Title: Unravelling the role of beta-CGRP in inflammatory bowel disease and its potential role
in gastrointestinal homeostasis
Version: 1 Date: 24 May 2024
Reviewer's report:
Scientific Quality: Grade C (Good)
Novelty of This Manuscript: Grade C (Fair)
Creativity or Innovation of This Manuscript: Grade C (Fair)
Scientific Significance of the Conclusion in This Manuscript: Grade C (Fair)
Language Quality: Grade B (Minor language polishing)
Conclusion: Minor revision
Conclusion:
This experiment tested 96 patients recently diagnosed with IBD and compared their morning
serum # - CGRP levels with 50 matched healthy controls and 50 patients with chronic migraine.
The results showed that the # - CGRP levels in IBD patients were lower than those in healthy
controls and chronic migraine patients. In terms of diagnosing subtypes of IBD, the # - CGRP
levels in ulcerative colitis and Crohn's disease are significantly lower than those in healthy
controls and chronic migraine patients. The conclusion is that compared with healthy controls
and chronic migraine patients, patients diagnosed with various IBDs recently have significantly
reduced serum # - CGRP levels, strongly supporting the role of this neuropeptide in the
pathophysiology of IBD from an early stage onwards. The authors also believe that # - CGRP
has a protective effect in gastrointestinal homeostasis. However, there are still several issues
that need attention:
1. Please describe the reasons for excluding the use of biological agents in the inclusion criteria.
Is there any relevant literature to prove that biological agents have an impact on CGRP? Or does
mesalazine and steroids have no effect on CGRP?
2. As mentioned earlier, # CGRP mainly exists in the intermuscular neurons of the small intestine
and colon. When selecting samples, please explain why not use colon specimens from IBD
patients to explore more accurate local changes, but rather to explore more comprehensive
changes in IBD patients? If it is indeed difficult to obtain specimens, can a small amount of
samples be used to explore the difference between circulating and local CGRP in advance?
3. The author mentioned in the discussion section that existing literature has shown a decrease
in the expression of CGRP and CGRP mRNA in the intestinal mucosa of UC patients. Can the
differences and focuses between this experiment and this literature be understood as differences
in the selection of disease stages for IBD patients? Or rather, focus on proving the causal
relationship between CGRP and IBD? Suggest adding a paragraph to describe the innovation
and highlights of this article.
4. Please carefully verify the accuracy of each cited literature, such as reference 31, which does
not seem to contain the keyword CGRP.
5. Can you add some literature related to basic experiments on the early effects of CGRP on
IBD to enhance the theoretical support of this article. Or provide some description of this in the
outlook section. Alternatively, animal experiments similar to this could be added.
Title: Unravelling the role of beta-CGRP in inflammatory bowel disease and its potential role
in gastrointestinal homeostasis
Version: 1 Date: 24 May 2024
Reviewer's report:
Scientific Quality: Grade C (Good)
Novelty of This Manuscript: Grade C (Fair)
Creativity or Innovation of This Manuscript: Grade C (Fair)
Scientific Significance of the Conclusion in This Manuscript: Grade C (Fair)
Language Quality: Grade B (Minor language polishing)
Conclusion: Minor revision
Conclusion:
This experiment tested 96 patients recently diagnosed with IBD and compared their morning
serum # - CGRP levels with 50 matched healthy controls and 50 patients with chronic migraine.
The results showed that the # - CGRP levels in IBD patients were lower than those in healthy
controls and chronic migraine patients. In terms of diagnosing subtypes of IBD, the # - CGRP
levels in ulcerative colitis and Crohn's disease are significantly lower than those in healthy
controls and chronic migraine patients. The conclusion is that compared with healthy controls
and chronic migraine patients, patients diagnosed with various IBDs recently have significantly
reduced serum # - CGRP levels, strongly supporting the role of this neuropeptide in the
pathophysiology of IBD from an early stage onwards. The authors also believe that # - CGRP
has a protective effect in gastrointestinal homeostasis. However, there are still several issues
that need attention:
1. Please describe the reasons for excluding the use of biological agents in the inclusion criteria.
Is there any relevant literature to prove that biological agents have an impact on CGRP? Or does
mesalazine and steroids have no effect on CGRP?
