Neutrophil recruitment in immunized mice depends on MIP-2 inducing the sequential release of MIP-1α, TNF-α and LTB4
| ISSN: | 1521-4141 0014-2980 |
|---|---|
| DOI: | 10.1002/eji.200636057 |
| Přístupová URL adresa: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6852e4e7b8b35ee9c987e957a3473d60 https://doi.org/10.1002/eji.200636057 |
| Rights: | OPEN |
| Přírůstkové číslo: | edsair.doi.dedup.....6852e4e7b8b35ee9c987e957a3473d60 |
| Autor: | Claudio Canetti, Karla Fernandes, C. D. L. Ramos, Fernando Q. Cunha, Mauro M. Teixeira, João Santana da Silva |
| Rok vydání: | 2006 |
| Předmět: |
CCR1
Chemokine Neutrophils medicine.drug_class Immunology Leukotriene B4 Receptors Interleukin-8B Leukocyte Count Mice Mediator Peritoneum Cell Movement medicine Animals Immunology and Allergy CXC chemokine receptors Antigens biology Tumor Necrosis Factor-alpha Neutrophil extracellular traps Macrophage Inflammatory Proteins Receptor antagonist Mice Inbred C57BL medicine.anatomical_structure Neutrophil Infiltration biology.protein Immunization Antibody |
| Zdroj: | European Journal of Immunology. 36:2025-2034 |
| ISSN: | 1521-4141 0014-2980 |
| DOI: | 10.1002/eji.200636057 |
| Popis: | Neutrophils are thought to play an important role in the tissue damage observed in various autoimmune diseases. Chemokines, cytokines and leukotrienes have recognized roles in the orchestration of neutrophil migration. We have recently shown that antigen-induced neutrophil migration into the peritoneum of immunized mice is mediated by macrophage-inflammatory protein (MIP)-1alpha which interacts with CCR1 and induces the sequential release of TNF-alpha and leukotriene B(4) (LTB(4)). The present study investigates the role of MIP-2 and CXCR2 in the cascade of events leading to mediator generation and neutrophil influx. Antigen challenge of immunized mice induced the expression of CXCR2 and the production of KC and MIP-2 proteins. Antigen-induced neutrophil migration was inhibited by a CXCR2 receptor antagonist (repertaxin) or an anti-MIP-2 antibody, but not by an anti-KC antibody. Administration of MIP-2 promoted a dose-dependent neutrophil migration in naive mice which was inhibited by repertaxin, anti-TNF-alpha, anti-MIP-1alpha antibodies or by MK886 (leukotriene synthesis inhibitor). MIP-2 administration induced the release of MIP-1alpha, TNF-alpha and LTB(4), and the release of the latter two was inhibited by anti-MIP-1alpha antibody treatment. Our studies highlight the intricate balance between mediator production and action during an immune-mediated inflammatory response and suggest a mediator cascade leading to neutrophil influx following antigen challenge of immunized mice: MIP-2 --> MIP-1alpha --> TNF-alpha --> LTB(4). |
| Databáze: | OpenAIRE |
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