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Mucin model for group B type III streptococcal infection in mice
Infection and Immunity
|February 1, 1980
Summary
This study investigated Streptococcus agalactiae virulence in mice using mucin. Iron was found not to be the factor reducing mouse resistance to this group B, type III streptococci infection.
Area of Science:
- Microbiology
- Immunology
- Infectious Diseases
Background:
- Streptococcus agalactiae (group B Streptococcus) is a significant human pathogen.
- Murine models are crucial for studying bacterial virulence and host resistance.
- Gastric mucin has been observed to enhance bacterial virulence in some models.
Purpose of the Study:
- To investigate the role of iron in mucin-mediated enhancement of Streptococcus agalactiae virulence.
- To determine if iron chelation or supplementation affects the outcome of experimental streptococcal infections.
Main Methods:
- Experimental murine infection model using intraperitoneal injection of Streptococcus agalactiae (group B, type III) in ICR Swiss mice.
- Assessment of virulence enhancement by measuring increased mortality.
- Testing the effect of mucin treated with Desferal (iron chelator) on virulence.
- Evaluating iron-dextran as a substitute for mucin in enhancing virulence.
Main Results:
- Intraperitoneal injection of Streptococcus agalactiae in hog gastric mucin significantly increased mortality in outbred ICR Swiss mice.
- Inbred C57BL6 mice showed resistance to the mucin-bacterial combination.
- Mucin treated to chelate iron retained its capacity to enhance Streptococcus agalactiae virulence.
- Iron-dextran failed to enhance the virulence of Streptococcus agalactiae.
Conclusions:
- Iron is not the resistance-lowering factor in the group B, type III Streptococcus agalactiae-mucin model.
- The mechanism by which gastric mucin enhances Streptococcus agalactiae virulence in susceptible mice requires further investigation.
- Host genetic factors (e.g., inbred C57BL6 mice) play a role in resistance to this infection model.