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PLoS One：从“有缘”到“无缘”（1）
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我第一次见识PLoS One是2003年在芬兰赫尔辛基大学，当时我正在该校Viki Biocenter的Biotechnology Institute作访问学者。不过，我既不是从网上检索到它，也不是上图书馆查阅到它，而是偶然从一位准备来实验室作博士后的同学手中的复印件上看到它。我粗略浏览了几页，顿时觉得耳目一新，不光是排版很光鲜，内容也有吸睛的魔力，有一种精致、高贵的感觉。
作为Open Access商业探索的先驱，PLoS One无疑功勋卓著，同时也赚得盆满钵满。可是，因其不菲的论文出版费，让人误以为它是“给钱就发表”的垃圾期刊，加上这些年的论文发表数骤增，又不乏国内学者疯狂“灌水”，让它的形象一落千丈，逐渐从“神坛”跌落到“凡间”。虽不敢说它是否会被贬入“地狱”，但其影响因子不断缩水（从4降到2）着实让粉丝们揪心不已。那么，PLoS One的“失宠”究竟是它的策略失误，还是唯利是图自毁名声？
我没有对它做过认真的研究，也不具备这方面的知识，当然不敢妄言。不过，我至少有两次跟它打交道的经历，足以感受到它是一份什么份量和格调的杂志。在前后几次与编辑的信件来往中，他面对我们表现的是怎样的态度呢？是严格把关还是随意放水？带着这个问题，我把几年前的电邮翻了出来，在此公开展示，给大家尤其是那些没给它投过稿只听过传言的人还原出一个真实的PLoS One!
编辑的第一封邮件（附评阅人意见）是这么写的：
PONE-D-11-22344
Live bacterial feeding simulates chronic and acute collagen-induced arthritis by predisposing nitric oxide-driven hypoxia in mice
PLoS ONE
Dear Dr Qing-Ping Zeng,
Thank you for submitting your manuscript to PLoS ONE. After careful consideration, we feel that it has merit, but is not suitable for publication as it currently stands. Therefore, my decision is "Major Revision."
We consider that the manuscript lacks precision in many aspects, and the data presented need to be completed and/or strengthened. We invite you to submit a revised version of the manuscript that addresses each and every point raised by the Reviewers (see Reviewers' comments below).
We encourage you to submit your revision within sixty days of the date of this decision.
When your files are ready, please submit your revision by logging on to http://pone.edmgr.com/ and following the Submissions Needing Revision link. Do not submit a revised manuscript as a new submission.
Please also include a rebuttal letter that responds to each point brought up by the academic editor and reviewer(s). This letter should be uploaded as a Response to Reviewers file.
In addition, please provide a marked-up copy of the changes made from the previous article file as a Manuscript with Tracked Changes file. This can be done using 'track changes' in programs such as MS Word and/or highlighting any changes in the new document.
If you choose not to submit a revision, please notify us.
Yours sincerely,
Pierre Bobé, Ph.D.
Academic Editor
PLoS ONE
Reviewers' comments:
Reviewer #1: Comments:
The title of the manuscript does not match the major findings and conclusion of the study. Also, it is not clear if the authors are trying to describe mechanisms involved in disease induction by bacterial feeding or proposing a new animal model for RA. Either ways the study is neither novel nor mechanistically adequate. The two major findings of the study linking nitric oxide and hypoxia with the pathogenesis of bacterial feeding-induced arthritis are rather preliminary and superficial. Only serum concentrations of nitric oxide and oxygen are measured. No 'cause and effect' relationship between either one of them with the disease process has been established objectively through rigorous experimentation (e.g., using specific NOS inhibitors or NOS-knockout mice, etc.). Only information from already published literature has been used to speculate the roles of nitric oxide and hypoxia in disease induction and progression. Also, the link between nitric oxide leading to hypoxia isentirely correlative, just based on the inverse levels of the two entities in serum. Neither any information about the local environment in the joints in regard to nitric oxide and hypoxia has been presented nor has any effort been made to show the direct role of nitric oxide or hypoxia in synovial hyperplasia. In addition, another main finding of this study that bacterial feeding can attenuate CIA is also not at all novel. As mentioned below, there are multiple published reports showing that bacterial infection/exposure can suppress the progression of arthritis in different models of arthritis, including CIA.
Novelty of the manuscript is further questionable considering several already published studies highlighting various aspects that are claimed by the authors to be novel. These include, for example, published work reportingautoimmune responses to microbes or microbial components (Toivanen A and Toivanen P, Best Pract Res Clin Rheumatol. 2004;18(5):689-703; Infante-Duarte et al., J Immunol. 2000; 165(11):6107-15), role of NO in the pathogenisis of RA (Nagy et al., Arthritis Res Ther. 2010;12(3):210; Nagy et al., Immunol Lett. 2007; 111(1):1-5) and immunosuppression by bacteria (Kelly D et al., Immunol Rev. 2012; 245(1):27-44; Mowat AM et al., Ann N Y Acad Sci. 2004;1029:1-8).
The role of cytokines and chemokines in the pathogenesis of arthritis is well defined. In this study, the authors have not clearly addressed these critical mediators in BIA.
In summary, the authors have taken two simple serum estimations (nitric oxide and oxygen levels) and developed a speculative theory about their roles in causing synovial hyperplasia. The proposed mechanisms are purely theoretical and not at all supported by experimental evidence.
In conclusion, based on the major concerns indicated above and these published reports, in my assessment the current manuscript is not suitable for publication in PLoS ONE.
