Bacterial sepsis and chemokines

Makiko Kobayashi, Yasuhiro Tsuda, Tsuyoshi Yoshida, Dan Takeuchi, Tokuichiro Utsonomiya, Hitoshi Takahashi, Fujio Suzuki

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Bacterial sepsis causes a high mortality rate when it occurs in patients with compromised host defenses. Severely burned patients, typical immunocompromised hosts, are extremely susceptible to infections from various pathogens, and a local wound infection frequently escalates into sepsis. In these patients, Staphylococcus aureus, Enterococcus faecalis and Pseudomonas aeruginosa are familiar pathogens that cause opportunistic infections. Also, polymicrobial sepsis frequently occurs in these patients. In this review, therefore, the roles of chemokines in thermally injured patients infected with these 3 pathogens and polymicrobial sepsis will be discussed. These infections in thermally injured patients may be controlled immunologically, because immunocompetent hosts are resistant to infections with these pathogens. Classically activated macrophages (M1Mφ) are major effector cells for host innate immune responses against these infections. However, M1Mφ are not generated in thermally injured patients whose alternatively activated macrophages (M2Mφ) predominate. M2Mφ appear in patients early after severe bum injuries. M2Mφ inhibit M1Mφ generation through the secretion of CCL17 and IL-10. As a modulator of Mφ, two different subsets of neutrophils (PMN-I, PMN-II) are described. PMN-I direct the polarization of resident Mφ into M1Mφ through the production of CCL3. M2Mφ are induced from resident Mφ by CCL2 released from PMN-II. Therefore, as an inhibitor of CCL2, glycyrrhizin protects individuals infected with S. aureus. Sepsis stemming from P. aeruginosa wound infection is also influenced by CCL2 released from immature myeloid cells. A large number of immature myeloid cells appear in association with burn injuries. Host resistance to S. aureus, E. faecalis, P. aeruginosa or polymicrobial infections may be improved in thermally injured patients through the induction of M1Mφ, elimination of CCL2 and/or depletion of M2Mφ induced by CCL2.

Original languageEnglish (US)
Pages (from-to)119-134
Number of pages16
JournalCurrent Drug Targets
Volume7
Issue number1
DOIs
StatePublished - Jan 2006

Fingerprint

Pathogens
Chemokines
Sepsis
Macrophages
Glycyrrhizic Acid
Pseudomonas aeruginosa
Staphylococcus aureus
Enterococcus faecalis
Interleukin-10
Wound Infection
Myeloid Cells
Modulators
Infection
Polarization
Opportunistic Infections
Wounds and Injuries
Immunocompromised Host
Coinfection
Innate Immunity
Neutrophils

Keywords

  • Burn injury
  • CCL2
  • CCL3
  • M1 macrophages
  • M2 macrophages
  • Opportunistic infections
  • PMN-I
  • PMN-II

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmaceutical Science

Cite this

Kobayashi, M., Tsuda, Y., Yoshida, T., Takeuchi, D., Utsonomiya, T., Takahashi, H., & Suzuki, F. (2006). Bacterial sepsis and chemokines. Current Drug Targets, 7(1), 119-134. https://doi.org/10.2174/138945006775270169

Bacterial sepsis and chemokines. / Kobayashi, Makiko; Tsuda, Yasuhiro; Yoshida, Tsuyoshi; Takeuchi, Dan; Utsonomiya, Tokuichiro; Takahashi, Hitoshi; Suzuki, Fujio.

In: Current Drug Targets, Vol. 7, No. 1, 01.2006, p. 119-134.

Research output: Contribution to journalArticle

Kobayashi, M, Tsuda, Y, Yoshida, T, Takeuchi, D, Utsonomiya, T, Takahashi, H & Suzuki, F 2006, 'Bacterial sepsis and chemokines', Current Drug Targets, vol. 7, no. 1, pp. 119-134. https://doi.org/10.2174/138945006775270169
Kobayashi M, Tsuda Y, Yoshida T, Takeuchi D, Utsonomiya T, Takahashi H et al. Bacterial sepsis and chemokines. Current Drug Targets. 2006 Jan;7(1):119-134. https://doi.org/10.2174/138945006775270169
Kobayashi, Makiko ; Tsuda, Yasuhiro ; Yoshida, Tsuyoshi ; Takeuchi, Dan ; Utsonomiya, Tokuichiro ; Takahashi, Hitoshi ; Suzuki, Fujio. / Bacterial sepsis and chemokines. In: Current Drug Targets. 2006 ; Vol. 7, No. 1. pp. 119-134.
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