ArticlePLoS neglected tropical diseases2026
S100A4 enhances the pro-fibrotic effect of macrophage to promote collagen capsule formation of Trichinella spiralis.
Article in PLoS neglected tropical diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundTrichinella spiralis is a zoonotic parasitic nematode capable of infecting humans and animals, causing trichinellosis. It poses a critical threat to human health, livestock industry and food safety. The muscle larva of T. spiralis is encased within a collagen capsule that is believed to protect it from host immunity. A strong macrophage-dominated inflammatory infiltrate accumulates around the capsule, yet how macrophages contribute to capsule formation remains unclear. Our objective was to investigate the effect of macrophage on collagen capsule formation. METHODOLOGY/PRINCIPAL
findingsThe results of immunofluorescence showed that S100A4 ⁺ cells accumulated in T. spiralis-infected muscle, and were composed predominantly of CD206 ⁺ macrophages. These macrophages were positioned in direct contact with α-SMA+ myofibroblasts. Moreover, numerous cells positive for both CD206 (M2 macrophage canonical marker) and α‑smooth muscle actin (α-SMA, biomarker of myofibroblasts) were observed. Western blot analysis revealed that S100A4 expression was restricted chiefly to M2 macrophage and its expression was markedly amplified by IL-4 together with excretory-secretory (ES) products from muscle larvae of T. spiralis. qPCR showed that inhibiting S100a4 transcription reduced Arg1 mRNA levels in macrophages activated by ES and IL-4. Immunofluorescence and western blot analysis showed the activated macrophages induced modest upregulation of α-SMA in fibroblasts. Immunohistochemistry revealed that inhibition of S100A4 by niclosamide reduced the expressions of CD206, TGF-β1 and collagen I in T. spiralis-infected muscle. Compared with albendazole alone, the combination of niclosamide and albendazole further reduced the larval burden in T. spiralis-infected mice. CONCLUSIONS/SIGNIFICANCE: In conclusion, infection with T. spiralis significantly upregulated S100A4 expression in skeletal muscle-infiltrating macrophages. S100A4 further promoted macrophage M2 polarization. The M2-like macrophages either drove fibroblast activation or acquired myofibroblast-like features, thereby fostering collagen capsule formation. Blocking S100A4 diminished macrophage M2 polarization, prevented collagen capsule formation, and represented a potential adjunctive strategy against trichinellosis.
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