A Mycobacterium leprae Hsp65 Mutant as a Candidate for Mitigating Lupus Aggravation in Mice
Author Information
Author(s): Marengo Eliana B., de Moraes Luciana V., Melo Robson L., Balan Andrea, Fernandes Beatriz L., Tambourgi Denise V., Rizzo Luiz Vicente, Sant'Anna Osvaldo Augusto
Primary Institution: Hospital Israelita Albert Einstein, São Paulo, Brazil
Hypothesis
The administration of point-mutated K409A Hsp65 can mitigate the progression of Systemic Lupus Erythematosus in mice.
Conclusion
The K409A mutant form of Hsp65 may delay the onset of Systemic Lupus Erythematosus, representing a potential new treatment approach for autoimmune diseases.
Supporting Evidence
- Administration of wild type M. leprae Hsp65 accelerated SLE progression.
- K409A pep increased survival time compared to Leader pep.
- Combined administration of K409A and Leader pep showed enhanced survival.
- Immunomodulatory effects of K409A were similar to its corresponding protein.
Takeaway
Scientists found that a special version of a protein from bacteria can help mice with a disease called lupus live longer.
Methodology
Mice were inoculated with synthetic peptides and observed for survival over a period of 315 days.
Limitations
The study was conducted in a mouse model, which may not fully replicate human disease.
Participant Demographics
Female [NZBxNZW]F1 mice, aged 45 days.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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