Establishment of a novel lupus mesenteric vasculitis mouse model and exploration of its exacerbation mechanisms - Scorecard - MDSpire
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Development of a New Mouse Model for Lupus Mesenteric Vasculitis and Investigation of Its Aggravation Mechanisms

  • By

  • Maki Fujishiro

  • Kunihiro Hayakawa

  • Yuko Kataoka

  • Marina Shinoura

  • Hiroyuki Tomita

  • Yuna Saito

  • Takuya Nishi

  • Keigo Ikeda

  • Kenji Takamori

  • Iwao Sekigawa

  • Shinji Morimoto

  • September 9, 2026

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Clinical Scorecard: Development of a New Mouse Model for Lupus Mesenteric Vasculitis and Investigation of Its Aggravation Mechanisms

At a Glance

CategoryDetail
ConditionLupus Mesenteric Vasculitis (LMV)
Key MechanismsToll-like receptor (TLR) 7/8 agonism and microbiota alterations
Target PopulationFemale NZBWF1 (BWF1) mice aged 8 weeks
Care SettingAnimal research facility

Key Highlights

  • R848 administration induced intestinal vasculitis and accelerated SLE pathology in BWF1 mice.
  • The model exhibited microbiota alterations and increased fecal propionic acid concentrations.
  • Broad-spectrum antibiotics tended to suppress LMV pathology during early induction.
  • Propionate administration appeared to attenuate intestinal vasculitis in affected mice.
  • The model allows for detailed investigation of LMV pathophysiology.

Guideline-Based Recommendations

Diagnosis

  • Diagnosis involves blood testing, imaging, and pathological examination.

Management

  • Steroids and immunosuppressants are effective treatments for LMV.

Monitoring & Follow-up

  • Monitoring for adverse effects associated with prolonged steroid and immunosuppressant use is recommended.

Risks

  • Prolonged use of steroids and immunosuppressants may lead to adverse effects.

Patient & Prescribing Data

BWF1 mice as a model for SLE-related LMV

R848 as a TLR7/8 agonist induces LMV pathology.

Clinical Best Practices

  • Utilize an integrated evaluation of imaging findings for diagnosis.
  • Consider microbiota involvement in LMV pathogenesis.

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