High susceptibility to lipopolysaccharide-induced lethal shock in encephalomyocarditis virus-infected mice.

Abstract

Secondary bacterial infection in humans is one of the pathological conditions requiring clinical attention. In this study, we examined the effect of lipopolysaccharide (LPS) on encephalomyocarditis virus (EMCV) infected mice. All mice inoculated with EMCV at 5 days before LPS challenge died within 24 h. LPS-induced TNF-α mRNA expression was significantly increased in the brain and heart at 5 days after EMCV infection. CD11b(+)/TLR4(+) cell population in the heart was remarkably elevated at 5 days after EMCV infection, and sorted CD11b(+) cells at 5 days after EMCV infection produced a large amount of TNF-α on LPS stimulation in vivo and in vitro. In conclusion, we found that the infiltration of CD11b(+) cells into infected organs is involved in the subsequent LPS-induced lethal shock in viral encephalomyocarditis. This new experimental model can help define the mechanism by which secondary bacterial infection causes a lethal shock in viral encephalomyocarditis.

• Authors: Hirofumi Ohtaki, Hiroyasu Ito, Masato Hoshi, Yosuke Osawa, Manabu Takamatsu, Akira Hara, Tetsuya Ishikawa, Hisataka Moriwaki, Kuniaki Saito, Mitsuru Seishima
• Journal: Scientific reports (Sci Rep) Vol. 2 Pg. 367 ( 2012) ISSN: 2045-2322 [Electronic] England
• PMID: 22509465 (Publication Type: Journal Article)

Chemical References

• CD11b Antigen
• DNA Primers
• Lipopolysaccharides
• RNA, Messenger
• Toll-Like Receptor 4
• Tumor Necrosis Factor-alpha

Topics

• Animals
• Base Sequence
• CD11b Antigen (immunology)
• Cardiovirus Infections (complications, immunology, metabolism, mortality)
• DNA Primers
• Encephalomyocarditis virus (pathogenicity)
• Flow Cytometry
• Lipopolysaccharides (toxicity)
• Mice
• Mice, Inbred C57BL
• RNA, Messenger (genetics)
• Real-Time Polymerase Chain Reaction
• Toll-Like Receptor 4 (genetics)
• Tumor Necrosis Factor-alpha (biosynthesis)