870. Does Staphylococcus aureus nasal colonization induce T-cell and inflammatory cytokine responses? Evidence from military trainees at high-risk for Staphylococcus aureus colonization and disease
Session: Poster Abstract Session: Bacterial Infections: Pathogenesis and Immunity
Friday, October 9, 2015
Room: Poster Hall
Background: Staphylococcus aureus is a major cause of skin and soft tissue infection (SSTI). Colonization of the anterior nares, the reservoir for S. aureus, is thought to be a risk factor for SSTI. Numerous studies have shown that both humoral and cellular immunity are involved in the host response to SSTI. By contrast, few studies have evaluated the host immune response to colonization among individuals without SSTI, and none to our knowledge have evaluated the impact of colonization on distributions of T-cell subsets and pro-inflammatory cytokines in serum.

Methods: From 4/2013-12/2014, we conducted a case-control study of SSTI among US Army Infantry trainees, a group known to be at increased risk for S. aureus colonization and disease. Trainees presenting to the medical clinic for non-infectious conditions (e.g. musculo-skeletal injury) were recruited as healthy controls. A nasal swab and blood sample was collected at the time of enrollment. Swabs were processed by standard methods to assess colonization status. T-cell populations in peripheral blood were assessed by flow cytometry. Serum concentrations of pro-inflammatory cytokines were assessed by 25-plex Luminex panel.

Results: Forty-seven participants without SSTI were included in the analysis. Of these, 20 (42.5%) were colonized with S. aureus. The proportion of γδ T-cells was higher among colonized as compared to non-colonized individuals (p<0.01). Moreover, proportions of Th1-cells (p<0.05) and γδ T-cells producing IFN-γ (p<0.01) were higher among colonized vs. non-colonized individuals. There were no differences between groups with respect to proportions of IL-17 producing T-cells (p=0.30). Colonized individuals also had higher serum concentrations of pro-inflammatory cytokines, specifically IFN-γ (p=0.004), MCP-1 (p=0.01), IL-1RA (p=0.02), Eotaxin (p=0.03), and MIP-1α (p=0.05). Concentrations of IL-17 did not differ between groups (p=0.14).

Conclusion: These findings suggest that nasal acquisition of S. aureus elicits a systemic immune response, namely an induction of pro-inflammatory cytokines and proliferation of Th1 and IFNγ-secreting cells. Further evaluation of this association in a longitudinal, observational study is warranted.

Lauren Nagy, PhD1, Carey Schlett, MPH2, Tianyuan Cui, MA3, Eugene Millar, PhD4, Katrina Crawford, MS5, D. Scott Merrell, PhD6, Jeffrey Lanier, MD7, Natasha Law, MA8, Nimfa Teneza-Mora, MD MPH9, Michael Ellis, MD, FIDSA10, Eric R. Hall, PhD11 and Dannett Bishop, Ph.D.1, (1)Wound Infections Department, Naval Medical Research Center, Silver Spring, MD, (2)Inf Dis Clin Res Prg, Uniform Serv Univ, Bethesda, MD, (3)Infectious Disease Clinical Research Program, Uniformed Services University, Rockville, MD, (4)Infectious Disease Clinical Research Program, Rockville, MD, (5)Uniformed Services University of the Health Sciences, Bethesda, MD, (6)Department of Microbiology, Uniformed Services University, Bethesda, MD, (7)Family Medicine, Martin Army Community Hospital, Fort Benning, GA, (8)Infectious Disease Clinical Research Program, Fort Benning, GA, (9)Naval Medical Research Center, Silver Spring, MD, (10)Department of Medicine, Uniformed Services University, Bethesda, MD, (11)U.S. Naval Medical Research Center, Silver Spring, MD

Disclosures:

L. Nagy, None

C. Schlett, None

T. Cui, None

E. Millar, None

K. Crawford, None

D. S. Merrell, None

J. Lanier, None

N. Law, None

N. Teneza-Mora, None

M. Ellis, None

E. R. Hall, None

D. Bishop, None

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