Serum levels of n-3 and n-6 polyunsaturated fatty acids in patients with systemic lupus erythematosus and their association with disease activity: a pilot study

Abstract

Objective: Polyunsaturated fatty acids (PUFAs) may modulate the inflammatory process in systemic autoimmune diseases, including systemic lupus erythematosus (SLE). The aim of this study was to assess the serum concentrations of essential 18-carbon PUFAs and their long-chain derivatives in patients with SLE and healthy controls, and to analyse their associations with laboratory and clinical features of the disease. Method: n-6 and n-3 PUFA composition was assessed in the sera of 30 SLE patients and 20 healthy controls using gas chromatography-mass spectrometry. We investigated the associations between PUFAs and disease activity measured with Systemic Lupus Erythematosus Activity Index (SLEDAI) scores, erythrocyte sedimentation rate, C-reactive protein, complement C3 and C4 concentrations, anti-nuclear antibody (ANA) titre, anti-double-stranded DNA (anti-dsDNA) antibody concentration, and medications. Results: Serum linoleic acid (LA) and α-linolenic acid concentrations were significantly higher in SLE patients compared with healthy controls. LA concentration correlated positively with the ANA titre and corticosteroid doses; eicosapentaenoic acid (EPA) and docosahexaenoic acid correlated inversely with anti-dsDNA antibody concentration. Patients treated with immunosuppressants had significantly lower concentrations of LA, arachidonic acid, and EPA. Conclusion: Both n-6 and n-3 PUFA precursors can participate in the inflammatory process in SLE patients. The mechanism of the PUFA metabolism disturbance needs further exploration.

A Review of Metabolomic Profiling in Rheumatoid Arthritis: Bringing New Insights in Disease Pathogenesis, Treatment and Comorbidities

“…Therefore, many immune-related inflammatory disorders, such as IBDs, diabetes mellitus, RA and systemic lupus erythematosus (SLE), have been associated with altered gut microbiota [ 63 , 65 , 66 ]. In SLE, bile acids, including deoxycholic acid, GCA, isohyodeoxycholic acid and arachidonic acid, were significantly correlated with the SLEDAI score [ 54 , 67 ]. Increased levels of primary bile acids, including cholic acid (CA), glycocholic acid (GCA), taurocholic acid (TCA) and glycochenodeoxycholic acid (GCDCA), were also observed in feces from SLE patients, and they showed power to predict the SLEDAI score [ 28 , 50 , 58 , 59 ].…”

Clinical Value of Serum Neuron-Specific Enolase Combined with Serum S100B Protein in the Diagnosis of Systemic Lupus Erythematosus

“…In the late 1970s, F. Michetti et al first detected S100B protein extracellular [ 29 ]. They found that the level of S100B was significantly increased in the cerebrospinal fluid of patients with multiple sclerosis in the acute phase, while the level of S100B protein was found to be lower in the stable phase of the disease, suggesting that this protein is not limited to nerve tissue [ 30 , 31 ]. Since then, its distribution has been found in specific cell types of nonneural tissue [ 32 ].…”

“…In the same model, inhibition of the protein can reduce behavioral and pathological changes [ 32 ]. Moreover, intracerebroventricular injection of S100B has also been reported to induce dentate neurogenesis and improve cognitive function in the model of experimental traumatic brain injury (lateral fluid shock) [ 31 ]. It was found that the level of S100B in patients with SLE was significantly higher compared to the control group, suggesting that the increase of S100B protein was related [ 35 ].…”

Life factors acting on systemic lupus erythematosus

“…In the last thirty years, numerous studies in murine SLE models such as NZBWF1, BXSB/MpJ, and MRL-1pr/1pr mice reported that fish and olive oils containing N-3 PUFA effectively attenuated plasma auto-antibodies, proteinuria, and kidney glomerulonephritis as well as increased lifespan of animals, compared with the phenotypes of mice fed with beef tallow that contained saturated fatty acids, N-6 PUFA, or N-9 monounsaturated fatty acids (N-9 MUFA) ( Figure 1 ) ( 7 – 12 ). Furthermore, an increasing number of human clinical trials demonstrated that consumption of N-3 PUFA had positive effects on autoimmune glomerulonephritis conditions, such as lupus nephritis and others ( 13 – 17 ). Since the earliest clinical trial in 1989, there have been seven major published clinical studies focusing on the relationship between N-3 PUFA and SLE.…”

“…In contrast, N-6 PUFA-containing corn oil, safflower oil, and sunflower oil, which all induced the production of plasma auto-antibodies, proteinuria, and glomerulonephritis by increasing mRNA expression levels of the above-mentioned CD4 + T cell-associated genes in the kidney and/or spleen, contributed to the development of autoimmune reactions in NZBWF1 mice ( 11 ). The N-6 PUFA precursor was also shown to participate in the inflammatory process in SLE patients in a clinical study ( 13 ). However, the precise molecular mechanisms of N-3 PUFA and N-6 PUFA effects in SLE models remain unclear, and further studies are needed to confirm and correctly interpret the results of the published accounts.…”