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Article
Peer-Review Record

C-X-C Motif Chemokine 3 Promotes the Inflammatory Response of Microglia after Escherichia coli-Induced Meningitis

Int. J. Mol. Sci. 2023, 24(13), 10432; https://doi.org/10.3390/ijms241310432
by Xinyi Qu 1,2,3,†, Beibei Dou 1,2,3,†, Ruicheng Yang 1,2,3, Chen Tan 1,2,3,4,5, Huanchun Chen 1,2,3,4,5 and Xiangru Wang 1,2,3,4,5,*
Reviewer 1: Anonymous
Reviewer 2:
Int. J. Mol. Sci. 2023, 24(13), 10432; https://doi.org/10.3390/ijms241310432
Submission received: 27 May 2023 / Revised: 18 June 2023 / Accepted: 19 June 2023 / Published: 21 June 2023
(This article belongs to the Special Issue Astrocyte-Endothelial Interactions at the Blood-Brain Barrier)

Round 1

Reviewer 1 Report

Dear Authors, 

The main question addressed by the research is the role of CXCL3/CXCR2 pathway in meningitis E. coli -induced neuroinflammation proving CXCL3 a promising target to prevent E. coli-induced neuroinflammation. According to authors, CXCL3/CXCR2 pathway in tumours was proved, while the role in meningitis E. coli -induced neuroinflammation was first investigated in this paper. 

The draft you submitted is a well-designed and performed study. 

The main goal of the paper was clearly introduced and assays were suitable to reach the desired results. The latter were clearly reported and analysed. 

The content of this paper is significant and with the sole exception of English issues at the very beginning of 'Discussion' paragraph, the draft is suitable for publication, from my point of view. 

Some small English issue was detected in the first part of 'Discussion' paragraph

Author Response

Comments and Suggestions for Authors

The main question addressed by the research is the role of CXCL3/CXCR2 pathway in meningitis E. coli -induced neuroinflammation proving CXCL3 a promising target to prevent E. coli-induced neuroinflammation. According to authors, CXCL3/CXCR2 pathway in tumours was proved, while the role in meningitis E. coli -induced neuroinflammation was first investigated in this paper. The draft you submitted is a well-designed and performed study. The main goal of the paper was clearly introduced and assays were suitable to reach the desired results. The latter were clearly reported and analyzed.

Re:

Thanks for your positive comment on our study.

 

The content of this paper is significant and with the sole exception of English issues at the very beginning of 'Discussion' paragraph, the draft is suitable for publication, from my point of view.

Re:

Thanks for your suggestions. We have rewritten the first paragraph of the discussion section based on the content of the article, please see the revised manuscript.

 

Comments on the Quality of English Language

Some small English issue was detected in the first part of 'Discussion' paragraph

Re: Thanks for your advice. Based on the research results, we have rewritten the first paragraph, please see the revised manuscript.

Reviewer 2 Report

Meningitis, a manifestation of Escherichia coli infection, involves inflammation of the meninges and subarachnoid space. CXCL3, a chemokine, shows high expression during E. coli meningitis. However, the role of CXCL3 in meningitis development remains unclear. This study used in vitro and in vivo assays to explore these contributions and identify potential therapeutic targets for central nervous system inflammation. The results showed up-regulated CXCL3 expression in brain cells and its receptor, CXCR2, in microglia. CXCL3 induced M1 microglia activation and inflammatory response. These findings highlight the importance of CXCL3 as a potential target for future research and prevention of E. coli-induced neuroinflammation.

I have only a few minor comments to further improve the manuscript.

The authors should read Manuscript multiple times to screen out multiple Grammatical mistakes.

Authors should also include mechanistic figure to show the findings.

Meningitis, a manifestation of Escherichia coli infection, involves inflammation of the meninges and subarachnoid space. CXCL3, a chemokine, shows high expression during E. coli meningitis. However, the role of CXCL3 in meningitis development remains unclear. This study used in vitro and in vivo assays to explore these contributions and identify potential therapeutic targets for central nervous system inflammation. The results showed up-regulated CXCL3 expression in brain cells and its receptor, CXCR2, in microglia. CXCL3 induced M1 microglia activation and inflammatory response. These findings highlight the importance of CXCL3 as a potential target for future research and prevention of E. coli-induced neuroinflammation.

I have only a few minor comments to further improve the manuscript.

The authors should read Manuscript multiple times to screen out multiple Grammatical mistakes.

Authors should also include mechanistic figure to show the findings.

Author Response

Comments and Suggestions for Authors

Meningitis, a manifestation of Escherichia coli infection, involves inflammation of the meninges and subarachnoid space. CXCL3, a chemokine, shows high expression during E. coli meningitis. However, the role of CXCL3 in meningitis development remains unclear. This study used in vitro and in vivo assays to explore these contributions and identify potential therapeutic targets for central nervous system inflammation. The results showed up-regulated CXCL3 expression in brain cells and its receptor, CXCR2, in microglia. CXCL3 induced M1 microglia activation and inflammatory response. These findings highlight the importance of CXCL3 as a potential target for future research and prevention of E. coli-induced neuroinflammation.

 

I have only a few minor comments to further improve the manuscript.

 

The authors should read Manuscript multiple times to screen out multiple Grammatical mistakes.

Re:

Thanks for your kind suggestion. The manuscript has been thoroughly revised and some grammatical errors have been corrected.

 

Authors should also include mechanistic figure to show the findings.

Re:

Thanks for your advice. We have added the molecular schematic, please see the revised manuscript.

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