| First Author | Wang MJ | Year | 2000 |
| Journal | Cell Immunol | Volume | 204 |
| Issue | 2 | Pages | 88-95 |
| PubMed ID | 11069716 | Mgi Jnum | J:65822 |
| Mgi Id | MGI:1927335 | Doi | 10.1006/cimm.2000.1697 |
| Citation | Wang MJ, et al. (2000) Differential expression and regulation of macrophage inflammatory protein (MIP)-1alpha and MIP-2 genes by alveolar and peritoneal macrophages in LPS-hyporesponsive C3H/HeJ mice. Cell Immunol 204(2):88-95 |
| abstractText | A point mutation in Toll-like receptor 4 (Tlr4) gene in C3H/HeJ mice underlies a defect in LPS-induced cytokine production by peritoneal macrophages (PMφ). Whether the C-C and the C-X-C chemokines are induced differently by LPS between alveolar macrophages (AMφ) and PMφ in this mice remains unclear. Thus, we examined the expression and regulation of macrophage inflammatory protein-1alpha (MIP-1alpha) and macrophage inflammatory protein-2 (MIP-2) in C3H/HeJ macrophages. These results showed that the accumulation of MIP-1alpha and MIP-2 mRNA increased dose dependently in response to LPS. PMφ responded to LPS to produce significantly higher levels of both chemokine mRNA and protein than AMφ. In addition, both macrophages produced much more MIP-2 than MIP-1alpha by the same doses of LPS stimulation. Moreover, the chemokine production by C3H/HeN macrophages was significantly higher than that of the C3H/HeJ macrophages. IFN-gamma suppressed the LPS-induced MIP-1alpha release but enhanced the LPS-induced MIP-2 secretion in both macrophages. These results show that the chemokine production was induced and regulated differentially in AMφ and PMφ. Copyright 2000 Academic Press. |
