{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T17:02:06Z","timestamp":1790614926381,"version":"4.1.0"},"reference-count":41,"publisher":"Microbiology Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,3,1]]},"abstract":"<jats:p>The ability of<jats:italic>Staphylococcus aureus<\/jats:italic>to avoid innate immune responses including neutrophil-mediated phagocytosis is crucial for the organism to cause infection. This multifactorial process involves several secreted and cell-surface-associated proteins. In this paper we report a novel mechanism of combating neutrophils that involves iron-regulated surface determinant protein H (IsdH). The IsdH protein is part of a complex that is only expressed under iron-restricted conditions in order to bind haemoglobin and extract and transport haem into the cytoplasm. A null mutant defective in expression of IsdH, and mutants expressing variants of IsdH with substitutions in residues predicted to be involved in ligand binding, were generated from<jats:italic>S. aureus<\/jats:italic>8325-4. The IsdH-defective mutants were shown by several measures to have reduced virulence compared with the wild-type. The mutant was engulfed more rapidly by human neutrophils in the presence of serum opsonins, survived poorly in fresh whole human blood and was less virulent in a mouse model of sepsis. The protective mechanism seems to stem from an accelerated degradation of the serum opsonin C3b.<\/jats:p>","DOI":"10.1099\/mic.0.025684-0","type":"journal-article","created":{"date-parts":[[2009,2,26]],"date-time":"2009-02-26T22:56:47Z","timestamp":1235689007000},"page":"667-679","source":"Crossref","is-referenced-by-count":64,"title":["Immune evasion by Staphylococcus aureus conferred by iron-regulated surface determinant protein IsdH"],"prefix":"10.1099","volume":"155","author":[{"given":"Livia","family":"Visai","sequence":"first","affiliation":[{"name":"Center for Tissue Engineering, Via Ferrata 1, 27100 Pavia, Italy"},{"name":"Department of Biochemistry, Viale Taramelli 3\/b, 27100 Pavia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naoko","family":"Yanagisawa","sequence":"additional","affiliation":[{"name":"Microbiology Department, Moyne Institute of Preventive Medicine, Trinity College, Dublin 2, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisabet","family":"Josefsson","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, University of Gothenburg, Gothenburg, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrej","family":"Tarkowski","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, University of Gothenburg, Gothenburg, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ilaria","family":"Pezzali","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Viale Taramelli 3\/b, 27100 Pavia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suzan H. 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