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LETTERS TO THE EDITOR
Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois
TO THE EDITOR: I am writing concerning the article "Adiponectin deficiency promotes endothelial activation and profoundly exacerbates sepsis-related mortality" by Teoh et al. (4). In the ABSTRACT, RESULTS, and DISCUSSION of the paper, the authors repeatedly assert that thioglycollate-injected adiponectin-knockout [APN-KO (in Ref. 4 Adipoq–/–)] mice have a "markedly greater" neutrophilic infiltrate in the peritoneal cavity and a "significantly greater" cytokine production compared with wild-type (WT) mice. However, the figures showing these data (Figs. 2 and 4 in Ref. 4) do not support these claims. In fact, no statistical significance is reported between thioglycollate-injected WT and APN-KO mice for either neutrophil numbers or cytokine levels. The graph bars seem to indicate that indeed the difference is not significant, perhaps with the exception of IL-12. Therefore, it appears incorrect to state that APN deficiency elicits "a heightened inflammatory response to thioglycollate-induced peritonitis," as the authors do in the DISCUSSION. The results by Teoh et al. are actually in agreement with our recent data obtained in the closely related model of zymosan-induced peritonitis, in which we demonstrate that APN-KO mice have a response comparable to that of WT mice in terms of cytokine production and minor differences in terms of cellular infiltrate (3).
Furthermore, Teoh et al. demonstrate that administration of recombinant mouse (rm)APN reduces inflammatory infiltrate and cytokine production in both WT and APN KO mice (Figs. 2 and 4 in Ref. 4). However, data presented on page E661 indicate that administration of rmAPN to WT mice did not increase circulating APN levels. Moreover, APN-KO mice injected with rmAPN had less than 50% serum APN compared with WT mice and yet had significantly lower inflammation than WT mice. Therefore, there seems to be no correlation between the the anti-inflammatory effects of rmAPN and its ability to raise circulating APN levels. This observation, together with data presented in their Figs. 2 and 4, appears to indicate that APN is not directly involved in regulating cytokine production and neutrophilic infiltrate in response to thioglycollate and that protection afforded by administration of rmAPN may be attributable to a nonspecific effect.
Since the role of APN as a regulator of inflammation is currently the subject of debate (1, 2), it important that data on this topic be presented and discussed in an accurate fashion to reflect the actual obervations.
REFERENCES
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