{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T16:00:58Z","timestamp":1758816058121,"version":"3.41.2"},"reference-count":33,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2017,2,9]],"date-time":"2017-02-09T00:00:00Z","timestamp":1486598400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100004752","name":"State Government of Victoria","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004752","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Helicobacter"],"published-print":{"date-parts":[[2017,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Complex I is the first enzyme complex in the mitochondrial respiratory chain, responsible for generating a large fraction of energy during oxidative phosphorylation. Recently, it has been identified that complex I deficiency can result in increased inflammation due to the generation of reactive oxygen species by innate immune cells. As a reduction in complex I activity has been demonstrated in human stomachs with atrophic gastritis, we investigated whether complex I deficiency could influence <jats:italic>Helicobacter pylori<\/jats:italic> pathogenesis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p><jats:italic>Ndufs6<\/jats:italic><jats:sup><jats:italic>gt<\/jats:italic>\/<jats:italic>gt<\/jats:italic><\/jats:sup> mice have a partial complex I deficiency. Complex I activity was quantified in the stomachs and immune cells of <jats:italic>Ndufs6<\/jats:italic><jats:sup><jats:italic>gt<\/jats:italic>\/<jats:italic>gt<\/jats:italic><\/jats:sup> mice by spectrophotometric assays. <jats:italic>Ndufs6<\/jats:italic><jats:sup><jats:italic>gt<\/jats:italic>\/<jats:italic>gt<\/jats:italic><\/jats:sup> mice were infected with <jats:italic>H.\u00a0pylori<\/jats:italic> and bacterial colonization assessed by colony\u2010forming assay, gastritis assessed histologically, and <jats:italic>H.\u00a0pylori \u2010<\/jats:italic>specific humoral response quantified by <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The immune cells and stomachs of <jats:italic>Ndufs6<\/jats:italic><jats:sup><jats:italic>gt<\/jats:italic>\/<jats:italic>gt<\/jats:italic><\/jats:sup> mice were found to have significantly decreased complex I activity, validating the model for assessing the effects of complex I deficiency in <jats:italic>H.\u00a0pylori<\/jats:italic> infection. However, there was no observable effect of complex I deficiency on either <jats:italic>H.\u00a0pylori<\/jats:italic> colonization, the resulting gastritis, or the humoral response.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Although complex I activity is described to suppress innate immune responses and is decreased during atrophic gastritis in humans, our data suggest it does not affect <jats:italic>H.\u00a0pylori<\/jats:italic> pathogenesis.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hel.12378","type":"journal-article","created":{"date-parts":[[2017,2,9]],"date-time":"2017-02-09T06:06:44Z","timestamp":1486620404000},"source":"Crossref","is-referenced-by-count":1,"title":["No evidence of a role for mitochondrial complex I in <i>Helicobacter pylori<\/i> pathogenesis"],"prefix":"10.1111","volume":"22","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1742-6203","authenticated-orcid":false,"given":"Garrett 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