Reviewer #2:
Fei Bao and colleagues investigated the possible role of live bacteria in inducing arthritis. According to their observations daily feeding of mice with bacteria (Escherichia coli) induced polyarthritis that is similar to collagen induced arthritis. They found a reverse correlation between the serum NO level and the blood oxygen saturation. The authors suggest that NO may contribute to the synovitis, induced by live bacterial feeding via the up regulation of proinflammatory cytokines. These are interesting observations; I have some comments to this work:
1: TNF<alpha> inhibitors are not used for the treatment of sepsis or pneumonia (or any other opportunistic infections) in humans, please clarify this in the introduction.
2: Please show the severity of bacteria induced arthritis following the applications of NO inhibitor with/without antibiotics.
3: Nitric oxide regulate mitochondrial biogenesis in different cell types, this should be included in discussion.
4: The introduction and the discussion would benefit from a significant shortening.
从编辑回信可知，第一位评阅人非常不客气，直截了当地说此文不适合在PLoS One发表，另一位评审者则提出了具体修改意见。这是我们在专业转型后第一次投稿，却差点让这个“处女作”被“凌迟处决”，还好编辑“慧眼识珠”，看到了本文的merit，给了我们一次大修的机会，不然世界将错过一次那么早知道“肠道感染引起类风湿性关节炎”的机会。由于我们的科学假说很solid，一轮实验做下来取得了很多有用数据，但写文章时却有所保留，没有完全囊括进去。现在看到评委这么一说（rather preliminary and superficial），我们在修改时不仅把全部数据都用上了，而且还补充了一些关键证据，让我们的理论完满坐实，就是想让评委无话可说，心服口服！
我们把修改稿寄出后，很快收到编辑的回信，他附上了评委的反馈意见：
PONE-D-11-22344R1
Nitric oxide-driven hypoxia initiates synovial angiogenesis, hyperplasia and inflammatory lesions in mice
PLoS ONE
Dear Dr Zeng,
Thank you for submitting your manuscript for review to PLoS ONE. After careful consideration, we feel that your manuscript will likely be suitable for publication if it is revised to address the points below. Therefore, my decision is "Minor Revision."
We invite you to submit a revised version of the manuscript that addresses the comments raised by the reviewers.
We encourage you to submit your revision within sixty days of the date of this decision.
When your files are ready, please submit your revision by logging on to http://pone.edmgr.com/ and following the Submissions Needing Revision link. Do not submit a revised manuscript as a new submission.
Please also include a rebuttal letter that responds to each point brought up by the academic editor and reviewer(s). This letter should be uploaded as a Response to Reviewers file.
In addition, please provide a marked-up copy of the changes made from the previous article file as a Manuscript with Tracked Changes file. This can be done using 'track changes' in programs such as MS Word and/or highlighting any changes in the new document.
If you choose not to submit a revision, please notify us.
Yours sincerely,
Pierre Bobé, Ph.D.
Academic Editor
PLoS ONE
Reviewers' comments:
Reviewer #1: The authors have made extensive revisions. The present title looks more appropriate to the study.
I would like to suggest an additional experiment. Authors showed that NO depletion using NOS inhibitor or anti-bacterial agent ameliorate synovitis which is interesting. Likewise it is worth studying that administration of a chemical agent that can potentially induce NO production in mice can also cause similar effects apart from bacterial infection. I think this will greatly strengthen the paper and gives a strong evidence for the direct involvement of NO in disease induction and progression.
Reviewer #2: Please show the severity of bacteria induced arthritis following the applications of specific NO inhibitors with/without antibiotics. This point should be addressed experimentally.
由于修改稿的完善程度远远超出评委们的预料（The authors have made extensive revisions），这次几乎没提什么咄咄逼人的意见，只是要求做一些小的修改，而补充实验也不太难，看来这是要接受发表的节奏啊！果然，文章经过小修后寄出，编辑很快就做出了接受发表的决定。本文第一作者是我的一位硕士研究生，这封接收函当时还作为喜讯在我校研究生院网站上公布，因那时连博士生和博士后都还没在IF大于4的SCI杂志上发表过论文啊！
PONE-D-11-22344R2
Nitric oxide-driven hypoxia initiates synovial angiogenesis, hyperplasia and inflammatory lesions in mice
PLoS ONE
Dear Dr Zeng,
I am pleased to inform you that your manuscript has been deemed suitable for publication in PLoS ONE.
Your manuscript will now be passed on to our Production staff, who will check your files for correct formatting and completeness. After this review, they may return your manuscript to you so that you can make necessary alterations and upload a final version.
Before uploading, you should check the PDF of your manuscript very closely. THERE IS NO AUTHOR PROOFING. You should therefore consider the corrected files you upload now as equivalent to a production proof. The text you supply at this point will be faithfully represented in your published manuscript exactly as you supply it. This is your last opportunity to correct any errors that are present in your manuscript files.
If you or your institution will be preparing press materials for this manuscript, you must inform our press team in advance. Please contact them at ONEpress@plos.org.
If you have any questions, concerns, or problems, please contact us at plosone@plos.org, and thank you for submitting your work to our journal.
With kind regards,
Pierre Bobé, Ph.D.
Academic Editor
PLoS ONE
看到这里，可能有人还是会坚持认为“正是因为要交很多钱，所以这么快就接受了”。他们会说：你看，评委建议拒稿，但编辑却决定大修，这难道不是受利益的驱使吗？且慢，等各位了解了我们下次的投稿经历，你就会知道PLoS One是否“唯利是图”？编辑是否“放水”？评委是否“合谋”？现在我说杂志很严格，编辑很敬业，评委也很认真，你肯定不信！
（待续）
投稿与审稿
https://blog.sciencenet.cn/blog-281238-1068458.html
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