摘要
用限量胰蛋白酶法定量研究了Ｐ－ＭｓｍＦｎ与其吞噬活性和分泌ＴＮＦ的关系，探讨Ｆｎ在细胞膜水平对巨噬细胞功能的调节作用。结果显示：随ｓｍＦｎ减少，Ｐ－Ｍ吞噬活性降低，该降低能被介质Ｆｎ所逆转，随介质Ｆｎ水平升高，ｓｍＦｎ增多，Ｐ－Ｍ吞噬活性亦增强。ｓｍＦｎ与吞噬活性呈显著正相关。ＬＰＳ（２０ｎｇ／ｍｌ）诱导ｓｍＦｎ减少的Ｐ－Ｍ产生ＴＮＦ－α呈双高峰变化，且高峰延迟，２４小时总量较对照组高。上述结果提示：Ｆｎ在细胞膜水平经ｓｍＦｎ调节Ｐ－Ｍ吞噬活性和分泌ＴＮＦ－α水平，ｓｍＦｎ是Ｆｎ调节Ｐ－Ｍ功能的桥梁，Ｆｎ制剂治疗创伤／感染病人对预防和减轻ＭＯＤ可能是有益的。
he
relationship of surface fibronectin of membrane(smFn)with
phagocytosis and tumornecrosis factor alpha(TNF-α)production of
peritoneal macrophages( p-M)were studiedquantatively by limited
trypsinization for researching the regulation of fibronectin
onmacrophages’ function on the cell membrane level.When
smFndecreased so long as trypsin level(1-50ug/ml) increased,the
phagocytosis of p-M also decreased,which might be reversable
byfibronectin; while fibronectin level in medium increased,both P-M
smFn and phagocytosis wereincreased,which were markedly positive
correlation (P<0.05 ).When p-M smFn were de-creased by trypsin,TNF-α
production of the p-M induced by endotpxin(20ng/ml)appeareddelayed
double peaks,which total during 24 hours was more than tht of
control.These resultsindicated that fibronectin on the cell membrace
level regulates macrophages’function throughsmFn。smFn is the
briedge that plasma fibronectin regulates monocyte-phagocyte
function.Fntherapy in traumatic or/ and infective patients may be
effective on preventiong multiple organ-damage.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
1994年第1期18-20,共3页
Chinese Journal of Immunology
