Abstract
ABSTRACTThe ulcer-causing pathogenHelicobacter pyloriuses directed motility, or chemotaxis, to both colonize the stomach and promote disease development. Previous work showed that mutants lacking the TlpB chemoreceptor, one of the receptors predicted to drive chemotaxis, led to less inflammation in the gerbil stomach than did the wild type. Here we expanded these findings and examined the effects on inflammation of completely nonchemotactic mutants and mutants lacking each chemoreceptor. Of note, all mutants colonized mice to the same levels as did wild-typeH. pylori. Infection by completely nonchemotactic mutants (cheWorcheY) resulted in significantly less inflammation after both 3 and 6 months of infection. Mutants lacking either the TlpA or TlpBH. pylorichemotaxis receptors also had alterations in inflammation severity, while mutants lacking either of the other two chemoreceptors (TlpC and HylB) behaved like the wild type. Fully nonchemotactic and chemoreceptor mutants adhered to cultured gastric epithelial cells and caused cellular release of the chemokine interleukin-8 in vitro similar to the release caused by the wild type. The situation appeared to be different in the stomach. Using silver-stained histological sections, we found that nonchemotacticcheYorcheWmutants were less likely than the wild type to be intimately associated with the cells of the gastric mucosa, although there was not a strict correlation between intimate association and inflammation. Because others have shown that in vivo adherence promotes inflammation, we propose a model in whichH. pyloriuses chemotaxis to guide it to a productive interaction with the stomach epithelium.
References
71
Referenced
102
10.1086/338772
10.1038/16495
10.1128/IAI.70.10.5877-5881.2002
10.1016/S0065-2911(08)60168-X
10.1084/jem.191.4.593
- Current protocols in molecular biology. 1995
10.1128/jb.179.15.4676-4683.1997
10.1146/annurev.mi.49.100195.002421
10.1073/pnas.0409873102
10.1073/pnas.93.25.14648
10.1016/S0378-1097(03)00423-3
10.1128/IAI.68.7.4335-4339.2000
10.1128/IAI.72.9.5181-5192.2004
10.1046/j.1083-4389.2002.00071.x
10.1136/jcp.48.1.41
10.1128/JB.188.7.2656-2665.2006
10.1128/IAI.01887-05
10.1128/IAI.69.5.2902-2908.2001
10.1099/00222615-37-2-123
10.1177/030098589503200506
10.1128/iai.64.7.2445-2448.1996
- Ferrero, R. L., and J. G. Fox. 2001. In vivo modeling of Helicobacter-associated gastrointestinal diseases, p. 565-582. In H. L. T. Mobley, G. Mendz, and S. L. Hazell (ed.), Helicobacter pylori: physiology and genetics. ASM Press, Washington, DC. / Helicobacter pylori: physiology and genetics. (2001)
10.1128/IAI.66.4.1349-1355.1998
10.1128/IAI.68.4.2016-2023.2000
10.1126/science.1084677
10.1073/pnas.95.7.3925
10.1128/jb.177.14.4121-4130.1995
- Hawkins, A. C., and C. S. Harwood. 2002. Chemotaxis of Ralstonia eutropha JMP134(pJP4) to the herbicide 2,4-dichlorophenoxyacetate. Appl. Environ. Microbiol.69:968-972. / Appl. Environ. Microbiol. (2002)
10.1128/IAI.71.5.2534-2541.2003
10.1128/iai.63.5.1732-1738.1995
10.1172/JCI11450
10.1128/iai.60.6.2475-2480.1992
10.1128/IAI.68.8.4598-4603.2000
10.1078/1438-4221-00173
10.1128/IAI.72.4.2358-2368.2004
10.1111/j.1462-5822.2005.00603.x
10.1016/S0016-5085(97)70155-0
10.1073/pnas.111581598
10.1099/0022-1317-51-11-958
10.1128/IAI.73.3.1820-1827.2005
10.1046/j.1523-5378.2003.00164.x
10.1038/35073084
10.1046/j.1523-5378.2003.00171.x
10.1126/science.287.5457.1497
10.1084/jem.192.11.1601
10.1016/S1286-4579(00)01274-0
10.1128/IAI.70.4.1984-1990.2002
10.1046/j.1365-2958.1997.4281787.x
10.1099/00221287-147-9-2493
10.1053/j.gastro.2006.05.001
10.1128/jb.176.9.2736-2739.1994
-
Roth, K. A., S. B. Kapadia, S. M. Martin, and R. G. Lorenz. 1999. Cellular immune responses are essential for the development of Helicobacter felis-associated gastric pathology. J. Immunol.163:1490-1497.
(
10.4049/jimmunol.163.3.1490
) / J. Immunol. (1999) 10.1046/j.1365-2036.2002.01301.x
10.1128/IAI.69.2.730-736.2001
10.1073/pnas.96.25.14559
10.1073/pnas.93.3.1259
10.1136/gut.43.1.2
10.4049/jimmunol.173.6.4197
10.1128/IAI.72.7.4138-4150.2004
10.1073/pnas.97.3.1263
10.1111/j.1365-2958.2006.05283.x
10.1128/IAI.73.2.803-811.2005
10.1038/41483
10.1128/IAI.67.6.3040-3046.1999
10.1038/ni1131
- Wang, J., T. G. Blanchard, and P. B. Ernst. 2001. Host inflammatory response to infection, p. 471-480. In H. L. T. Mobley, G. Mendz, and S. L. Hazell (ed.), Helicobacter pylori: physiology and genetics. ASM Press, Washington, DC. / Helicobacter pylori: physiology and genetics. (2001)
10.1053/gast.2002.37074
10.1073/pnas.130079797
10.1016/0378-1119(85)90120-9
10.1046/j.1365-2958.1997.2861650.x
10.1111/j.1574-6968.1997.tb12738.x
Dates
Type | When |
---|---|
Created | 18 years, 3 months ago (May 22, 2007, 12:39 p.m.) |
Deposited | 2 years, 3 months ago (May 11, 2023, 7:11 p.m.) |
Indexed | 2 months, 1 week ago (June 23, 2025, 1:42 p.m.) |
Issued | 18 years, 1 month ago (Aug. 1, 2007) |
Published | 18 years, 1 month ago (Aug. 1, 2007) |
Published Print | 18 years, 1 month ago (Aug. 1, 2007) |
@article{Williams_2007, title={Helicobacter pyloriChemotaxis Modulates Inflammation and Bacterium-Gastric Epithelium Interactions in Infected Mice}, volume={75}, ISSN={1098-5522}, url={http://dx.doi.org/10.1128/iai.00082-07}, DOI={10.1128/iai.00082-07}, number={8}, journal={Infection and Immunity}, publisher={American Society for Microbiology}, author={Williams, Susan M. and Chen, Yu-Ting and Andermann, Tessa M. and Carter, J. Elliot and McGee, David J. and Ottemann, Karen M.}, year={2007}, month=aug, pages={3747–3757} }