Adiponectin and inflammation
American Journal of Physiology. Endocrinology and Metabolism
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 adiponectinknockout Adipoq Ϫ/Ϫ )] mice have a "markedly greater" neutrophilic infiltrate in the peritoneal cavity and a "significantly greater" cytokine production compared with wild-type (WT) mice.
... , 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