Protective effect of green tea and epigallocatechin-3-gallate in a LPS-induced systemic inflammation model

• Published in: The Journal of nutritional biochemistry 2022-03, Vol.101, p.108920-108920, Article 108920
• Main Authors: Azambuja, Juliana Hofstätter, Mancuso, Rubia Isler, Via, Fernanda Isabel Della, Torello, Cristiane Okuda, Saad, Sara Teresinha Olalla
• Format: Article
• Language: English
• Subjects: Animals; Catechin - analogs & derivatives; Catechin - pharmacology; Epigallocatechin-3-gallate; Green tea; Humans; Inflammation; Inflammation - immunology; Inflammation - therapy; Lipopolysaccharides - immunology; Lymphocytes - immunology; Macrophage Activation; Macrophages; Macrophages - immunology; Male; Mice; Mice, Inbred BALB C; Myeloid Cells - immunology; Protective Agents; T regulatory lymphocytes, neutrophils and MDSCs; Tea
• ISSN: 0955-2863; 1873-4847
• DOI: 10.1016/j.jnutbio.2021.108920

Inflammation causes severe dysregulation of organ functions, via the development of oxidative stress and inflammation damage. Polyphenol compounds found in green tea (GTE), including the most important component epigallocatechin-3-gallate (EGCG), have a great therapeutic potential. Here, protective properties of GTE and EGCG against lipopolysaccharide (LPS)-induced inflammation are explored. To this end, the effects of GTE and EGCG were studied on LPS challenged macrophages. Mice received GTE (250 mg/kg/d/p.o) or EGCG (25 mg/kg/d/i.p.) for 7 d, before the inflammation shock was provoked with a single intraperitoneal injection of LPS. The frequencies of lymphocytes CD4+, CD8+, NK1-1+ and CD4+CD25highFOXP3+ (Treg), macrophages CD11b+F480+, monocytes CD11b+Ly6Clow/high, neutrophils CD11b+Ly6G+, MDSCs CD11b+Gr-1high, M2/N2-like phenotype CD206+ and M1-like phenotype CD86+ in spleen, bone marrow and peripheral blood were determined. In vitro studies revealed that GTE and EGCG significantly attenuated LPS-induced CD80 expression and increased the CD163 expression, showing a potential to reduce the macrophage inflammatory phenotype. In vivo, GTE and EGCG inhibited the inflammation, mainly by reducing M1-macrophages and increasing Treg cells in the bone marrow. In addition, GTE and EGCG increase M2-macrophages, N2-neutrophils and Tregs in the spleen and blood and block the migration of monocytes from the bone marrow to the peripheral blood. These findings indicate that EGCG and GTE prevent LPS-induced inflammatory damage contributing to restoring the immune system homeostasis [Display omitted] .