Innate Immune Mechanism of Neutrophil Extracellular Trap Formation is Impaired in at-Risk Term Low Birth Weight Newborns

被引:1
|
作者
Das, Doli [1 ]
Singh, Vikas V. [1 ]
Chauhan, Sudhir K. [1 ,5 ]
Rai, Richa [1 ,6 ]
Kumar, Ashok [2 ]
Jain, Madhu [3 ]
Rai, Geeta [1 ,4 ]
机构
[1] Banaras Hindu Univ, Inst Sci, Dept Mol & Human Genet, Varanasi, India
[2] Banaras Hindu Univ, Inst Med Sci, Dept Pediat, Varanasi, India
[3] Banaras Hindu Univ, Inst Med Sci, Dept Obstet & Gynecol, Varanasi, India
[4] Banaras Hindu Univ, Inst Sci, Dept Mol & Human Genet, Varanasi 221005, India
[5] Oslo Univ Hosp, Inst Canc Res, Dept Canc Immunol, Oslo, Norway
[6] Icahn Sch Med Mt Sinai, Tisch Canc Inst, Div Hematol & Oncol, New York, NY USA
关键词
low birth weight; NETosis; Neutrophil extracellular trap; placenta; toll-like receptor; NEONATAL NEUTROPENIA; MOLECULAR-MECHANISMS; NET FORMATION; NETOSIS; SEPSIS; INFANTS; GROWTH; INFECTION; ELASTASE; RELEASE;
D O I
10.1080/08880018.2023.2218409
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Low birth weight (LBW) is a leading cause of newborn's mortality however the underlying defects in cellular immunity and immune mechanisms leading to severe neonatal infections in term LBW (tLBW) newborns are not well understood. Neutrophil extracellular traps (NETs), or NETosis, is an innate immune defense mechanism of neutrophils involved in trapping and killing of microbes. The efficiency of NET formation in cord blood derived neutrophils of tLBW and normal birth weight (NBW) newborns in the presence of toll like receptor (TLR) agonist inductions was evaluated. The NET formation was observed to be substantially impaired in tLBW newborns along with NET proteins expression, extracellular deoxyribonucleic acid (DNA) release and reactive oxygen species generation. The placental tissues from tLBW newborns delivery also showed minimal NETosis. These findings suggest impaired NET formation to be an important factor underlying the deficient immune status of tLBW newborns making them susceptible to life- threatening infections.
引用
收藏
页码:568 / 586
页数:19
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