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Several studies have demonstrated the antagonist relationship between the two organisms via several molecular mechanisms, including competition for nutrients as well as via direct killing by hydrogen peroxide. During nasal colonization, the pneumococcus is in direct contact with the fatty acid\n                      <jats:italic toggle=\"yes\">h<\/jats:italic>\n                      18:0, which is released into the extracellular environment by\n                      <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                      . We report that\n                      <jats:italic toggle=\"yes\">h<\/jats:italic>\n                      18:0 is specifically toxic to the pneumococcus among the pathogenic streptococci, providing a unique mechanism for interspecies competition during colonization. Exposure of cells to\n                      <jats:italic toggle=\"yes\">h<\/jats:italic>\n                      18:0 revealed that\n                      <jats:italic toggle=\"yes\">S. pneumoniae<\/jats:italic>\n                      could rapidly adapt to and overcome the observed toxicity. Whole-genome analysis revealed the mechanism underlying this resistance being linked to a truncation of a glycosyltransferase in the capsule biosynthesis locus and a genomic inversion in the phase variation locus, leading to altered cell surface charge and membrane lipid composition. These physiological differences in the resistant isolates may aid in repelling toxic, charged fatty acids such as\n                      <jats:italic toggle=\"yes\">h<\/jats:italic>\n                      18:0 from the cell membrane.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        The pneumococcus and\n                        <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                        are two of the most well-characterized residents of the human nasopharynx; yet much remains unknown regarding how the two bacteria interact. Here, we describe the potential of\n                        <jats:italic toggle=\"yes\">S. aureus<\/jats:italic>\n                        -produced\n                        <jats:italic toggle=\"yes\">h<\/jats:italic>\n                        18:0, whose function and biological impact are still being described, to act as an interspecies competition molecule against\n                        <jats:italic toggle=\"yes\">S. pneumoniae<\/jats:italic>\n                        , and how the pneumococcus can adapt to overcome its toxicity.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/jb.00223-25","type":"journal-article","created":{"date-parts":[[2025,9,19]],"date-time":"2025-09-19T13:00:11Z","timestamp":1758286811000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Mechanisms of 10-hydroxyoctadecanoic acid resistance in\n                    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