title: Temporary upregulation of anti-inflammatory cytokine IL-13 expression in the brains of CD14 deficient mice in the early stage of prion infection.
abstract: CD14 deficient (CD14(-/-)) mice survived longer than wild-type (WT) C57BL/6J mice when inoculated with prions intracerebrally, accompanied by increased expression of anti-inflammatory cytokine IL-10 by microglia in the early stage of infection. To assess the immune regulatory effects of CD14 in detail, we compared the gene expression of pro- and anti-inflammatory cytokines in the brains of WT and CD14(-/-) mice infected with the Chandler strain. Gene expression of the anti-inflammatory cytokine IL-13 in prion-infected CD14(-/-) mice was temporarily upregulated at 75dpi, whereas IL-13 gene expression was not upregulated in prion-infected WT mice. Immunofluorescence staining showed that IL-13 was mainly expressed in neurons of the thalamus at 75dpi. These results suggest that CD14 can suppress IL-13 expression in neurons during the early stage of prion infection.
authors.affiliation: Laboratory of Veterinary Hygiene, Graduate School of Veterinary Medicine, Hokkaido University, Nishi 9, Kita 18, Kita-ku, Sapporo 060-0818, Japan.
authors.forename: Rie
authors.initials: R
authors.lastname: Hasebe
authors.affiliation: Laboratory of Veterinary Hygiene, Graduate School of Veterinary Medicine, Hokkaido University, Nishi 9, Kita 18, Kita-ku, Sapporo 060-0818, Japan.
authors.forename: Akio
authors.initials: A
authors.lastname: Suzuki
authors.affiliation: Laboratory of Veterinary Hygiene, Graduate School of Veterinary Medicine, Hokkaido University, Nishi 9, Kita 18, Kita-ku, Sapporo 060-0818, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Yamasaki
authors.affiliation: Laboratory of Veterinary Hygiene, Graduate School of Veterinary Medicine, Hokkaido University, Nishi 9, Kita 18, Kita-ku, Sapporo 060-0818, Japan. Electronic address: horiuchi@vetmed.hokudai.ac.jp.
authors.forename: Motohiro
authors.initials: M
authors.lastname: Horiuchi
mesh_terms: D000818:Animals; D001921:Brain / Q000276:immunology* / Q000378:metabolism*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D005260:Female; D018836:Inflammation Mediators / Q000378:metabolism; D018793:Interleukin-13 / Q000235:genetics* / Q000378:metabolism; D053661:Interleukin-13 Receptor alpha1 Subunit / Q000235:genetics / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D020297:Mice, Congenic; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009474:Neurons / Q000276:immunology / Q000378:metabolism; D018620:PrPSc Proteins / Q000378:metabolism; D017096:Prion Diseases / Q000235:genetics / Q000276:immunology* / Q000378:metabolism*; D013788:Thalamus / Q000276:immunology / Q000378:metabolism; D013997:Time Factors; D059467:Transcriptome; D015854:Up-Regulation
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D018793:Interleukin-13; D053661:Interleukin-13 Receptor alpha1 Subunit; D018950:Lipopolysaccharide Receptors; D018620:PrPSc Proteins
keywords: CD14; IL-13; Pathogenesis; Prion disease