1150. Staphylococcus aureus Colonisation is Associated with Elevated Intra-Nasal Levels of Neutrophil Chemotaxins and the Neutrophil-Inhibitory Peptide Resistin
Session: Poster Abstract Session: Innate and Adaptive Immunity to Infections
Saturday, October 22, 2011
Room: Poster Hall B1
Handouts
  • IDSA SA colonisation & nasal secretions.pdf (633.5 kB)
  • Background: 

    Persistent S. aureus colonisation predisposes to infection. Current decolonisation therapy temporarily reduces bacterial burden. Investigating colonisation pathophysiology may identify new therapeutic targets. Bacterial factors involved in colonisation are conserved across S. aureus lineages. Despite universal exposure, one third of adults are colonised. This implies host-specific factors may determine in whom colonisation occurs. Host determinants of colonisation are poorly understood. Atopic dermatitis, characterised by a Th2-skewed immune response, and impaired neutrophil function have been implicated as potential risk factors by epidemiological studies. The hypothesis that colonisation is associated with these factors was investigated.

    Methods: 

    Patients were classified as persistently, transiently and non-colonised on the basis of two nasal swabs taken ≥5 days apart (S. aureus from both, one or neither swab). Th1, Th2 and Th17 signalling, complement activation and phagocyte recruitment factors were measured in nasal secretions and serum by Luminex® assay and ELISA. S. aureus isolates were strain-typed.

    Results: 

    63 persistently and 55 non-colonised individuals were recruited. Persistent colonisation was associated with significantly elevated intra-nasal levels of IL1β (114.2 vs. 52.2pg/ml, p=0.01), G-CSF (129.5 vs. 54.1pg/ml, p=0.02) and resistin (29.5 vs. 4.5ng/ml, p=0.01). Serum immune profiles did not differ with colonisation status. Intra-nasal levels of IL1β, G-CSF and resistin were strongly positively correlated with each other (r=0.58-0.72). Immune profiles did not differ by isolate lineage. Demographics, co-morbidity or illness severity did not vary by colonisation status.

    Conclusion: 

    IL1β and G-CSF are phagocyte chemotaxins. Resistin is a macrophage-derived peptide that inhibits the neutrophil respiratory burst. Colonisation appears to elicit intra-nasal phagocyte recruitment. Failure to eradicate S. aureus may be associated with resistin-mediated impairment of intra-cellular killing as opposed to a Th2-skewed response. Research is underway investigating the cause of elevated intra-nasal resistin and whether inhibiting resistin gene transcription enhances S. aureus eradication.


    Subject Category: E. Innate and adaptive immunity to infections, including vaccine immunology

    Jonathan Lambourne, MD, PhD1, Richard Holliman, MD, MSc, DSc1,2 and Jodi Lindsay, MSc, PhD1, (1)Centre for Infection, Division of Cellular & Molecular Medicine, St George’s University of London, London, United Kingdom, (2)Department of Microbiology, St George’s Healthcare NHS Trust, London, United Kingdom

    Disclosures:

    J. Lambourne, None

    R. Holliman, None

    J. Lindsay, None

    Findings in the abstracts are embargoed until 12:01 a.m. EST Thursday, Oct. 20 with the exception of research findings presented at IDSA press conferences.