Plasma Zonulin as a Biomarker of Divergent Channels Latency in Systemic Lupus Erythematosus?

Background: Systemic lupus erythematosus (SLE) is an autoimmune disorder with a chronic intermittent course, a characteristic that suggests an involvement of divergent channels. According to Chinese medicine, divergent channels divert the pathogens to joints, where they are held transiently in a latent state, in order to keep them away from internal organs. The purpose of the present work is to determine whether, in SLE subjects, the levels of certain markers of gut leakage (zonulin), fungal translocation or proliferation of [(1→3)-β-D-glucan], and protective mechanisms (FGF21) are associated with the type of organ involvement or with the type of joint involvement (small vs. large joints) and to explore potential connections with the Chinese medicine perspective on SLE, conceptualized as pathology of the divergent channels. Methods: The study had a cross-sectional design and included an SLE group (n = 33) and a control group (n = 24) of subjects. Plasma levels of zonulin, (1→3)-β-D-glucan, and FGF21 were measured using indirect ELISA. Results: Despite the fact that SLE patients exhibited higher plasma zonulin levels when compared to controls [4.709 (1.996-10.426), n = 33 vs. 1.973 (1.371-3.05925), n = 24, p = 0.004], [median (IQR)], there was no difference in plasma zonulin levels between SLE patients with large joint involvement and controls. Plasma (1→3)-β-D-glucan was also higher in the SLE group than in controls [119.444 (82.746-277.66), n = 33 vs. 77.893 (47.524-124.7495), n = 24, p = 0.01]. Cutaneous involvement was significantly more frequent in patients with large joint (p = 0.03) and small joint (p = 0.006) involvement than in those without articular involvement. Conclusions: Plasma zonulin may be correlated with the degree of SLE latency in joints (divergent channels activation). The engagement of divergent channels, reflected by articular involvement, appears to be associated with a greater propensity for sinew channel activation as a potential mechanism of pathogen evacuation.