S Wang1, H Zhou2, T Feng3, R Wu2, X Sun1, N Guan2, L Qu4, Z Gao4, J Yan5, N Xu6, J Zhao7, C Qi8. 1. Oncology Institute, The Affiliated Hospital of Nanjing Medical University, Changzhou No. 2 People's Hospital, Changzhou 213003, China; Central Lab, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou 213003, China. 2. Central Lab, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou 213003, China. 3. Oncology Institute, The Affiliated Hospital of Nanjing Medical University, Changzhou No. 2 People's Hospital, Changzhou 213003, China. 4. Department of Vascular Surgery, Shanghai Changzheng Hospital, Shanghai 200003, China. 5. Department of Medicine, James Graham Brown Cancer Center, University of Louisville, Louisville, KY 40202, USA. 6. Section of Clinical Chemistry & Pharmacology, Department of Laboratory Medicine, Lund University, S-221 85 Lund, Sweden. 7. Department of Cardiology, The Affiliated Hospital of Nanjing Medical University, Changzhou No. 2 People's Hospital, Changzhou 213003, China. Electronic address: zhaojz09@gmail.com. 8. Oncology Institute, The Affiliated Hospital of Nanjing Medical University, Changzhou No. 2 People's Hospital, Changzhou 213003, China; Central Lab, The Affiliated Hospital of Nanjing Medical University, Changzhou No.2 People's Hospital, Changzhou 213003, China. Electronic address: qichunjian@gmail.com.
Abstract
AIM: To investigate the immunomodulatory effects of β-(1,3/1,6)-d-glucan on atherosclerosis as well as on the molecular mechanisms of its transition. METHODS AND RESULTS: Human monocytic leukemia (THP-1) cells were differentiated into the macrophage phenotype by incubation with oxLDL in the absence or presence of β-glucan. β-glucan attenuated CD86 and CD80 expression and simultaneously reduced secretion of the inflammatory cytokines IL-2, IL-8, IL-12, TNF-α and IFN-γ. Western blot analysis showed that oxLDL treatment induced phosphorylation of p38 MAPK and ERK1/2 in PMA-differentiated THP-1 cells. However, β-glucan inhibited p38 MAPK activation. In experiments with monocytes derived from healthy donors, β-glucan inhibited IL-8, IL-12 and TNF-α production. The anti-inflammatory effects of β-glucan were also observed in atherosclerotic plaque cells. CONCLUSIONS: β-glucan inhibited oxLDL-induced pro-inflammatory effects in macrophages via regulation of p38 MAPK phosphorylation. This novel finding may provide insight for new therapeutic strategies.
AIM: To investigate the immunomodulatory effects of β-(1,3/1,6)-d-glucan on atherosclerosis as well as on the molecular mechanisms of its transition. METHODS AND RESULTS:Human monocytic leukemia (THP-1) cells were differentiated into the macrophage phenotype by incubation with oxLDL in the absence or presence of β-glucan. β-glucan attenuated CD86 and CD80 expression and simultaneously reduced secretion of the inflammatory cytokines IL-2, IL-8, IL-12, TNF-α and IFN-γ. Western blot analysis showed that oxLDL treatment induced phosphorylation of p38MAPK and ERK1/2 in PMA-differentiated THP-1 cells. However, β-glucan inhibited p38MAPK activation. In experiments with monocytes derived from healthy donors, β-glucan inhibited IL-8, IL-12 and TNF-α production. The anti-inflammatory effects of β-glucan were also observed in atherosclerotic plaque cells. CONCLUSIONS: β-glucan inhibited oxLDL-induced pro-inflammatory effects in macrophages via regulation of p38MAPK phosphorylation. This novel finding may provide insight for new therapeutic strategies.