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This study aimed to investigate the anti-virulence efficacy of tigecycline against\n              <jats:italic>S. aureus<\/jats:italic>\n              . We used highly virulent\n              <jats:italic>S. aureus<\/jats:italic>\n              strains SA75 and JP30 to evaluate the effect of tigecycline on virulence, both of them isolated from the clinic. The MIC value of tigecycline against SA75 was 0.125 \u00b5g\/mL, and that against JP30 was 0.25 \u00b5g\/mL. Tigecycline did not affect the growth ability of bacteria at 0.015 \u00b5g\/mL. Thus, subsequent discussions will focus on the effect of antibiotics at the latter subinhibitory concentrations that did not affect growth. First, the sub-MICs of tigecycline not only enhanced the sensitivity of\n              <jats:italic>S. aureus<\/jats:italic>\n              to oxidants and human whole blood but also weakened the hemolytic activity and cell adhesion level of\n              <jats:italic>S. aureus<\/jats:italic>\n              . Second, it undermined the survival of\n              <jats:italic>S. aureus<\/jats:italic>\n              in RAW264.7 and attenuated the macrophage inflammatory response induced by\n              <jats:italic>S. aureus<\/jats:italic>\n              . On the contrary, tigecycline decreased the hemolytic activity, as well as the skin abscess formation and bacterial burden in mice. Most importantly, it significantly decreased the expression of\n              <jats:italic>hla<\/jats:italic>\n              ,\n              <jats:italic>hlgB<\/jats:italic>\n              ,\n              <jats:italic>hlgC<\/jats:italic>\n              ,\n              <jats:italic>spa<\/jats:italic>\n              ,\n              <jats:italic>sbi<\/jats:italic>\n              ,\n              <jats:italic>saeR<\/jats:italic>\n              ,\n              <jats:italic>sak<\/jats:italic>\n              ,\n              <jats:italic>tst<\/jats:italic>\n              , and\n              <jats:italic>coa<\/jats:italic>\n              genes by RT-qPCR and the protein expression of \u03b1-toxin. Altogether, the sub-MICs of tigecycline might be a promising agent to attenuate the virulence of\n              <jats:italic>S. aureus<\/jats:italic>\n              and its host immune response by inhibiting the SaeRS two-component system and the product of \u03b1-toxin.\n            <\/jats:p>\n            <jats:sec>\n              <jats:title>IMPORTANCE<\/jats:title>\n              <jats:p>\n                In this study, the sub-MICs of tigecycline decreased the resistance of\n                <jats:italic>S. aureus<\/jats:italic>\n                to oxidants and human whole blood. Moreover, tigecycline weakened the cell adhesion level of\n                <jats:italic>S. aureus<\/jats:italic>\n                and skin abscess formation in mice by reducing bacterial burden. Remarkably, tigecycline decreased the hemolytic activity and significantly downregulated the expression of various virulence genes and \u03b1-toxin. This research highlighted that the sub-MICs of tigecycline might be a promising agent to attenuate the virulence of\n                <jats:italic>S. aureus<\/jats:italic>\n                by inhibiting the product of \u03b1-toxin.\n              <\/jats:p>\n            <\/jats:sec>\n          <\/jats:sec>","DOI":"10.1128\/spectrum.01344-24","type":"journal-article","created":{"date-parts":[[2025,3,19]],"date-time":"2025-03-19T13:01:51Z","timestamp":1742389311000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":2,"title":["Sub-inhibitory concentrations of tigecycline could attenuate the virulence of\n            <i>Staphylococcus aureus<\/i>\n            by inhibiting the product of \u03b1-toxin"],"prefix":"10.1128","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-2321-5817","authenticated-orcid":false,"given":"Junhong","family":"Shi","sequence":"first","affiliation":[{"name":"Department of Clinical 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