Lipopolysaccharide-induced cytokine and receptor expression and neutrophil infiltration in the liver of osteopetrosis (op/op) mutant mice.
Lipopolysaccharide-induced cytokine and receptor expression and neutrophil infiltration in the liver of osteopetrosis (op/op) mutant mice.
复制标题
脂多糖诱导骨石症(op/op)突变小鼠肝脏中的细胞因子和受体表达以及中性粒细胞浸润。
DOI:
10.1034/j.1600-0676.2000.020006465.x
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发表时间:
2000
期刊:
影响因子:
--
通讯作者:
Shultz,LD
中科院分区:
文献类型:
--
作者:
Jiang,S;Naito,M;Kaizu,C;Kuwata,K;Hasegawa,G;Mukaida,N;Shultz,LD
Background/AimsMice homozygous for the osteopetrosis (op) mutation are genetically deficient in macrophage colony‐stimulating factor (M‐CSF/CSF‐1) and are characterized by defective differentiation and function of macrophages. The aim of this study is to assess the contribution of M‐CSF to lipopolysaccharide (LPS)‐induced cytokine expression and neutrophil infiltration in the liver.MethodsWe investigated the effects of LPS administration in M‐CSF‐deficientop/opmutant mice. The expression of cytokines and receptors in the liver was studied by immunohistochemistry and RT‐PCR. Neutrophil infiltration in the liver was also examined.ResultsAfter LPS administration, cytokine production and expression of LPS receptors, such as CD14 and scavenger receptor class A (MSR‐A), were induced at lower levels inop/opmice than those in littermate mice. Neutrophil infiltration in the liver ofop/opmice did not differ significantly from that of littermate mice. Anti‐IL‐8 receptor homologue and anti‐C5a receptor antibody reduced the number of infiltrating neutrophils.ConclusionsThese findings indicate that deficient macrophage activation following LPS injection inop/opmice is associated with decreased expression of CD14 and MSR‐A in the liver. Thus, M‐CSF plays a critical role in LPS‐induced macrophage activation but does not exert a dominant role in neutrophil infiltration in the liver.