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

Area of Science:

• Immunology
• Virology
• Pathology

Background:

• Secondary bacterial infections are a significant clinical concern.
• Encephalomyocarditis virus (EMCV) infection can lead to severe outcomes.
• Lipopolysaccharide (LPS) is a key component of Gram-negative bacteria.

Purpose of the Study:

• To investigate the impact of lipopolysaccharide (LPS) on mice previously infected with encephalomyocarditis virus (EMCV).
• To elucidate the mechanisms underlying LPS-induced lethality in EMCV-infected mice.

Main Methods:

• Mice were infected with EMCV and subsequently challenged with LPS.
• Tumor necrosis factor-alpha (TNF-α) mRNA expression was measured in brain and heart.
• Flow cytometry was used to analyze CD11b(+) and TLR4(+) cell populations in the heart.
• CD11b(+) cells were sorted and stimulated with LPS in vitro and in vivo.

Main Results:

• EMCV-infected mice challenged with LPS exhibited 100% mortality within 24 hours.
• LPS challenge significantly increased TNF-α mRNA expression in the brain and heart of EMCV-infected mice.
• A marked elevation in CD11b(+)/TLR4(+) cells was observed in the heart post-EMCV infection.
• Sorted CD11b(+) cells produced substantial amounts of TNF-α upon LPS stimulation.

Conclusions:

• Infiltration of CD11b(+) cells into infected organs contributes to LPS-induced lethal shock in EMCV.
• This study establishes a novel experimental model for studying lethal shock in viral encephalomyocarditis.
• Understanding these mechanisms is crucial for managing secondary bacterial infections in viral diseases.