title: Enterococcus faecalis translocation in mice with severe burn injury: a pathogenic role of CCL2 and alternatively activated macrophages (M2aMphi and M2cMphi).
abstract: Here, we investigated a role of CCL2 on the increased susceptibility of severely burned mice to Enterococcus faecalis translocation. After inoculation of Mphi from MLMphi of normal mice, 80% of the SCIDbgMN mice orally infected with the lethal dose of E. faecalis survived, and all mice inoculated with MLMphi from thermally injured mice died. At this time, SCIDbgMN mice inoculated with MLMphi from thermally injured CCL2(-/-) mice were shown to be resistant (90% survival). M1Mphi were not induced by E. faecalis antigen in cultures of MLMphi from thermally injured wild-type mice, and MLMphi from thermally injured CCL2(-/-) mice converted to M1Mphi after the antigen stimulation. MLMphi from wild-type mice 2 days postburn injury possessed M2a- and M2cMphi properties, and those from mice 7-21 days postburn injury carried M2bMphi properties. However, MLMphi from thermally injured CCL2(-/-) mice did not show any typical properties for M2a- or M2cMphi. CCL17 and CXCL13 (biomarkers for M2a- and M2cMphi), but not CCL1 (a biomarker of M2bMphi), were produced by MLMphi from thermally injured CCL2(-/-) mice treated with rCCL2. These results indicate that CCL2 converts resident MLMphi to M2a- and M2cMphi, detected early after burn injury, and decreases host antibacterial innate immunity against sepsis stemming from oral E. faecalis infection.
authors.affiliation: Department of Internal Medicine, The University of Texas Medical Branch, Galveston, TX 77555-0435, USA.
authors.forename: Kenji
authors.initials: K
authors.lastname: Shigematsu
authors.forename: Akira
authors.initials: A
authors.lastname: Asai
authors.forename: Makiko
authors.initials: M
authors.lastname: Kobayashi
authors.forename: David N
authors.initials: DN
authors.lastname: Herndon
authors.forename: Fujio
authors.initials: F
authors.lastname: Suzuki
mesh_terms: D000818:Animals; D000943:Antigens, Differentiation / Q000235:genetics / Q000276:immunology; D018988:Bacterial Translocation / Q000187:drug effects / Q000235:genetics / Q000276:immunology*; D002056:Burns / Q000235:genetics / Q000276:immunology*; D054414:Chemokine CCL17 / Q000235:genetics / Q000276:immunology; D018932:Chemokine CCL2 / Q000235:genetics / Q000276:immunology*; D054382:Chemokine CXCL13 / Q000235:genetics / Q000276:immunology; D013293:Enterococcus faecalis / Q000502:physiology*; D016908:Gram-Positive Bacterial Infections; D007113:Immunity, Innate / Q000235:genetics; D008262:Macrophage Activation / Q000187:drug effects / Q000235:genetics / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D018345:Mice, Knockout; D016513:Mice, SCID; D018805:Sepsis / Q000235:genetics / Q000276:immunology; D013997:Time Factors
chemical_list: D000943:Antigens, Differentiation; C499538:Ccl17 protein, mouse; C491768:Ccl2 protein, mouse; D054414:Chemokine CCL17; D018932:Chemokine CCL2; D054382:Chemokine CXCL13; C486386:Cxcl13 protein, mouse