Lipopolysaccharide aggravates cerebral pathology in B10.PL-derived CD1-/-, beta2m-/-, TCRalpha-/-, and TCRdelta-/- knockout mice

Folia Biol (Krakow). 2006;54(3-4):139-44. doi: 10.3409/173491606778557446.

Abstract

Adult B10.PL-derived immunological genes knockout mice injected with 100 microg lipopolysaccharide (LPS) showed severe hydrocephalus and meningitis. A consequence of the hydrocephalus is pineal hyperplasia, sponginess of periventricular parenchyma, gliosis and, at the last stage of hydrocephalus formation, disappearance of the ependymal layer and the Gomori-positive subependymal astrocytes. Possible mechanisms for the aggravation of cerebral pathology induced by LPS are discussed.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, CD1 / genetics
  • Antigens, CD1 / physiology*
  • Brain / drug effects*
  • Brain / pathology
  • Female
  • Lipopolysaccharides / toxicity*
  • Mice
  • Mice, Knockout
  • Receptors, Antigen, T-Cell / genetics
  • Receptors, Antigen, T-Cell / physiology*
  • beta 2-Microglobulin / genetics
  • beta 2-Microglobulin / physiology*

Substances

  • Antigens, CD1
  • Lipopolysaccharides
  • Receptors, Antigen, T-Cell
  • beta 2-Microglobulin