The role of IL-4 on RANKL induced by lipoproteins in osteoblasts

• Grant number: 15/00410-0
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: July 01, 2015
• End date: February 28, 2018
• Field of knowledge: Health Sciences - Dentistry - Periodontology
• Principal Investigator: Pedro Paulo Chaves de Souza
• Grantee: Thaís Floriano Marcelino
• Host Institution: Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil
• Associated research grant: 14/05283-3 - The effect of bradykinin on osteoclastogenesis in vitro and LPS-induced bone resorption in vivo, AP.JP

Abstract

Inflammatory reactions close to the skeleton generally lead to bone loss, for example in pathological conditions such as rheumatoid arthritis, periodontal disease, loosened joint prosthesis and peri-implantitis. Some of these reactions are caused by infection. In periodontitis, Porphyromonas gingivalis (P.g.) is an important pathogenic microorganism. Besides having lipopolysaccharide in its structure, P.g. also produces a lipoprotein that is an important virulence factor responsible for triggering bone loss by different mechanisms. One of the mechanisms by which lipoproteins induce bone loss is the enhancement on RANKL production. On the other hand, in chronicle inflammatory conditions, some bone-protective cytokines are produced, for example IL-4. One of the mechanisms by which IL-4 protects from bone loss is blocking the enhancement on RANKL production caused by pro-inflammatory cytokines. Therefore, the aim of this investigation is to analyze the role of IL-4 on the expression of RANKL induced by a synthetic lipoprotein, Pam2CSK4. RANKL production will be analyzed in an osteoblasts primary culture by quantitative real time PCR and ELISA. The identification of the IL-4 protective mechanisms is important for the understanding of periodontal disease aiming to develop new therapeutic strategies. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

PERSSON, EMMA; SOUZA, PEDRO P. C.; FLORIANO-MARCELINO, THAIS; CONAWAY, HOWARD HERSCHEL; HENNING, PETRA; LERNER, ULF H.. Activation of Shc1 Allows Oncostatin M to Induce RANKL and Osteoclast Formation More Effectively Than Leukemia Inhibitory Factor. FRONTIERS IN IMMUNOLOGY, v. 10, MAY 28 2019. (14/05283-3, 15/00410-0)

DE SOUZA, PEDRO P. C.; HENNING, PETRA; LERNER, ULF H.. Stimulation of Osteoclast Formation by Oncostatin M and the Role of WNT16 as a Negative Feedback Regulator. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v. 23, n. 6, p. 22-pg., 2022-03-01. (14/05283-3, 15/00410-0)

HENNING, PETRA; MOVERARE-SKRTIC, SOFIA; WESTERLUND, ANNA; CHAVES DE SOUZA, PEDRO PAULO; FLORIANO-MARCELINO, THAIS; NILSSON, KARIN H.; EL SHAHAWY, MAHA; OHLSSON, CLAES; LERNER, ULF H.. WNT16 is Robustly Increased by Oncostatin M in Mouse Calvarial Osteoblasts and Acts as a Negative Feedback Regulator of Osteoclast Formation Induced by Oncostatin M. JOURNAL OF INFLAMMATION RESEARCH, v. 14, p. 4723-4741, 2021. (15/00410-0, 14/05283-3)