title: The interaction between different types of activated RAW 264.7 cells and macrophage inflammatory protein-1 alpha.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Radiation and Medical Oncology, Zhongnan Hospital, Wuhan University, 169, Donghu Road, Wuchang District, Wuhan, Hubei 430071, PR China.
authors.forename: Zhongshi
authors.initials: Z
authors.lastname: He
authors.forename: Hui
authors.initials: H
authors.lastname: Zhang
authors.forename: Chunxu
authors.initials: C
authors.lastname: Yang
authors.forename: Yajuan
authors.initials: Y
authors.lastname: Zhou
authors.forename: Yong
authors.initials: Y
authors.lastname: Zhou
authors.forename: Guang
authors.initials: G
authors.lastname: Han
authors.forename: Ling
authors.initials: L
authors.lastname: Xia
authors.forename: Wen
authors.initials: W
authors.lastname: Ouyang
authors.forename: Fuxiang
authors.initials: F
authors.lastname: Zhou
authors.forename: Yunfeng
authors.initials: Y
authors.lastname: Zhou
authors.forename: Conghua
authors.initials: C
authors.lastname: Xie
mesh_terms: D000818:Animals; D001119:Arginase / Q000378:metabolism; D002460:Cell Line; D054405:Chemokine CCL3 / Q000378:metabolism*; D002633:Chemotaxis; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D007249:Inflammation; D018793:Interleukin-13 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism; D008264:Macrophages / Q000166:cytology* / Q000378:metabolism; D051379:Mice; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D011014:Pneumonia / Q000378:metabolism; D011658:Pulmonary Fibrosis / Q000378:metabolism; D011994:Recombinant Proteins / Q000378:metabolism
chemical_list: C496534:Ccl3 protein, mouse; D054405:Chemokine CCL3; D018793:Interleukin-13; D008070:Lipopolysaccharides; D011994:Recombinant Proteins; D015847:Interleukin-4; D009569:Nitric Oxide; D001119:Arginase