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The interaction between different types of activated RAW 264.7 cells and macrophage inflammatory protein-1 alpha.
- Source :
-
Radiation Oncology . 2011, Vol. 6 Issue 1, p86-92. 7p. - Publication Year :
- 2011
-
Abstract
- <bold>Background: </bold>Two major ways of macrophage (MΦ) activation can occur in radiation-induced pulmonary injury (RPI): classical and alternative MΦ activation, which play important roles in the pathogenesis of RPI. MΦ can produce chemokine MΦ inflammatory protein-1α (MIP-1α), while MIP-1α can recruit MΦ. The difference in the chemotactic ability of MIP-1α toward distinct activated MΦ is unclear. We speculated that there has been important interaction of MIP-1α with different activated MΦ, which might contribute to the pathogenesis of RPI.<bold>Methods: </bold>Classically and alternatively activated MΦ were produced by stimulating murine MΦ cell line RAW 264.7 cells with three different stimuli (LPS, IL-4 and IL-13); Then we used recombinant MIP-1α to attract two types of activated MΦ. In addition, we measured the ability of two types of activated MΦ to produce MIP-1α at the protein or mRNA level.<bold>Results: </bold>Chemotactic ability of recombinant MIP-1α toward IL-13-treated MΦ was the strongest, was moderate for IL-4-treated MΦ, and was weakest for LPS-stimulated MΦ (p<0.01). The ability of LPS-stimulated MΦ to secrete MIP-1α was significantly stronger than that of IL-4-treated or IL-13-treated MΦ (p<0.01). The ability of LPS-stimulated MΦ to express MIP-1α mRNA also was stronger than that of IL-4- or IL-13-stimulated MΦ (p<0.01).<bold>Conclusions: </bold>The chemotactic ability of MIP-1α toward alternatively activated MΦ (M2) was significantly greater than that for classically activated MΦ (M1). Meanwhile, both at the mRNA and protein level, the capacity of M1 to produce MIP-1α is better than that of M2. Thus, chemokine MIP-1α may play an important role in modulating the transition from radiation pneumonitis to pulmonary fibrosis in vivo, through the different chemotactic affinity for M1 and M2. [ABSTRACT FROM AUTHOR]
- Subjects :
- *MACROPHAGES
*RADIATION
*CHEMOKINES
*PROTEINS
*PULMONARY fibrosis
Subjects
Details
- Language :
- English
- ISSN :
- 1748717X
- Volume :
- 6
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Radiation Oncology
- Publication Type :
- Academic Journal
- Accession number :
- 64083362
- Full Text :
- https://doi.org/10.1186/1748-717X-6-86