Trypanosoma cruzi, the causative agent of Chagas disease, modulates interleukin-6-induced STAT3 phosphorylation via gp130 cleavage in different host cells

► Inactive cruzipain triggers TLR2 and IL-6 secretion, leading to cardioprotection. ► Cruzipain enzymatically cleaves the IL-6 receptor gp130 in different host cells. ► This is reverted when the enzyme is complexed with chagasin, a parasite inhibitor. ► Cruzipain induces the release of Ig-like domain of gp130 on human leukocytes. ► Trypomastigote supernatants abolish STAT3 phosphorylation in splenocytes.