PMID- 38064816
OWN - NLM
STAT- MEDLINE
DCOM- 20240118
LR  - 20240118
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 127
DP  - 2024 Jan 25
TI  - Cold-inducible RNA-binding protein induces inflammatory responses via NF-kappaB 
      signaling pathway in normal human bronchial epithelial cells infected with 
      streptococcus pneumoniae.
PG  - 111338
LID - S1567-5769(23)01665-X [pii]
LID - 10.1016/j.intimp.2023.111338 [doi]
AB  - BACKGROUND: Community-acquired pneumonia causes significant illness and death 
      worldwide, requiring further investigation and intervention. The invasion of 
      Streptococcus pneumoniae (S. pneumoniae, S.p) can lead to serious conditions like 
      meningitis, sepsis, or pneumonia. Extracellular Cold-inducible RNA-binding 
      protein (eCIRP) acts as a damage-associated molecular pattern that triggers 
      inflammatory responses and plays an important role in both acute and chronic 
      inflammatory diseases. It remains unclear whether CIRP is involved in the process 
      of S. pneumoniae infection in normal human bronchial epithelial cells (BEAS-2B). 
      METHODS: Cell counting kit (CCK)-8 assay was used to detect the activity of 
      BEAS-2B cells. The subcellular localization of CIRP was detected by 
      immunofluorescence. The mRNA and protein levels of CIRP, nuclear factor kappa-B 
      (NF-kappaB) p65, toll like receptor-4 (TLR4), interleukin-6 (IL-6) were detected 
      using quantitative real-time PCR (PCR) and Western Blot (WB). The protein 
      expressions of CIRP, IL-1beta, IL-6, tumor necrosis factor-alpha (TNF-alpha) and monocyte 
      chemoattractant protein-1 (MCP-1) were assessed by enzyme-linked immunosorbent 
      assay (ELISA). RESULTS: CIRP affects the activity of BEAS-2B cells induced by S. 
      pneumoniae infection. After infection, CIRP translocates from the nucleus to the 
      cytoplasm, thereby inducing the production of pro-inflammatory cytokines (IL-1beta, 
      IL-6, TNF-alpha, and MCP-1). Additionally, the NF-kappaB p65 protein increases in 
      infected cells but decreases with si-CIRP interference. Treatment with TLR4 
      neutralizing antibodies or NF-kappaB inhibitor effectively reduces the expressions of 
      IL-1beta, IL-6, TNF-alpha, and MCP-1. CONCLUSIONS: The infection with S. pneumoniae 
      upregulates CIRP expression and translocates it from the nucleus to the cytoplasm 
      in BEAS-2B cells, leading to the release of proinflammatory factors via 
      activation of NF-kappaB signaling pathway. CIRP as a key mediator in S. 
      pneumoniae-induced inflammation offers potential targets for therapeutic 
      intervention against community-acquired pneumonia.
CI  - Copyright (c) 2023 Elsevier B.V. All rights reserved.
FAU - Zhang, Rong
AU  - Zhang R
AD  - Emergency Department of the Affiliated Xuzhou Municipal Hospital of Xuzhou 
      Medical University, Xuzhou, Jiangsu 221000, China.
FAU - Fang, Kun
AU  - Fang K
AD  - Emergency Department of the Affiliated Xuzhou Municipal Hospital of Xuzhou 
      Medical University, Xuzhou, Jiangsu 221000, China.
FAU - Mu, Chunyan
AU  - Mu C
AD  - Xuzhou Medical University, Xuzhou, Jiangsu 221000, China.
FAU - Zhang, Liang
AU  - Zhang L
AD  - Emergency Department of the Affiliated Xuzhou Municipal Hospital of Xuzhou 
      Medical University, Xuzhou, Jiangsu 221000, China. Electronic address: 
      qilipiaoxiangqq@163.com.
LA  - eng
PT  - Journal Article
DEP - 20231207
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (NF-kappa B)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (RNA-Binding Proteins)
SB  - IM
MH  - Humans
MH  - *NF-kappa B/metabolism
MH  - Streptococcus pneumoniae
MH  - Toll-Like Receptor 4/genetics/metabolism
MH  - Interleukin-6/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Signal Transduction
MH  - Epithelial Cells/metabolism
MH  - *Pneumonia/metabolism
MH  - RNA-Binding Proteins/metabolism
OTO - NOTNLM
OT  - BEAS-2B
OT  - Cold-inducible RNA-binding protein
OT  - NF-kappaB signaling
OT  - Streptococcus pneumoniae
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/12/09 05:43
MHDA- 2024/01/18 06:43
CRDT- 2023/12/08 18:02
PHST- 2023/08/28 00:00 [received]
PHST- 2023/11/20 00:00 [revised]
PHST- 2023/11/29 00:00 [accepted]
PHST- 2024/01/18 06:43 [medline]
PHST- 2023/12/09 05:43 [pubmed]
PHST- 2023/12/08 18:02 [entrez]
AID - S1567-5769(23)01665-X [pii]
AID - 10.1016/j.intimp.2023.111338 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2024 Jan 25;127:111338. doi: 10.1016/j.intimp.2023.111338. 
      Epub 2023 Dec 7.