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• W2273919079 abstract "We have reported that TLR11 contributes to the murine response to flagellin and resistance to infection with Salmonella spp., including those responsible for typhoid fever in humans (Mathur et al., 2012Mathur R. Oh H. Zhang D. Park S.G. Seo J. Koblansky A. Hayden M.S. Ghosh S. Cell. 2012; 151: 590-602Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar). Here, we respond to the Correspondence in this issue of Cell by Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar, which claims that mice lacking TLR11 are not more susceptible to infection with Salmonella species and that TLR11 does not recognize Salmonella flagellin. We previously reported that murine TLR11 is important for resistance to ascending uropathogenic E. coli (UPEC) infections (Zhang et al., 2004Zhang D. Zhang G. Hayden M.S. Greenblatt M.B. Bussey C. Flavell R.A. Ghosh S. Science. 2004; 303: 1522-1526Crossref PubMed Scopus (877) Google Scholar), orally administered S. typhimurium infection (Mathur et al., 2012Mathur R. Oh H. Zhang D. Park S.G. Seo J. Koblansky A. Hayden M.S. Ghosh S. Cell. 2012; 151: 590-602Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar, Shi et al., 2012Shi Z. Cai Z. Yu J. Zhang T. Zhao S. Smeds E. Zhang Q. Wang F. Zhao C. Fu S. et al.J. Biol. Chem. 2012; 287: 43417-43423Crossref PubMed Scopus (16) Google Scholar), and infection with S. typhi (Mathur et al., 2012Mathur R. Oh H. Zhang D. Park S.G. Seo J. Koblansky A. Hayden M.S. Ghosh S. Cell. 2012; 151: 590-602Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar). We demonstrated TLR11-dependent responses to both Salmonella spp. and UPEC (Mathur et al., 2012Mathur R. Oh H. Zhang D. Park S.G. Seo J. Koblansky A. Hayden M.S. Ghosh S. Cell. 2012; 151: 590-602Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar, Shi et al., 2012Shi Z. Cai Z. Yu J. Zhang T. Zhao S. Smeds E. Zhang Q. Wang F. Zhao C. Fu S. et al.J. Biol. Chem. 2012; 287: 43417-43423Crossref PubMed Scopus (16) Google Scholar, Zhang et al., 2004Zhang D. Zhang G. Hayden M.S. Greenblatt M.B. Bussey C. Flavell R.A. Ghosh S. Science. 2004; 303: 1522-1526Crossref PubMed Scopus (877) Google Scholar) and identified flagellin, FliC, as the relevant PAMP in both UPEC and S. typhimurium (Mathur et al., 2012Mathur R. Oh H. Zhang D. Park S.G. Seo J. Koblansky A. Hayden M.S. Ghosh S. Cell. 2012; 151: 590-602Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar). In the 4 years since publication of our study (Mathur et al., 2012Mathur R. Oh H. Zhang D. Park S.G. Seo J. Koblansky A. Hayden M.S. Ghosh S. Cell. 2012; 151: 590-602Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar), we have found that the susceptibility of TLR11 knockout mice has undergone a gradual phenotypic drift—in particular, we have observed increased variability in lethality following administration of high doses of S. typhi. However, we disagree with Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar with regard to the ability of TLR11 to recognize flagellin, as we have found this interaction to be readily reproducible, though clearly occurring through a mechanism that is distinct from the recognition of Toxoplasma gondii profilin (Hatai et al., 2016Hatai H. Lepelley A. Zeng W. Hayden M.S. Ghosh S. PLoS ONE. 2016; 11: e0148987Crossref Scopus (36) Google Scholar). We propose that this discrepancy is based on dissimilar methodologies used by Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar in their interrogation of the role of TLR11 in bacterial flagellin recognition. After becoming aware of discrepant infection results obtained by Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar, we repeated these experiments and, again, observed significant differences in S. typhi dissemination comparing WT and TLR11 knockout mice (Figure 1A). Similarly, we observed increased mortality and subjective indicators of illness (data not shown) in tlr11−/− mice compared with WT controls. However, we subsequently have obtained less consistent results with recent experiments showing almost no difference in susceptibility to infection with S. typhi (Figure 1B). Our recent results are therefore more similar to the infection data of Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar, and we are unable to fully explain the differences in lethality now observed upon prolonged infection. The majority of experiments in our Cell paper were performed before or shortly after