Animal models and experimental medicine · 2026
Phenotypic profiling of pristane-induced mimicking human systemic lupus erythematosus in Macaca fascicularis.
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Jonny Jonny, Wirjopranoto Soetojo, Nidom Chairul A, Sudiana I Ketut, Putranto Terawan A, Pratiwi Elisa D, Mawaddah Tiza W, Nidom Astria N, Nidom Reviany V, Indrasari Setyarina, Rosytania Irma Y, Yana Hiqmah Y, Kusumastuti Sanindita
Аннотация
BACKGROUND: The development of nonhuman primate models that replicate human systemic lupus erythematosus (SLE) remains limited. This study aimed to develop a pristane-induced SLE model in Macaca fascicularis and evaluate its capacity to mimic human-like clinical and laboratory immunological alterations.
METHODS: An experimental, single-arm investigation was performed using six female M. fascicularis (2-3 years old, 3-4 kg), which received a single intraperitoneal pristane injection (5 mL/kg body weight) to induce SLE and were monitored biweekly.
RESULTS: Throughout the 24-week study period, all macaques developed hallmark SLE-like changes without requiring a booster, including a pronounced increase in antinuclear antibody titers (p = 0.002), with anti-dsDNA positivity detected at the study endpoint. Significant decline was observed in hemoglobin, leukocyte, and lymphocyte count (p < 0.05), reflecting hematologic perturbations consistent with human SLE. Physiologic deterioration, manifested as hyperthermia and weight loss, also emerged early (p = 0.001). Biochemical assessment demonstrated mild hepatic and renal dysfunction marked by elevated serum glutamic pyruvic transaminase (SGPT) and urea concentrations (p < 0.05). Uniform proteinuria further indicated renal involvement, although the absence of hematuria suggests a spectrum of renal injury that may be less severe than that observed in advanced human SLE and may require longer observation.
CONCLUSION: Overall, the reproducibility of autoantibody elevation and multisystem involvement demonstrates the model's translational potential. This nonhuman primate model offers a significant framework for investigating SLE pathogenesis and assessing novel therapy approaches.
METHODS: An experimental, single-arm investigation was performed using six female M. fascicularis (2-3 years old, 3-4 kg), which received a single intraperitoneal pristane injection (5 mL/kg body weight) to induce SLE and were monitored biweekly.
RESULTS: Throughout the 24-week study period, all macaques developed hallmark SLE-like changes without requiring a booster, including a pronounced increase in antinuclear antibody titers (p = 0.002), with anti-dsDNA positivity detected at the study endpoint. Significant decline was observed in hemoglobin, leukocyte, and lymphocyte count (p < 0.05), reflecting hematologic perturbations consistent with human SLE. Physiologic deterioration, manifested as hyperthermia and weight loss, also emerged early (p = 0.001). Biochemical assessment demonstrated mild hepatic and renal dysfunction marked by elevated serum glutamic pyruvic transaminase (SGPT) and urea concentrations (p < 0.05). Uniform proteinuria further indicated renal involvement, although the absence of hematuria suggests a spectrum of renal injury that may be less severe than that observed in advanced human SLE and may require longer observation.
CONCLUSION: Overall, the reproducibility of autoantibody elevation and multisystem involvement demonstrates the model's translational potential. This nonhuman primate model offers a significant framework for investigating SLE pathogenesis and assessing novel therapy approaches.