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Review
. 2010 Mar;160(5-6):107-11.
doi: 10.1007/s10354-010-0765-6.

Update on the role of Toll-like receptors during bacterial infections and sepsis

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Review

Update on the role of Toll-like receptors during bacterial infections and sepsis

Sylvia Knapp. Wien Med Wochenschr. 2010 Mar.

Abstract

Toll-like receptors (TLRs) are recognition molecules that importantly contribute to the innate immune response to bacterial and viral infections. Once TLRs sense the presence of invading pathogens a signal transduction cascade is initiated that eventually leads to the production of pro-inflammatory mediators and attraction of neutrophils to the site of infection. While the ultimate goal of this defense pathway is the successful elimination of invading microbes, prolonged or exaggerated stimulation of TLR-associated events can lead to systemic inflammation and clinical symptoms of sepsis. This brief review summarizes the impact of selected TLRs in the host response to clinically important bacteria and provides insights into TLR-associated therapeutic approaches during sepsis and inflammation.

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Comment in

  • Editorial: sepsis.
    Knapp S, Frass M. Knapp S, et al. Wien Med Wochenschr. 2010 Mar;160(5-6):105-6. doi: 10.1007/s10354-010-0764-7. Wien Med Wochenschr. 2010. PMID: 20364411 No abstract available.

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References

    1. J Immunol. 2008 Mar 1;180(5):3478-84 - PubMed
    1. Arthritis Rheum. 2005 Sep;52(9):2656-65 - PubMed
    1. Blood. 2004 Dec 15;104(13):4071-9 - PubMed
    1. J Exp Med. 2005 Dec 5;202(11):1575-85 - PubMed
    1. Annu Rev Immunol. 2003;21:335-76 - PubMed

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