Reviewer's report 
 Bifidobacterium infantis strains with and without a combination of Oligofructose and Inulin (OFI) Title: 
attenuate inflammation in DSS-induced colitis in rats 
 1  24 July 2006 Version: Date: 
 Francisco Guarner Reviewer: 
Reviewer's report: 
General 
The article by Dr. Osman and coworkers reports original research on the role of bacteria on intestinal 
mucosal inflammation. These authors looked at the mechanisms by which bifidobacteria may induce 
antiinflammatory effects in a rat model of inflammation, by using two specific bifidobacteria strains with and 
without a prebiotic mixture that increases numbers and activity of bifidobacteria in the gut. The data 
presented are interesting and consistent with previous work by other investigators. The information on short 
chain fatty acids, MDA and bacterial translocation is highly original. 
------------------------------------------------------------------------------- 
Major Compulsory Revisions (that the author must respond to before a decision on publication can be reached) 
No major revisions are required 
------------------------------------------------------------------------------- 
Minor Essential Revisions (such as missing labels on figures, or the wrong use of a term, which the author 
can be trusted to correct) 
The authors did not detect TNF-alpha protein in tissue homogenates from rats with DSS colitis. This 
cytokine is present even in normal rat colonic tissue, as shown by a large number of publications in the past. 
In this paper, Il-1 was shown to be present in notable amounts, that were influenced by prebiotic and 
probiotic treatment. Il-1 and TNF are two Th1 cytokines with a parlell profile, and therefore it is diifficult to understand why IL-1 was incresed and TNF undetectable. Thus, the lack of detection of TNF is likely to 
reflect a technical problem (degradation of the protein during tissue homogenization - was a protease 
inhibitor added? - or lack of sensitivity by the Elisa kit, etc.). It would be desirable that the authors omit their comments on the role of TNF on intestinal inflammation. In this study TNF was not detected -most likely by 
technical reasons- and the authors should not conclude or suggest that TNF is not playing a role in intestinal
inflammation (Discussion, page 16, last paragraph), against the evidence achieved by a huge number of 
experimental and clinical studies. 
The data on translocation are very interesting, and perhaps the strongest part of the paper. But again there 
are data difficult to understand in table 1. In particular, the effect of DSM 15158 with or without prebiotic on 
bacterial translocation to the liver. Sometimes there is translocation in large numbers in a single rat, and no translocation in the rest of the group. Since figures can be very disperse, you may indicate number of rats postive for translocation per group rather than concentration of bacteria recovered from the liver (Then you 
should use a cualitative statistical test, like Chi-square or simliar). The authors may also consider the 
posibility of omiting the data on translocation to the liver, and show only translocation to mesenteric lymph nodes which is more reliable. ------------------------------------------------------------------------------- 
Discretionary Revisions (which the author can choose to ignore) 
There is no information on morphological lesions. Usually lesions are scored by histological examination 
using the criteria proposed by Cooper and co-workers (see reference 14). These data are very relevant to 
show whether the anti-inflammatory effect is associated with reduction of the mucosal injury. 
 Accept after minor essential revisions What next?: 
 An article of importance in its field Level of interest: 
 Acceptable Quality of written English: 
 No Statistical review: 
Declaration of competing interests: 
I declare that I have no competing interests 
Reviewer's report 
 Bifidobacterium infantis strains with and without a combination of Oligofructose and Inulin (OFI) Title: 
attenuate inflammation in DSS-induced colitis in rats 
 1  24 July 2006 Version: Date: 
 Francisco Guarner Reviewer: 
Reviewer's report: 
General 
The article by Dr. Osman and coworkers reports original research on the role of bacteria on intestinal 
mucosal inflammation. These authors looked at the mechanisms by which bifidobacteria may induce 
antiinflammatory effects in a rat model of inflammation, by using two specific bifidobacteria strains with and 
without a prebiotic mixture that increases numbers and activity of bifidobacteria in the gut. The data 
presented are interesting and consistent with previous work by other investigators. The information on short 
chain fatty acids, MDA and bacterial translocation is highly original. 
------------------------------------------------------------------------------- 
Major Compulsory Revisions (that the author must respond to before a decision on publication can be reached) 
No major revisions are required 
------------------------------------------------------------------------------- 
Minor Essential Revisions (such as missing labels on figures, or the wrong use of a term, which the author 
can be trusted to correct) 
The authors did not detect TNF-alpha protein in tissue homogenates from rats with DSS colitis. This 
cytokine is present even in normal rat colonic tissue, as shown by a large number of publications in the past. 