moving our colony from Yale University to Columbia University, and there have been significant changes in the housing and breeding of the TLR11 mouse colony since 2012. This includes movement within the Columbia University vivarium, as well as maintenance of the strain as a heterozygous rather than homozygous knockout colony. Pyrosequencing of the current colony indicates alteration of the intestinal microbiome in tlr11−/− mice relative to wild-type mice; however, additional studies will be necessary to determine if there have been changes over time and if these changes contribute to the phenotypic variability that we have observed. Such an environmental, potentially facility specific, effect on the relationship between TLR genotype and phenotype would not be unprecedented. For example, it was reported that tlr5−/− mice develop obesity (Vijay-Kumar et al., 2010Vijay-Kumar M. Aitken J.D. Carvalho F.A. Cullender T.C. Mwangi S. Srinivasan S. Sitaraman S.V. Knight R. Ley R.E. Gewirtz A.T. Science. 2010; 328: 228-231Crossref PubMed Scopus (1527) Google Scholar) and spontaneous colitis (Vijay-Kumar et al., 2007Vijay-Kumar M. Sanders C.J. Taylor R.T. Kumar A. Aitken J.D. Sitaraman S.V. Neish A.S. Uematsu S. Akira S. Williams I.R. Gewirtz A.T. J. Clin. Invest. 2007; 117: 3909-3921PubMed Google Scholar). However, the composition of the microbiome alters the penetrance of these TLR5-dependent phenotypes (Singh et al., 2015Singh V. Yeoh B.S. Carvalho F. Gewirtz A.T. Vijay-Kumar M. Gut Microbes. 2015; 6: 279-283Crossref PubMed Scopus (26) Google Scholar), which is consistent with our failure to observe either colitis or obesity in any tlr5−/− mice in a colony we have maintained since 2004. Changes in the composition of the intestinal microbiome also alter the susceptibility of mice to infection with Salmonella (Littman and Pamer, 2011Littman D.R. Pamer E.G. Cell Host Microbe. 2011; 10: 311-323Abstract Full Text Full Text PDF PubMed Scopus (371) Google Scholar). Therefore, it is conceivable that changes in the microbiome, either over time or between facilities, contribute to the variable phenotype of tlr11−/− mice with respect to Salmonella susceptibility. The second claim made by Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar is that TLR11 does not mediate the response to Salmonella flagellin. In support of this conclusion, Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar performed experiments using splenic dendritic cells and lamina propria macrophages. Splenic dendritic cells express TLR5, which also recognizes bacterial flagellin. Consequently, it is expected that, as observed, loss of TLR11 in these cells should not abolish the response to Salmonella flagellin. Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar have also used lamina propria macrophages, which express TLR11 but do not express TLR5 (Mathur et al., 2012Mathur R. Oh H. Zhang D. Park S.G. Seo J. Koblansky A. Hayden M.S. Ghosh S. Cell. 2012; 151: 590-602Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar). Rather than seeing no response, as would be predicted if flagellin responses were mediated solely by TLR5, Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar see a response to FliC that is unchanged in cells lacking TLR11. Although neither the cell purity nor the expression of TLR11 and TLR5 is examined in the cells sorted by Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar, the response to extracellular FliC indicates either the presence of a contaminating PAMP or the presence of contaminating TLR5-expressing cells. In addition to in vitro experiments, Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar provide in vivo data suggesting that loss of TLR11 has no effect on IL-6 or IL-12 production after flagellin injection. However, we reiterate that we do not propose that the in vivo response to flagellin is entirely TLR11 dependent; there is ample evidence implicating TLR5 in systemic flagellin responses. Therefore, as multiple cell types in the TLR11 knockout animals express TLR5, it is not very surprising that removing TLR11 does not completely abolish induction of IL6 or IL-12. Finally, Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar use a single experiment to conclude that Salmonella flagellin is not recognized by TLR11. However, the experiment presented by Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar fails to adequately support their conclusion. We have twice identified bacterial flagellin, from UPEC