Evidence for participation of the macrophage in Shiga-like toxin II-induced lethality in mice

Microb Pathog. 1990 Aug;9(2):95-103. doi: 10.1016/0882-4010(90)90083-3.

Abstract

Seven strains of inbred mice were compared for their susceptibility to the lethal effects of Shiga-like toxin II (SLT II). A/J mice, which are unable to produce the C5 component of complement, did not differ from C5 normal mice in susceptibility to SLT II. CBA/NJ mice (hemizygous for X-linked immunodeficiency) did not differ from the B-cell sufficient CBA/J strain. C3H/HeJ mice, defective in macrophage response to lipopolysaccharide (Lpsd), showed a consistently and significantly longer mean time to death than did the normally responsive C3H/HeN strain. C57BL/10ScN mice, which also carry the Lpsd allele, showed a similar but smaller difference in mean time to death compared with the C57BL/10SnJ strain. Production of tumor necrosis factor could be induced in vitro by SLT II treatment of C3H/HeN, but not C3H/HeJ macrophages. These results imply that antibody and complement production do not modulate SLT II lethality in mice, but that the macrophage may contribute to SLT II-induced injury.

MeSH terms

  • Alleles
  • Animals
  • Bacterial Toxins / toxicity*
  • Complement C5 / metabolism
  • Dexamethasone / pharmacology
  • Lipopolysaccharides / pharmacology
  • Macrophages / metabolism*
  • Mice
  • Mice, Inbred A
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Shiga Toxin 2
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Bacterial Toxins
  • Complement C5
  • Lipopolysaccharides
  • Shiga Toxin 2
  • Tumor Necrosis Factor-alpha
  • Dexamethasone