2. As mentioned earlier, # CGRP mainly exists in the intermuscular neurons of the small intestine
and colon. When selecting samples, please explain why not use colon specimens from IBD
patients to explore more accurate local changes, but rather to explore more comprehensive
changes in IBD patients? If it is indeed difficult to obtain specimens, can a small amount of
samples be used to explore the difference between circulating and local CGRP in advance?
3. The author mentioned in the discussion section that existing literature has shown a decrease
in the expression of CGRP and CGRP mRNA in the intestinal mucosa of UC patients. Can the
differences and focuses between this experiment and this literature be understood as differences
in the selection of disease stages for IBD patients? Or rather, focus on proving the causal
relationship between CGRP and IBD? Suggest adding a paragraph to describe the innovation
and highlights of this article.
4. Please carefully verify the accuracy of each cited literature, such as reference 31, which does
not seem to contain the keyword CGRP.
5. Can you add some literature related to basic experiments on the early effects of CGRP on
IBD to enhance the theoretical support of this article. Or provide some description of this in the
outlook section. Alternatively, animal experiments similar to this could be added.
Please review this paper.
user
Title: Unravelling the role of beta-CGRP in inflammatory bowel disease and its potential role
in gastrointestinal homeostasis
Version: 1 Date: 24 May 2024
Reviewer's report:
Scientific Quality: Grade C (Good)
Novelty of This Manuscript: Grade C (Fair)
Creativity or Innovation of This Manuscript: Grade C (Fair)
Scientific Significance of the Conclusion in This Manuscript: Grade C (Fair)
Language Quality: Grade B (Minor language polishing)
Conclusion: Minor revision
Conclusion:
This experiment tested 96 patients recently diagnosed with IBD and compared their morning
serum # - CGRP levels with 50 matched healthy controls and 50 patients with chronic migraine.
The results showed that the # - CGRP levels in IBD patients were lower than those in healthy
controls and chronic migraine patients. In terms of diagnosing subtypes of IBD, the # - CGRP
levels in ulcerative colitis and Crohn's disease are significantly lower than those in healthy
controls and chronic migraine patients. The conclusion is that compared with healthy controls
and chronic migraine patients, patients diagnosed with various IBDs recently have significantly
reduced serum # - CGRP levels, strongly supporting the role of this neuropeptide in the
pathophysiology of IBD from an early stage onwards. The authors also believe that # - CGRP
has a protective effect in gastrointestinal homeostasis. However, there are still several issues
that need attention:
1. Please describe the reasons for excluding the use of biological agents in the inclusion criteria.
Is there any relevant literature to prove that biological agents have an impact on CGRP? Or does
mesalazine and steroids have no effect on CGRP?
2. As mentioned earlier, # CGRP mainly exists in the intermuscular neurons of the small intestine
and colon. When selecting samples, please explain why not use colon specimens from IBD
patients to explore more accurate local changes, but rather to explore more comprehensive
changes in IBD patients? If it is indeed difficult to obtain specimens, can a small amount of
samples be used to explore the difference between circulating and local CGRP in advance?
3. The author mentioned in the discussion section that existing literature has shown a decrease
in the expression of CGRP and CGRP mRNA in the intestinal mucosa of UC patients. Can the
differences and focuses between this experiment and this literature be understood as differences
in the selection of disease stages for IBD patients? Or rather, focus on proving the causal
relationship between CGRP and IBD? Suggest adding a paragraph to describe the innovation
and highlights of this article.
4. Please carefully verify the accuracy of each cited literature, such as reference 31, which does
not seem to contain the keyword CGRP.
5. Can you add some literature related to basic experiments on the early effects of CGRP on
IBD to enhance the theoretical support of this article. Or provide some description of this in the
outlook section. Alternatively, animal experiments similar to this could be added.
assistant