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脂蛋白(a)，一种调理素，增强了巨噬细胞对非典型肺炎链球菌的吞噬作用。

Lipoprotein(a), an Opsonin, Enhances the Phagocytosis of Nontypeable by Macrophages.

机构信息

Research Center of Plasma Lipoprotein Immunology, Inner Mongolia Agricultural University, Hohhot, China.

Laboratory of Biochemistry, Baotou Medical College, Baotou, China.

出版信息

J Immunol Res. 2021 Nov 2;2021:2185568. doi: 10.1155/2021/2185568. eCollection 2021.

DOI:10.1155/2021/2185568
PMID:34765679
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8577944/
Abstract

We recently showed that both nontypeable (NTHi) and its surface plasminogen- (Plg-) binding proteins interact with lipoprotein(a) (Lp(a)) in a lysine-dependent manner. Because Lp(a) can be taken up by macrophages, we postulated that it serves as an opsonin to enhance phagocytosis of NTHi by macrophages. Based on colony-forming unit (CFU) counts, Lp(a) was found to increase U937 macrophage-mediated phagocytosis of NTHi49247 and NTHi49766 by 34% and 43%, respectively, after 120 min. In contrast, Lp(a) did not enhance phagocytosis of BL21 or JM109, which were unable to bind to Lp(a). As with U937 macrophages, Lp(a) was capable of increasing phagocytosis of NTHi49247 by peripheral blood mononuclear cell-derived macrophages. Opsonic phagocytosis by Lp(a) was inhibited by the addition of recombinant kringle IV type 10 (rKIV), a lysine-binding competitor; moreover, Lp(a) did not increase phagocytosis of NTHi by U937 macrophages that were pretreated with a monoclonal antibody against the scavenger receptor CD36. Taken together, our observation suggests that Lp(a) might serve as a lysine-binding opsonin to assist macrophages in rapid recognition and phagocytosis of NTHi.

摘要

我们最近表明，非典型性（NTHi）及其表面纤溶酶原-（Plg-）结合蛋白均以赖氨酸依赖性方式与脂蛋白（a）（Lp（a））相互作用。因为 Lp（a）可以被巨噬细胞摄取，所以我们推测它作为一种调理素来增强巨噬细胞对 NTHi 的吞噬作用。根据菌落形成单位（CFU）计数，Lp（a）被发现分别增加了 U937 巨噬细胞介导的对 NTHi49247 和 NTHi49766 的吞噬作用 34%和 43%，在 120 分钟后。相比之下，Lp（a）不会增强 BL21 或 JM109 的吞噬作用，因为它们不能与 Lp（a）结合。与 U937 巨噬细胞一样，Lp（a）能够增加外周血单核细胞衍生的巨噬细胞对 NTHi49247 的吞噬作用。添加重组kringle IV 型 10（rKIV）（一种赖氨酸结合竞争物）可抑制 Lp（a）的调理吞噬作用；此外，Lp（a）不会增加用针对清道夫受体 CD36 的单克隆抗体预处理的 U937 巨噬细胞对 NTHi 的吞噬作用。综上所述，我们的观察结果表明，Lp（a）可能作为一种赖氨酸结合调理素，有助于巨噬细胞快速识别和吞噬 NTHi。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/19a73aa5a476/JIR2021-2185568.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/90f0e7c66a31/JIR2021-2185568.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/27547377c5ff/JIR2021-2185568.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/fe20f1257611/JIR2021-2185568.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/531479bc393f/JIR2021-2185568.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/ffa2b71d68ca/JIR2021-2185568.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/f7bf19d664eb/JIR2021-2185568.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/19a73aa5a476/JIR2021-2185568.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/90f0e7c66a31/JIR2021-2185568.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/27547377c5ff/JIR2021-2185568.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/fe20f1257611/JIR2021-2185568.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/531479bc393f/JIR2021-2185568.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/ffa2b71d68ca/JIR2021-2185568.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/f7bf19d664eb/JIR2021-2185568.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e899/8577944/19a73aa5a476/JIR2021-2185568.007.jpg

相似文献

[1]
Lipoprotein(a), an Opsonin, Enhances the Phagocytosis of Nontypeable by Macrophages.

J Immunol Res. 2021

[2]
Antibodies to the HMW1/HMW2 and Hia adhesins of nontypeable haemophilus influenzae mediate broad-based opsonophagocytic killing of homologous and heterologous strains.

Clin Vaccine Immunol. 2014-5

[3]
Relationship between intracellular survival in macrophages and virulence of Haemophilus influenzae type b.

J Infect Dis. 1991-6

[4]
Low-density lipoprotein as an opsonin promoting the phagocytosis of Pseudomonas aeruginosa by U937 cells.

J Microbiol. 2019-5-11

[5]
Survival of nontypeable Haemophilus influenzae in macrophages.

FEMS Microbiol Lett. 2001-9-11

[6]
LDL acts as an opsonin enhancing the phagocytosis of group A Streptococcus by monocyte and whole human blood.

Med Microbiol Immunol. 2016-4

[7]
High-density lipoprotein acts as an opsonin to enhance phagocytosis of group A streptococcus by U937 cells.

Microbiol Immunol. 2015-7

[8]
Phagocytosis of live versus killed or fluorescently labeled bacteria by macrophages differ in both magnitude and receptor specificity.

Immunol Cell Biol. 2017-5

[9]
Human antibodies specific for the high-molecular-weight adhesion proteins of nontypeable Haemophilus influenzae mediate opsonophagocytic activity.

Infect Immun. 2003-12

[10]
Calcium restores the macrophage response to nontypeable haemophilus influenzae in chronic obstructive pulmonary disease.

Am J Respir Cell Mol Biol. 2015-6

本文引用的文献

[1]
Low-density lipoprotein as an opsonin promoting the phagocytosis of Pseudomonas aeruginosa by U937 cells.

J Microbiol. 2019-5-11

[2]
Oxidized phospholipids as a unifying theory for lipoprotein(a) and cardiovascular disease.

Nat Rev Cardiol. 2019-5

[3]
Plasminogen-binding proteins as an evasion mechanism of the host's innate immunity in infectious diseases.

Biosci Rep. 2018-10-2

[4]
The adhesins of non-typeable Haemophilus influenzae.

Expert Rev Anti Infect Ther. 2018-2-21

[5]
Lipoprotein(a) in clinical practice: New perspectives from basic and translational science.

Crit Rev Clin Lab Sci. 2017-12-20

[6]
The renaissance of lipoprotein(a): Brave new world for preventive cardiology?

Prog Lipid Res. 2017-9-6

[7]
The role of CD36 receptor in the pathogenesis of atherosclerosis.

Adv Clin Exp Med. 2017-7

[8]
Nontypeable Haemophilus influenzae and chronic obstructive pulmonary disease: a review for clinicians.

Crit Rev Microbiol. 2017-5-25

[9]
Lipoprotein(a) and its role in inflammation, atherosclerosis and malignancies.

Clin Res Cardiol Suppl. 2017-3

[10]
Structure, function, and genetics of lipoprotein (a).

J Lipid Res. 2016-8

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