Identification of formyl peptides from Listeria monocytogenes and Staphylococcus aureus as potent chemoattractants for mouse neutrophils.
Identification of formyl peptides from Listeria monocytogenes and Staphylococcus aureus as potent chemoattractants for mouse neutrophils.
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DOI：
10.4049/jimmunol.181.2.1429
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发表时间：
2008-07-15
期刊：
影响因子：
--
通讯作者：
Ye RD
中科院分区：
文献类型：
--
作者：
Southgate EL;He RL;Gao JL;Murphy PM;Nanamori M;Ye RD
原型甲酰肽N-甲酰-Met-Leu-Phe（fMLF）是大肠杆菌培养上清液中发现的主要化学引诱物，也是人甲酰肽受体（FPR）1的强效激动剂。与此一致，fMLF在纳摩尔浓度下诱导人中性粒细胞的杀菌功能。然而，它对小鼠FPR（mFPR）1和小鼠嗜中性粒细胞的作用要弱得多，需要微摩尔浓度才能激活细胞。为了确定其他细菌是否产生更有效的mFPR 1激动剂，我们检查了单核细胞增生李斯特菌和金黄色葡萄球菌的甲酰基肽激活小鼠中性粒细胞的能力。从L.单核细胞增多症和四肽（N-甲酰-Met-Ile-Phe-Leu（fMIFL））。发现金黄色葡萄球菌在1-10 nM诱导小鼠嗜中性粒细胞趋化性，在10-100 nM诱导超氧化物产生，类似于fMLF对人嗜中性粒细胞的效力。使用表达mFPR 1和mFPR 2（小鼠中性粒细胞中FPR的主要形式）的转染细胞系，我们发现mFPR 1负责fMIVIL和fMIFL的高效力。相比之下，mFPR 2的活化需要微摩尔浓度的两种肽。mfpr 1的基因缺失导致中性粒细胞超氧化物产生的废除和响应于fMIVIL和fMIFL的脱粒，进一步证明mFPR 1是用于检测这些甲酰肽的主要受体。因此，L.单核细胞增多症和S.金黄色葡萄球菌在激活小鼠中性粒细胞方面的效力是fMLF的100倍。mFPR 1检测细菌衍生的甲酰肽的能力表明，这种重要的宿主防御机制在小鼠中是保守的。
The prototypic formyl peptide N-formyl-Met-Leu-Phe (fMLF) is a major chemoattractant found in Escherichia coli culture supernatants and a potent agonist at human formyl peptide receptor (FPR) 1. Consistent with this, fMLF induces bactericidal functions in human neutrophils at nanomolar concentrations. However, it is a much less potent agonist for mouse FPR (mFPR) 1 and mouse neutrophils, requiring micromolar concentrations for cell activation. To determine whether other bacteria produce more potent agonists for mFPR1, we examined formyl peptides from Listeria monocytogenes and Staphylococcus aureus for their abilities to activate mouse neutrophils. A pentapeptide (N-formyl-Met-Ile-Val-Ile-Leu (fMIVIL)) from L. monocytogenes and a tetrapeptide (N-formyl-Met-Ile-Phe-Leu (fMIFL)) from S. aureus were found to induce mouse neutrophil chemotaxis at 1-10 nM and superoxide production at 10-100 nM, similar to the potency of fMLF on human neutrophils. Using transfected cell lines expressing mFPR1 and mFPR2, which are major forms of FPRs in mouse neutrophils, we found that mFPR1 is responsible for the high potency of fMIVIL and fMIFL. In comparison, activation of mFPR2 requires micromolar concentrations of the two peptides. Genetic deletion of mfpr1 resulted in abrogation of neutrophil superoxide production and degranulation in response to fMIVIL and fMIFL, further demonstrating that mFPR1 is the primary receptor for detection of these formyl peptides. In conclusion, the formyl peptides from L. monocytogenes and S. aureus are 100-fold more potent than fMLF in activating mouse neutrophils. The ability of mFPR1 to detect bacterially derived formyl peptides indicates that this important host defense mechanism is conserved in mice.
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DOI：
10.1016/0006-291x(90)91143-g
发表时间：
1990-05-16
影响因子：
3.1
作者：
BOULAY, F;TARDIF, M;VIGNAIS, P
通讯作者：
VIGNAIS, P
影响因子：
4.4
作者：
He, R;Tan, L;Ye, RD
通讯作者：
Ye, RD
影响因子：
3.9
作者：
LINDAHL, KF;DABHI, VM;WANG, CR
通讯作者：
WANG, CR
N-甲基肽通过与两种N-甲基肽受体（FPR）亚型的差异相互作用诱导小鼠中性粒细胞趋化性的两种不同浓度最佳。 FPR2的分子表征，第二小鼠中性粒细胞FPR。
影响因子：
15.3
作者：
Hartt, J K;Barish, G;Murphy, P M;Gao, J L
通讯作者：
Gao, J L
影响因子：
32.4
作者：
Gulden, PH;Fischer, P;Pamer, EG
通讯作者：
Pamer, EG