Reviewer's report
Title:A redundant role for dectin-1 in experimental colitis models.
Version: 1Date:25 November 2011
Reviewer: Satish Keshav
Reviewer's report:
Review of: A redundant role for dectin-1 in experimental colitis models
Sigrid .E.M. Heinsbroek1§, Anneke Oei2, Joris J. Roelofs3, Shobhit Dhawan1,
Anje te Velde1, Siamon Gordon4, Wouter J. de Jonge1
When assessing the work, please consider the following points:
1. Is the question posed by the authors well defined? Yes
2. Are the methods appropriate and well described? Yes
3. Are the data sound? Yes
4. Does the manuscript adhere to the relevant standards for reporting and data
deposition?
5. Are the discussion and conclusions well balanced and adequately supported
by the data? Mainly yes, see below
6. Are limitations of the work clearly stated? Yes
7. Do the authors clearly acknowledge any work upon which they are building,
both published and unpublished? Yes
8. Do the title and abstract accurately convey what has been found? See below
9. Is the writing acceptable? Yes
Comments (all are discretionary revisions):
Overall this is a well-conducted study, concentrating on two out of many possible
models of intestinal inflammation. There seems to be little or no effect of genetic
deficiency of dectin-1 in these models.
Title and abstract:
The term “redundant role” implies that there is some effect that is possibly
compensated for. At the moment, however, this is speculative. An alternative title
that describes the main findings might be: “Genetic deletion of dectin-1 does not
affect the course of murine experimental colitis”
Results:
Controls for immunohistochemistry, such as isotype-matched antibody, and
dectin-1 -/- should be shown and mentioned in legend.
The TNF response by isolated macrophages to fecal extracts is much lower than
then IL-10 response, and this difference is not seen with zymozan. This merits
some discussion.
In figure 3, the levels of IL-10 are much lower in dectin1 -/- than wild-type,
although not statistically significant. In two instances, the levels are zero. This
seems like an experiment to repeat to see if indeed there is some biological
effect.
Discussion:
The antigens that elicit ASCA reactivity are not definitively known, although
Candida albicans is suspected/assumed, see, for example: Gastroenterology.
2006 May;130(6):1764-75.
Candida albicans is an immunogen for anti-Saccharomyces cerevisiae antibody
markers of Crohn's disease, and Am J Gastroenterol. 2009 Jul;104(7):1745-53.
Candida albicans colonization and ASCA in familial Crohn's disease.
The summary statement “we showed that dectin-1 is able to induce a cytokine
response towards mouse faeces” is based on indirect evidence, i.e. that the
genetic absence results in change in the response of macrophages in vitro,
rather than a formal demonstration, for instance by blocking dectin-1 signalling,
and probably should be modified. For the rest, the conclusion that this does not
substantially affect at least two models of intestinal inflammation seems fair, and
is an important contribution to the literature on the subject.
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests
Reviewer's report
Title:A redundant role for dectin-1 in experimental colitis models.
Version: 1Date:25 November 2011
Reviewer: Satish Keshav
Reviewer's report:
Review of: A redundant role for dectin-1 in experimental colitis models
Sigrid .E.M. Heinsbroek1§, Anneke Oei2, Joris J. Roelofs3, Shobhit Dhawan1,
Anje te Velde1, Siamon Gordon4, Wouter J. de Jonge1
When assessing the work, please consider the following points:
1. Is the question posed by the authors well defined? Yes
2. Are the methods appropriate and well described? Yes
3. Are the data sound? Yes
4. Does the manuscript adhere to the relevant standards for reporting and data
deposition?
5. Are the discussion and conclusions well balanced and adequately supported
by the data? Mainly yes, see below
6. Are limitations of the work clearly stated? Yes
7. Do the authors clearly acknowledge any work upon which they are building,
both published and unpublished? Yes
8. Do the title and abstract accurately convey what has been found? See below
9. Is the writing acceptable? Yes
Comments (all are discretionary revisions):
Overall this is a well-conducted study, concentrating on two out of many possible
models of intestinal inflammation. There seems to be little or no effect of genetic
deficiency of dectin-1 in these models.
Title and abstract:
The term “redundant role” implies that there is some effect that is possibly
compensated for. At the moment, however, this is speculative. An alternative title
that describes the main findings might be: “Genetic deletion of dectin-1 does not
affect the course of murine experimental colitis”
Results:
Controls for immunohistochemistry, such as isotype-matched antibody, and
dectin-1 -/- should be shown and mentioned in legend.
