PMID- 33347836
OWN - NLM
STAT- MEDLINE
DCOM- 20211014
LR  - 20220910
IS  - 1678-4782 (Electronic)
IS  - 0021-7557 (Print)
IS  - 0021-7557 (Linking)
VI  - 97
IP  - 5
DP  - 2021 Sep-Oct
TI  - The critical function of miR-1323/Il6 axis in children with Mycoplasma pneumoniae 
      pneumonia.
PG  - 552-558
LID - S0021-7557(20)30251-5 [pii]
LID - 10.1016/j.jped.2020.11.004 [doi]
AB  - OBJECTIVE: Mycoplasma pneumoniae pneumonia (MPP) is a common respiratory 
      infection in children. Tumor necrosis factor-alpha (TNF-alpha), interleukin-17 (IL-17), 
      and IL-6 have correlation with Mycoplasma pneumoniae lung infection and MPP 
      pathogenesis. METHOD: miRNAs participate in the pathogenesis of various diseases 
      by regulating the development and differentiation of the immune cell. Blood was 
      collected and total RNA was isolated. miRNA microarrays were performed to 
      identify differentially expressed miRNAs in MPP patients. The levels of relative 
      miRNAs and mRNAs were evaluated by qRT-PCR. RESULTS: There are 23 differentially 
      expressed miRNAs in MPP children's plasma, 15 miRNAs had enhanced expression and 
      8 had depressed expression. MPP patients showed lower mir-1323 level in blood 
      samples than healthy controls. MPP patients with pleural effusion had much higher 
      Il6 and Il17a mRNA levels than those without pleural effusion. The expression 
      level of Il6 had a negative correlation with miR-1323 level. In the human THP-1 
      cell line, the level of miR-1323 was significantly reduced through 
      lipopolysaccharides treatment. In THP-1 cells, overexpression or silencing of 
      miR-1323 significantly reduced or promoted Il6 expression. CONCLUSION: In 
      conclusion, miR-1323 targets the mRNA of Il6 and inhibits the expression of Il6. 
      The pathogenesis of MPP inhibits the expression of miR-1323 in macrophages, 
      triggers the overexpression of Il6, and enhances inflammation response.
CI  - Copyright (c) 2020 Sociedade Brasileira de Pediatria. Published by Elsevier Editora 
      Ltda. All rights reserved.
FAU - Yin, Linlin
AU  - Yin L
AD  - Cangzhou Central Hospital, Department of Clinical Laboratory, Hebei, China. 
      Electronic address: Yinlinlin818@163.com.
FAU - Ma, Yajun
AU  - Ma Y
AD  - Tengzhou Central People's Hospital, Department of Clinical Laboratory, Shandong, 
      China.
FAU - Wang, Wenlong
AU  - Wang W
AD  - Cangzhou Central Hospital, Department of Clinical Laboratory, Hebei, China.
FAU - Zhu, Yitang
AU  - Zhu Y
AD  - Cangzhou Central Hospital, Department of Clinical Laboratory, Hebei, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20201219
PL  - Brazil
TA  - J Pediatr (Rio J)
JT  - Jornal de pediatria
JID - 2985188R
RN  - 0 (MIRN1323 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Child
MH  - Humans
MH  - Leukocyte Count
MH  - *MicroRNAs/genetics
MH  - Mycoplasma pneumoniae/genetics
MH  - *Pneumonia, Mycoplasma
MH  - Tumor Necrosis Factor-alpha
PMC - PMC9432136
OTO - NOTNLM
OT  - Il6
OT  - MPP
OT  - Macrophage
OT  - Mycoplasma pneumonia
OT  - miR-1323
EDAT- 2020/12/22 06:00
MHDA- 2021/10/15 06:00
PMCR- 2020/12/19
CRDT- 2020/12/21 20:10
PHST- 2020/08/19 00:00 [received]
PHST- 2020/11/02 00:00 [revised]
PHST- 2020/11/05 00:00 [accepted]
PHST- 2020/12/22 06:00 [pubmed]
PHST- 2021/10/15 06:00 [medline]
PHST- 2020/12/21 20:10 [entrez]
PHST- 2020/12/19 00:00 [pmc-release]
AID - S0021-7557(20)30251-5 [pii]
AID - 10.1016/j.jped.2020.11.004 [doi]
PST - ppublish
SO  - J Pediatr (Rio J). 2021 Sep-Oct;97(5):552-558. doi: 10.1016/j.jped.2020.11.004. 
      Epub 2020 Dec 19.