In this paper, Il-1 was shown to be present in notable amounts, that were influenced by prebiotic and 
probiotic treatment. Il-1 and TNF are two Th1 cytokines with a parlell profile, and therefore it is diifficult to understand why IL-1 was incresed and TNF undetectable. Thus, the lack of detection of TNF is likely to 
reflect a technical problem (degradation of the protein during tissue homogenization - was a protease 
inhibitor added? - or lack of sensitivity by the Elisa kit, etc.). It would be desirable that the authors omit their comments on the role of TNF on intestinal inflammation. In this study TNF was not detected -most likely by 
technical reasons- and the authors should not conclude or suggest that TNF is not playing a role in intestinal
inflammation (Discussion, page 16, last paragraph), against the evidence achieved by a huge number of 
experimental and clinical studies. 
The data on translocation are very interesting, and perhaps the strongest part of the paper. But again there 
are data difficult to understand in table 1. In particular, the effect of DSM 15158 with or without prebiotic on 
bacterial translocation to the liver. Sometimes there is translocation in large numbers in a single rat, and no translocation in the rest of the group. Since figures can be very disperse, you may indicate number of rats postive for translocation per group rather than concentration of bacteria recovered from the liver (Then you 
should use a cualitative statistical test, like Chi-square or simliar). The authors may also consider the 
posibility of omiting the data on translocation to the liver, and show only translocation to mesenteric lymph nodes which is more reliable. ------------------------------------------------------------------------------- 
Discretionary Revisions (which the author can choose to ignore) 
There is no information on morphological lesions. Usually lesions are scored by histological examination 
using the criteria proposed by Cooper and co-workers (see reference 14). These data are very relevant to 
show whether the anti-inflammatory effect is associated with reduction of the mucosal injury. 
 Accept after minor essential revisions What next?: 
 An article of importance in its field Level of interest: 
 Acceptable Quality of written English: 
 No Statistical review: 
Declaration of competing interests: 
I declare that I have no competing interests 
Please review this paper.
user
Reviewer's report 
 Bifidobacterium infantis strains with and without a combination of Oligofructose and Inulin (OFI) Title: 
attenuate inflammation in DSS-induced colitis in rats 
 1  24 July 2006 Version: Date: 
 Francisco Guarner Reviewer: 
Reviewer's report: 
General 
The article by Dr. Osman and coworkers reports original research on the role of bacteria on intestinal 
mucosal inflammation. These authors looked at the mechanisms by which bifidobacteria may induce 
antiinflammatory effects in a rat model of inflammation, by using two specific bifidobacteria strains with and 
without a prebiotic mixture that increases numbers and activity of bifidobacteria in the gut. The data 
presented are interesting and consistent with previous work by other investigators. The information on short 
chain fatty acids, MDA and bacterial translocation is highly original. 
------------------------------------------------------------------------------- 
Major Compulsory Revisions (that the author must respond to before a decision on publication can be reached) 
No major revisions are required 
------------------------------------------------------------------------------- 
Minor Essential Revisions (such as missing labels on figures, or the wrong use of a term, which the author 
can be trusted to correct) 
The authors did not detect TNF-alpha protein in tissue homogenates from rats with DSS colitis. This 
cytokine is present even in normal rat colonic tissue, as shown by a large number of publications in the past. 
In this paper, Il-1 was shown to be present in notable amounts, that were influenced by prebiotic and 
probiotic treatment. Il-1 and TNF are two Th1 cytokines with a parlell profile, and therefore it is diifficult to understand why IL-1 was incresed and TNF undetectable. Thus, the lack of detection of TNF is likely to 
reflect a technical problem (degradation of the protein during tissue homogenization - was a protease 
inhibitor added? - or lack of sensitivity by the Elisa kit, etc.). It would be desirable that the authors omit their comments on the role of TNF on intestinal inflammation. In this study TNF was not detected -most likely by 
technical reasons- and the authors should not conclude or suggest that TNF is not playing a role in intestinal
inflammation (Discussion, page 16, last paragraph), against the evidence achieved by a huge number of 
experimental and clinical studies. 
The data on translocation are very interesting, and perhaps the strongest part of the paper. But again there 
are data difficult to understand in table 1. In particular, the effect of DSM 15158 with or without prebiotic on 
bacterial translocation to the liver. Sometimes there is translocation in large numbers in a single rat, and no translocation in the rest of the group. Since figures can be very disperse, you may indicate number of rats postive for translocation per group rather than concentration of bacteria recovered from the liver (Then you 
should use a cualitative statistical test, like Chi-square or simliar). The authors may also consider the 
posibility of omiting the data on translocation to the liver, and show only translocation to mesenteric lymph nodes which is more reliable. ------------------------------------------------------------------------------- 
Discretionary Revisions (which the author can choose to ignore) 
There is no information on morphological lesions. Usually lesions are scored by histological examination 
using the criteria proposed by Cooper and co-workers (see reference 14). These data are very relevant to 
show whether the anti-inflammatory effect is associated with reduction of the mucosal injury. 
 Accept after minor essential revisions What next?: 
 An article of importance in its field Level of interest: 
 Acceptable Quality of written English: 
 No Statistical review: 
Declaration of competing interests: 
I declare that I have no competing interests 
assistant