Evidence map›Paper›PMID 36517836›Full record

ArticleJournal of translational medicine2022

Monophosphoryl lipid A ameliorates radiation-induced lung injury by promoting the polarization of macrophages to the M1 phenotype.

Xingdong Guo, Lehui Du, Na Ma, Pei Zhang, Yuan Wang, Yanan Han, Xiang Huang, Qian Zhang, Xin Tan, Xiao Lei and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 26 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Xingdong Guo *Department of Radiation Oncology, Chinese PLA General Hospital, Beijing, China.
Lehui Du *Department of Radiation Oncology, Chinese PLA General Hospital, Beijing, China.
Na Ma *Department of Radiation Oncology, Chinese PLA General Hospital, Beijing, China.
Pei ZhangDepartment of Radiation Oncology, Chinese PLA General Hospital, Beijing, China.
Yuan WangDepartment of Radiation Oncology, Chinese PLA General Hospital, Beijing, China.
Yanan HanDepartment of Radiation Oncology, Chinese PLA General Hospital, Beijing, China.
Xiang HuangDepartment of Radiation Oncology, Chinese PLA General Hospital, Beijing, China.
Qian ZhangDepartment of Radiation Oncology, Chinese PLA General Hospital, Beijing, China.
Xin TanDepartment of Radiation Oncology, Chinese PLA General Hospital, Beijing, China.
Xiao LeiDepartment of Radiation Oncology, Chinese PLA General Hospital, Beijing, China. 18601758966@163.com.ORCID 0000-0002-0428-1749
Baolin QuDepartment of Radiation Oncology, Chinese PLA General Hospital, Beijing, China. baolinqu301@163.com.
Chinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRadiation-induced lung injury (RILI) often occurs during clinical chest radiotherapy and acute irradiation from accidental nuclear leakage. This study explored the role of monophosphoryl lipid A (MPLA) in RILI. MATERIALS AND

methodsThe entire thoracic cavity of C57BL/6N mice was irradiated at 20 Gy with or without pre-intragastric administration of MPLA. HE staining, Masson trichrome staining, and TUNEL assay were used to assess lung tissue injury after treatment. The effect of irradiation on the proliferation of MLE-12 cells was analyzed using the Clonogenic assay. The effect of MPLA on the apoptosis of MLE-12 cells was analyzed using flow cytometry. Expression of γ-H2AX and epithelial-mesenchymal transition (EMT) markers in MLE-12 cells was detected by immunofluorescence and Western blot, respectively.

resultsMPLA attenuated early pneumonitis and late pulmonary fibrosis after thoracic irradiation and reversed radiation-induced EMT in C57 mice. MPLA further promoted proliferation and inhibited apoptosis of irradiated MLE-12 cells in vitro. Mechanistically, the radioprotective effect of MPLA was mediated by exosomes secreted by stimulated macrophages. Macrophage-derived exosomes modulated DNA damage in MLE-12 cells after irradiation. MPLA promoted the polarization of RAW 264.7 cells to the M1 phenotype. The exosomes secreted by M1 macrophages suppressed EMT in MLE-12 cells after irradiation.

conclusionMPLA is a novel treatment strategy for RILI. Exosomes derived from macrophages are key to the radioprotective role of MPLA in RILI.

Indexed as

Lung InjuryRadiation InjuriesAnimalsLipid ALungMacrophagesMiceMice, Inbred C57BLPhenotypeLipid Amonophosphoryl lipid AEpithelial-mesenchymal transitionExosomesMacrophagesMonophosphoryl lipid ARadiation-induced lung injuryRadioprotection

Identifiers

PMID36517836
PMCPMC9753357
OpenAlexW4311469593

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.