title: Apolipoprotein E-deficient mice develop an anti-Chlamydophila pneumoniae T helper 2 response and resist vascular infection.
abstract: BACKGROUND
  Hypercholesterolemia could inhibit the immune response against various pathogens. No information is available about its impact on the immune response toward Chlamydophila pneumoniae.
  
  
  METHODS
  Apolipoprotein E (apoE)-deficient and wild-type mice fed a normal diet were infected with a single intranasal inoculation of viable C. pneumoniae.
  
  
  RESULTS
  Whereas interferon gamma concentrations (T helper 1 response) were similar in the lungs and spleen of apoE-deficient and wild-type mice, increased concentrations of interleukin 10, interleukin 6, and interleukin 4 (T helper 2 response) were found in the lungs of apoE-deficient mice. The spleen B lymphocyte percentage and interleukin 4 levels and serum specific antibody titers were higher in apoE-deficient mice. C. pneumoniae infection was facilitated neither in the lungs nor in the aorta of these mice. On the contrary, the number of apoE-deficient mice with detectable levels of bacterial DNA in the aorta was clearly decreased. When low-density lipoprotein receptor-deficient mice fed a normal diet were similarly infected, no difference in the interleukin 4 concentration and infection level was observed in the lungs and no protection was found in the aorta.
  
  
  CONCLUSIONS
  Mild hypercholesterolemia in mice does not facilitate C. pneumoniae persistence in the vascular wall. ApoE deficiency, rather than mild hypercholesterolemia, probably favors the development of an unusual anti-C. pneumoniae T helper 2 response and protects against vascular infection.
authors.affiliation: INSERM Unité 858, Institute of Molecular Medicine of Rangueil, Institut Fédératif de Recherche F150, and University Paul Sabatier, Toulouse Cedex 4, France.
authors.forename: Dani
authors.initials: D
authors.lastname: Nazzal
authors.forename: Nicole
authors.initials: N
authors.lastname: Therville
authors.forename: Houda
authors.initials: H
authors.lastname: Yacoub-Youssef
authors.forename: Virginie
authors.initials: V
authors.lastname: Garcia
authors.forename: Mogens
authors.initials: M
authors.lastname: Thomsen
authors.forename: Thierry
authors.initials: T
authors.lastname: Levade
authors.forename: Bruno
authors.initials: B
authors.lastname: Segui
authors.forename: Hervé
authors.initials: H
authors.lastname: Benoist
mesh_terms: D000818:Animals; D001011:Aorta / Q000382:microbiology; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D023521:Chlamydophila Infections / Q000276:immunology* / Q000382:microbiology; D016993:Chlamydophila pneumoniae / Q000276:immunology / Q000472:pathogenicity*; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications; D008168:Lung / Q000382:microbiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018410:Pneumonia, Bacterial / Q000276:immunology* / Q000382:microbiology; D018418:Th2 Cells / Q000276:immunology; D014652:Vascular Diseases / Q000276:immunology* / Q000382:microbiology
chemical_list: D001057:Apolipoproteins E; D016207:Cytokines