Role of interleukin-1 and tumour necrosis factor in leukocyte recruitment to acute dermal inflammation
The cytokines IL-1 and TNF-α are involved in inflammation and their production is stimulated by various agents, especially endotoxin (LPS). Here, using the human IL-1 receptor antagonist (IL-1RA) and a new monoclonal antibody (mAb 7F11) to rabbit TNF, the role of endogenous IL-l and TNF production i...
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| Format: | Article |
| Language: | English |
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Wiley
1992-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/S0962935192000528 |
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| _version_ | 1850166185752002560 |
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| author | Andrew C. Issekutz Nancy Lopes Thomas B. Issekutz |
| author_facet | Andrew C. Issekutz Nancy Lopes Thomas B. Issekutz |
| author_sort | Andrew C. Issekutz |
| collection | DOAJ |
| description | The cytokines IL-1 and TNF-α are involved in inflammation and their production is stimulated by various agents, especially endotoxin (LPS). Here, using the human IL-1 receptor antagonist (IL-1RA) and a new monoclonal antibody (mAb 7F11) to rabbit TNF, the role of endogenous IL-l and TNF production in acute (3h) leukocyte (PMNL) recruitment to dermal inflammation in rabbits has been studied. IL-1RA inhibited by 27% the PMNL accumulation in reactions induced by killed Escherichia coli (p < 0.05) but not by LPS. The monoclonal antibody to TNF inhibited by 27% and 38% (p < 0.002) the PMNL accumulation in LPS and E. coli reactions respectively, but a combination of the mAb with IL-1RA was not more effective. Treatment of human umbilical vein endothelium with LPS for 3 h activated endothelium to induce PMNL transendothelial migration in vitro, which was not inhibited by IL-1RA, antibody to TNF-α, IL-1 or to IL-8. In conclusion, TNF and IL-1 may partially mediate acute PMNL infiltration in vivo to LPS and Gram negative bacteria, but there is a major IL-1/TNF independent mechanism, at least in dermal inflammation, which may be due to direct LPS activation of the microvasculature or perhaps the generation of cytokines other than IL-1 and TNF. |
| format | Article |
| id | doaj-art-dd504e70841145ea910d933bcdb43aab |
| institution | OA Journals |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 1992-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-dd504e70841145ea910d933bcdb43aab2025-08-20T02:21:30ZengWileyMediators of Inflammation0962-93511466-18611992-01-011534735310.1155/S0962935192000528Role of interleukin-1 and tumour necrosis factor in leukocyte recruitment to acute dermal inflammationAndrew C. Issekutz0Nancy Lopes1Thomas B. Issekutz2Departments of Pediatrics, Microbiology and Immunology, Dalhousie University, 5850 University Avenue, Halifax, Nova Scotia, B3J 3G9, CanadaDepartments of Pediatrics, Microbiology and Immunology, Dalhousie University, 5850 University Avenue, Halifax, Nova Scotia, B3J 3G9, CanadaDepartments of Pediatrics, Microbiology and Immunology, Dalhousie University, 5850 University Avenue, Halifax, Nova Scotia, B3J 3G9, CanadaThe cytokines IL-1 and TNF-α are involved in inflammation and their production is stimulated by various agents, especially endotoxin (LPS). Here, using the human IL-1 receptor antagonist (IL-1RA) and a new monoclonal antibody (mAb 7F11) to rabbit TNF, the role of endogenous IL-l and TNF production in acute (3h) leukocyte (PMNL) recruitment to dermal inflammation in rabbits has been studied. IL-1RA inhibited by 27% the PMNL accumulation in reactions induced by killed Escherichia coli (p < 0.05) but not by LPS. The monoclonal antibody to TNF inhibited by 27% and 38% (p < 0.002) the PMNL accumulation in LPS and E. coli reactions respectively, but a combination of the mAb with IL-1RA was not more effective. Treatment of human umbilical vein endothelium with LPS for 3 h activated endothelium to induce PMNL transendothelial migration in vitro, which was not inhibited by IL-1RA, antibody to TNF-α, IL-1 or to IL-8. In conclusion, TNF and IL-1 may partially mediate acute PMNL infiltration in vivo to LPS and Gram negative bacteria, but there is a major IL-1/TNF independent mechanism, at least in dermal inflammation, which may be due to direct LPS activation of the microvasculature or perhaps the generation of cytokines other than IL-1 and TNF.http://dx.doi.org/10.1155/S0962935192000528 |
| spellingShingle | Andrew C. Issekutz Nancy Lopes Thomas B. Issekutz Role of interleukin-1 and tumour necrosis factor in leukocyte recruitment to acute dermal inflammation Mediators of Inflammation |
| title | Role of interleukin-1 and tumour necrosis factor in leukocyte recruitment to acute dermal inflammation |
| title_full | Role of interleukin-1 and tumour necrosis factor in leukocyte recruitment to acute dermal inflammation |
| title_fullStr | Role of interleukin-1 and tumour necrosis factor in leukocyte recruitment to acute dermal inflammation |
| title_full_unstemmed | Role of interleukin-1 and tumour necrosis factor in leukocyte recruitment to acute dermal inflammation |
| title_short | Role of interleukin-1 and tumour necrosis factor in leukocyte recruitment to acute dermal inflammation |
| title_sort | role of interleukin 1 and tumour necrosis factor in leukocyte recruitment to acute dermal inflammation |
| url | http://dx.doi.org/10.1155/S0962935192000528 |
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