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Review
. 2014 Jul 23:5:355.
doi: 10.3389/fimmu.2014.00355. eCollection 2014.

Does Type I Interferon Limit Protective Neutrophil Responses during Pulmonary Francisella Tularensis Infection?

Affiliations
Review

Does Type I Interferon Limit Protective Neutrophil Responses during Pulmonary Francisella Tularensis Infection?

Yoichi Furuya et al. Front Immunol. .
No abstract available

Keywords: Francisella tularensis; immune evasion; mucosal immunity; neutrophil; type I interferon.

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Figures

Figure 1
Figure 1
A model depicting the proposed roles of IFN-I and neutrophils during F. tularensis infection is shown. Pulmonary infection with F. tularensis triggers IFN-I production from innate immune cells such as alveolar macrophages. IFN-I may sensitize F. tularensis-infected neutrophils for cell death and contribute to an overall reduction in neutrophil numbers at the site of infection. IFN-I may also directly limit neutrophil recruitment via inhibition of IL-17 producing γδT cells or suppression of other neutrophil chemoattractants. Suppression of neutrophil recruitment may prevent tissue damage associated with excessive infiltration of neutrophils as well as lead to inadequate bacterial clearance, resulting in an unfavorable outcome. An optimal neutrophil response may require moderate recruitment at an early time point to aid in prompt clearance of bacteria without causing significant inflammation later during pulmonary tularemia.

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References

    1. Allen LA. Interview with Dr. Lee-Ann Allen regarding pivotal advance: Francisella tularensis LVS evades killing by human neutrophils via inhibition of the respiratory burst and phagosome escape. Interview by Helene F. Rosenberg. J Leukoc Biol (2006) 80(6):1222–310.1189/jlb.1306287 - DOI - PubMed
    1. Hall JD, Woolard MD, Gunn BM, Craven RR, Taft-Benz S, Frelinger JA, et al. Infected-host-cell repertoire and cellular response in the lung following inhalation of Francisella tularensis Schu S4, LVS, or U112. Infect Immun (2008) 76(12):5843–5210.1128/IAI.01176-08 - DOI - PMC - PubMed
    1. Singh A, Rahman T, Malik M, Hickey AJ, Leifer CA, Hazlett KR, et al. Discordant results obtained with Francisella tularensis during in vitro and in vivo immunological studies are attributable to compromised bacterial structural integrity. PLoS One (2013) 8(3):e58513.10.1371/journal.pone.0058513 - DOI - PMC - PubMed
    1. Stetson DB, Medzhitov R. Recognition of cytosolic DNA activates an IRF3-dependent innate immune response. Immunity (2006) 24(1):93–10310.1016/j.immuni.2005.12.003 - DOI - PubMed
    1. Henry T, Brotcke A, Weiss DS, Thompson LJ, Monack DM. Type I interferon signaling is required for activation of the inflammasome during Francisella infection. J Exp Med (2007) 204(5):987–9410.1084/jem.20062665 - DOI - PMC - PubMed

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