A direct effect of sulfatide against development of fibrosis

In an interesting article, Zhou and Liu [1] suggest that development of fibrosis in the liver might be due to LDL-associated sulfatide activation of type II NKT cells which somehow should be responsible for fibrosis development [1]. Fibrosis in the liver is a huge problem, also for later development of cirrhosis. Although we agree that sulfatide stimulates type II NKT cells [2], we think another explanation for fibrosis may be important. Recently, we have published that the sphingolipid, sulfatide, inhibits formation of fibrosis from fibroblast cells [3]. Sulfatide alter gene expression of fibroblast in gene pathways associated with cell cycle/growth, transforming growth factor-β function, and encoding of proteins involved in intracellular signaling [3]. It fits well with the fact that in the pancreatic islets of Langerhans, there is insulin which is a trophic factor for cell growth but no fibrosis development likely due to presence of sulfatide. On the other hand, when insulin is injected for therapeutic reason in subcutaneous tissue, the patient must change anatomic area because of development of fibrosis in the injection site as sulfatide is absent. This is, as mentioned, not a problem in the pancreas where the sphingolipid is present in relatively high amounts [4]. It might well be that the attachment of sulfatide to LDL masks its effect and hence sulfatide is not able to inhibit the fibrosis which fits well with the condition [5]. Thus, there is a direct effect of sulfatide against the development of fibrosis which may be a suitable explanation for the effect in the liver.

CRediT authorship contribution statement

Rikke Thea: Conceptualization, Writing – original draft, Writing – review & editing. Karsten Buschard: Conceptualization, Writing – original draft, Writing – review & editing.

Conflict of interest

The authors have declared that no conflict of interest exists.