoxin exposure causes the release of IL-17 from T lymphocytes and that this cytokine release requires the presence of macrophages. Once released, endogenous IL-17 acts in part by inducing local release of neutrophil-mobilizing cytokines such as IL-6 and MIP-2, from nonlymphocyte, nonmacrophage cells, and this contributes to recruitment of neutrophils in the airways. These IL-17-related mechanisms constitute potential targets for pharmacotherapy against exaggerated neutrophil recruitment in airway disease.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Dermatologi och venereologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Dermatology and Venereal Diseases (hsv//eng)
Keyword
- Administration
- Intranasal
- Animals
- Antibodies
- Monoclonal/administration & dosage
- Bronchoalveolar Lavage Fluid/cytology/immunology
- Dose-Response Relationship
- Immunologic
- Inflammation/blood/immunology
- inhibitors/immunology/*physiology
- Injections
- Intraperitoneal
- Interleukin-17/analysis/antagonists & inhibitors/immunology/*physiology
- Interleukin-6/antagonists & inhibitors/metabolism/secretion
- Lipopolysaccharides/*administration & dosage
- Lung/*immunology/pathology
- Male
- Mice
- Mice
- Inbred C57BL
- Monokines/antagonists & inhibitors/metabolism/secretion
- Neutrophil Infiltration/*immunology
- Neutrophils/immunology/metabolism/pathology/secretion
- Solubility
- T-Lymphocytes/immunology/metabolism
Publication and Content Type
- ref (subject category)
- art (subject category)
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