The TNF response by isolated macrophages to fecal extracts is much lower than
then IL-10 response, and this difference is not seen with zymozan. This merits
some discussion.
In figure 3, the levels of IL-10 are much lower in dectin1 -/- than wild-type,
although not statistically significant. In two instances, the levels are zero. This
seems like an experiment to repeat to see if indeed there is some biological
effect.
Discussion:
The antigens that elicit ASCA reactivity are not definitively known, although
Candida albicans is suspected/assumed, see, for example: Gastroenterology.
2006 May;130(6):1764-75.
Candida albicans is an immunogen for anti-Saccharomyces cerevisiae antibody
markers of Crohn's disease, and Am J Gastroenterol. 2009 Jul;104(7):1745-53.
Candida albicans colonization and ASCA in familial Crohn's disease.
The summary statement “we showed that dectin-1 is able to induce a cytokine
response towards mouse faeces” is based on indirect evidence, i.e. that the
genetic absence results in change in the response of macrophages in vitro,
rather than a formal demonstration, for instance by blocking dectin-1 signalling,
and probably should be modified. For the rest, the conclusion that this does not
substantially affect at least two models of intestinal inflammation seems fair, and
is an important contribution to the literature on the subject.
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests
Please review this paper.
user
Reviewer's report
Title:A redundant role for dectin-1 in experimental colitis models.
Version: 1Date:25 November 2011
Reviewer: Satish Keshav
Reviewer's report:
Review of: A redundant role for dectin-1 in experimental colitis models
Sigrid .E.M. Heinsbroek1§, Anneke Oei2, Joris J. Roelofs3, Shobhit Dhawan1,
Anje te Velde1, Siamon Gordon4, Wouter J. de Jonge1
When assessing the work, please consider the following points:
1. Is the question posed by the authors well defined? Yes
2. Are the methods appropriate and well described? Yes
3. Are the data sound? Yes
4. Does the manuscript adhere to the relevant standards for reporting and data
deposition?
5. Are the discussion and conclusions well balanced and adequately supported
by the data? Mainly yes, see below
6. Are limitations of the work clearly stated? Yes
7. Do the authors clearly acknowledge any work upon which they are building,
both published and unpublished? Yes
8. Do the title and abstract accurately convey what has been found? See below
9. Is the writing acceptable? Yes
Comments (all are discretionary revisions):
Overall this is a well-conducted study, concentrating on two out of many possible
models of intestinal inflammation. There seems to be little or no effect of genetic
deficiency of dectin-1 in these models.
Title and abstract:
The term “redundant role” implies that there is some effect that is possibly
compensated for. At the moment, however, this is speculative. An alternative title
that describes the main findings might be: “Genetic deletion of dectin-1 does not
affect the course of murine experimental colitis”
Results:
Controls for immunohistochemistry, such as isotype-matched antibody, and
dectin-1 -/- should be shown and mentioned in legend.
The TNF response by isolated macrophages to fecal extracts is much lower than
then IL-10 response, and this difference is not seen with zymozan. This merits
some discussion.
In figure 3, the levels of IL-10 are much lower in dectin1 -/- than wild-type,
although not statistically significant. In two instances, the levels are zero. This
seems like an experiment to repeat to see if indeed there is some biological
effect.
Discussion:
The antigens that elicit ASCA reactivity are not definitively known, although
Candida albicans is suspected/assumed, see, for example: Gastroenterology.
2006 May;130(6):1764-75.
Candida albicans is an immunogen for anti-Saccharomyces cerevisiae antibody
markers of Crohn's disease, and Am J Gastroenterol. 2009 Jul;104(7):1745-53.
Candida albicans colonization and ASCA in familial Crohn's disease.
The summary statement “we showed that dectin-1 is able to induce a cytokine
response towards mouse faeces” is based on indirect evidence, i.e. that the
genetic absence results in change in the response of macrophages in vitro,
rather than a formal demonstration, for instance by blocking dectin-1 signalling,
and probably should be modified. For the rest, the conclusion that this does not
substantially affect at least two models of intestinal inflammation seems fair, and
is an important contribution to the literature on the subject.
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests
assistant