Pristane is a colorless, odorless liquid primarily obtained from natural sources such as shark liver oil and is also found in small quantities in various plants and marine organisms[1]. Pristane is extensively used in medical research for its ability to induce autoimmune diseases in animal models, making it a valuable tool for studying the pathogenesis of conditions such as rheumatoid arthritis (RA) and lupus[4][5][6][7].
In vitro, Pristane treatment (5-400μM) on mouse strain-derived thymus lymphoma BW5147 cells for 48h induced apoptosis in a time- and dose-dependent manner via the mitochondrial pathway proved by the release of cytochrome c[2]. Pristane (1mM) stimulated bone marrow-derived macrophages (BMM) for 6 or 24h induced autophagy in BMMs and upregulated TLR3 expression by activating the STAT1-IRF1 pathway[3].
In vivo, BALB/c mice received a single i.p. injection of 0.5mL Pristane revealed the development of immune complex‐mediated glomerulonephritis, a hallmark of SLE. The autoimmune syndrome induced by Pristane in BALB/c mice resembles idiopathic SLE in humans including the development of anti-nuclear antibodies[4]. 0.5mL Pristane‐injected Swiss Jim Lambert mice developed severe glomerulonephritis characterized by proteinuria, mesangial proliferation, and glomerular immune complex deposits like in BALB/c mice. Unexpectedly, the predominant autoantibodies induced by Pristane in SJL mice were not those associated with Pristane-induced disease in BALB/c mice but, anti-ribosomal P, another lupus-related specificity. The autoantibodies were strongly reactive with the C-terminal 22 amino acids of the ribosomal P2 protein, indicating that they exhibited similar fine specificities to anti-P Abs in human SLE[6]. In contrast, C57BL/6J mice administrated with Pristane (0.5mL) via intraperitoneal injection exhibited milder nephritis, characterized by decreased levels of CD3 and CD4 in total leukocytes with upregulation of CD11b, Ly6G, Ly6C, F4/80, and CD86[6]. LEW rats administrated with 150μl of Pristane with an intradermal injection at the base of the tail developed severe arthritis with a sudden onset 2 to 3 weeks after treatment. By day 122, the clinically affected joints were severely compromised by the erosions and cartilage was almost completely lost[7].
References:
[1] Avigan J, Milne G W A, Highet R J. The occurrence of pristane and phytane in man and animals. 1967 Dec;144(1),0–131.
[2] Calvani N, Caricchio R, Tucci M, et al. Induction of apoptosis by the hydrocarbon oil pristane: implications for pristane-induced lupus. J Immunol. 2005 Oct 1;175(7):4777-82.
[3] Zhu W H, Xu J, Jiang C S, et al. Pristane induces autophagy in macrophages, promoting a STAT1-IRF1-TLR3 pathway and arthritis. Clin Immunol. 2017 Feb:175:56-68.
[4] Satoh M, Kumar A, Kanwar Y S, Reeves W H. Anti-nuclear antibody production and immune-complex glomerulonephritis in BALB/c mice treated with pristane. Proc Natl Acad Sci USA. 1995 Nov 21;92(24):10934-8.
[5] Satoh M, Hamilton KJ, Ajmani AK, et al. Autoantibodies toribosomal P antigens with immune complex glomerulonephritisin SJL mice treated with pristane. J Immunol. 1996;157(7):3200‐3206.
[6] Zhou Y L, Yang B B, Long H J, et al. Immune cell alterations in a pristane-induced lupus model in C57BL/6J mice. Rheumatology & Autoimmunity. 2024 Nov 27. 2767-1410
[7] Vingsbo C, Sahlstrand P, Brun J G, et al. Pristane-induced arthritis in rats: a new model for rheumatoid arthritis with a chronic disease course influenced by both major histocompatibility complex and non-major histocompatibility complex genes. Am J Pathol. 1996 Nov;149(5):1675-83.