Serum amyloid A is a chemoattractant: induction of migration, adhesion, and tissue infiltration of monocytes and polymorphonuclear leukocytes.

Serum amyloid A is a chemoattractant: induction of migration, adhesion, and tissue infiltration of monocytes and polymorphonuclear leukocytes.
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DOI:
10.1084/jem.180.1.203
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发表时间:
1994-07-01
期刊:
The Journal of experimental medicine
影响因子:
--
通讯作者:
Oppenheim JJ
Oppenheim JJ
中科院分区:
其他
文献类型:
--
作者:
Badolato R;Wang JM;Murphy WJ;Lloyd AR;Michiel DF;Bausserman LL;Kelvin DJ;Oppenheim JJ

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血清淀粉样蛋白A(SAA)是一种急性期蛋白,在血液中与高密度脂蛋白结合; SAA主要由肝细胞分泌,在炎症反应期间其在血液中的浓度增加高达1000倍。目前,其生物学功能尚不清楚。由于某些形式的继发性淀粉样变性是由SAA衍生的肽在组织中沉积引起的,白细胞似乎参与了这一过程,因此我们研究了人SAA对人单核细胞和多形核细胞(PMN)的影响。当重组人SAA(rSAA)的浓度相当于急性期(> 0.8 μ M)时,它诱导单核细胞和多形核白细胞定向迁移。rSAA与高密度脂蛋白的预孵育阻断了单核细胞和PMN的这种趋化活性。rSAA还可调节粘附蛋白CD 11b和白细胞粘附分子1的表达,并诱导PMN和单核细胞与脐静脉内皮细胞单层的粘附。当皮下注射到小鼠中时,rSAA在注射部位募集PMN和单核细胞。在这些数据的基础上,我们认为SAA可能参与增强单核细胞和中性粒细胞迁移到炎症组织在急性期反应。
Serum amyloid A (SAA) is an acute phase protein that in the blood is bound to high density lipoproteins; SAA is secreted mainly by hepatocytes, and its concentration increases in the blood up to 1000 times during an inflammatory response. At present, its biological function is unclear. Since some forms of secondary amyloidosis are caused by deposition in tissues of peptides derived from the SAA and leukocytes seem to be involved in this process, we investigated the effect of human SAA on human monocytes and polymorphonuclear cells (PMN). When recombinant human SAA (rSAA) was used at concentrations corresponding to those found during the acute phase (> 0.8 microM), it induced directional migration of monocytes and polymorphonuclear leukocytes. Preincubation of rSAA with high density lipoproteins blocked this chemoattractant activity for both monocytes and PMN. rSAA also regulated the expression of the adhesion proteins CD11b and leukocyte cell adhesion molecule 1 and induced the adhesion of PMN and monocytes to umbilical cord vein endothelial cell monolayers. When subcutaneously injected into mice, rSAA recruited PMN and monocytes at the injection site. On the basis of these data, we suggest that SAA may participate in enhancing the migration of monocytes and PMN to inflamed tissues during an acute phase response.