and Salmonella, as the ligand for TLR11 using unbiased biochemical approaches and have confirmed the association between Salmonella FliC and TLR11 using pull-down assays (Mathur et al., 2012Mathur R. Oh H. Zhang D. Park S.G. Seo J. Koblansky A. Hayden M.S. Ghosh S. Cell. 2012; 151: 590-602Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar). Furthermore, we find a clear and reproducible interaction between TLR11 and flagellin in subsequent studies (Hatai et al., 2016Hatai H. Lepelley A. Zeng W. Hayden M.S. Ghosh S. PLoS ONE. 2016; 11: e0148987Crossref Scopus (36) Google Scholar). The negative data presented by Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar rely on a dissimilar, plate-based method utilizing a truncated, unprocessed, and secreted form of TLR11 (Raetz et al., 2013Raetz M. Kibardin A. Sturge C.R. Pifer R. Li H. Burstein E. Ozato K. Larin S. Yarovinsky F. J. Immunol. 2013; 191: 4818-4827Crossref PubMed Scopus (80) Google Scholar). These two methods produce distinct observations in the case of TLR11 binding to T. gondii profilin (TPRF): we find increased interaction at pH7 compared to pH6 (Hatai et al., 2016Hatai H. Lepelley A. Zeng W. Hayden M.S. Ghosh S. PLoS ONE. 2016; 11: e0148987Crossref Scopus (36) Google Scholar), while Song et al., 2016Song J. Wilhelm C.L. Wangdi T. Maira-Litran T. Lee S.-J. Raetz M. Sturge C.R. Mirpuri J. Pei J. Grishin N.V. et al.Cell. 2016; 164 (this issue): 827-828Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar reported decreased binding above pH6 (Raetz et al., 2013Raetz M. Kibardin A. Sturge C.R. Pifer R. Li H. Burstein E. Ozato K. Larin S. Yarovinsky F. J. Immunol. 2013; 191: 4818-4827Crossref PubMed Scopus (80) Google Scholar). We find that the requirements for TLR11 binding to TPRF and FliC are distinct. Specifically, FliC is preferentially bound by the cleaved form of TLR11, while TPRF is almost exclusively bound by the uncleaved form in in vitro binding assays (Hatai et al., 2016Hatai H. Lepelley A. Zeng W. Hayden M.S. Ghosh S. PLoS ONE. 2016; 11: e0148987Crossref Scopus (36) Google Scholar). Consequently, it cannot be assumed that a recombinant, truncated, and uncleaved TLR11 ectodomain capable of binding TPRF would bind to FliC under the same conditions. In summary, our current results suggest a loss of susceptibility to infection relative to that previously reported. While we speculate that the phenotype may correlate with changes in the intestinal flora, as has been reported for the variable penetrant phenotypes attributed to loss of TLR5 (Singh et al., 2015Singh V. Yeoh B.S. Carvalho F. Gewirtz A.T. Vijay-Kumar M. Gut Microbes. 2015; 6: 279-283Crossref PubMed Scopus (26) Google Scholar, Vijay-Kumar et al., 2010Vijay-Kumar M. Aitken J.D. Carvalho F.A. Cullender T.C. Mwangi S. Srinivasan S. Sitaraman S.V. Knight R. Ley R.E. Gewirtz A.T. Science. 2010; 328: 228-231Crossref PubMed Scopus (1527) Google Scholar, Vijay-Kumar et al., 2007Vijay-Kumar M. Sanders C.J. Taylor R.T. Kumar A. Aitken J.D. Sitaraman S.V. Neish A.S. Uematsu S. Akira S. Williams I.R. Gewirtz A.T. J. Clin. Invest. 2007; 117: 3909-3921PubMed Google Scholar), further studies will be necessary to fully test this hypothesis, which may be informative in understanding the biology of Salmonella infection. A Mouse Model of Salmonella Typhi InfectionMathur et al.CellOctober 26, 2012In BriefTlr11 knockout mice are susceptible to S. Typhi infection and model human typhoid fever, providing the opportunity to test vaccine strategies in an animal model. Full-Text PDF Open ArchiveAbsence of TLR11 in Mice Does Not Confer Susceptibility to Salmonella TyphiSong et al.CellFebruary 25, 2016In BriefSalmonella enterica serovar Typhi (S. Typhi) causes typhoid fever, a systemic disease of humans that is estimated to cause more than 200,000 annual deaths (Butler, 2011; Crump and Mintz, 2010; Parry et al., 2002). Unlike other Salmonella enterica serovars, which can infect a broad range of animals, S. Typhi can only infect humans, which has hampered the development of a convenient animal model for the study of typhoid fever. Recently, it was reported in Cell (Mathur et al., 2012) that mice lacking Toll-like receptor 11 (TLR11) could be lethally infected with S. Full-Text PDF Open Archive" @default.
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• W2273919079 title "Mice Lacking TLR11 Exhibit Variable Salmonella typhi Susceptibility" @default.
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