대식세포에서 Pam3CSK4로 유도된 면역관용의 NF-κB/MAPK 신호 조절을 통한 항염증 효과

• 영문명: Anti-inflammatory Effect of Tolerance Induced by Pam3CSK4 in Murine Macrophage RAW 264.7 Cells via Inhibitor of NF-κB/MAPK Signaling Pathway
• 발행기관: 대한약학회
• 저자명: 한상철(Sang Chul Han) 강나진(Na Jin Kang) 박경민(Kyung min Park) 박지선(Ji seon Park) 엄영은(Young eun Eum) 강희경(Hee Kyoung Kang) 유은숙(Eun Sook Yoo)
• 간행물 정보: 『약학회지』제62권 제5호(2018년), 306~312쪽, 전체 7쪽
• 주제분류: 의약학 > 기타의약학
• 파일형태: PDF
• 발행일자: 2018.10.30

영문 초록

Endotoxin tolerance is an essential mechanism for immune-homeostatic response that suppresses excessive inflammatory cytokine production. It is induced by repeated exposure to endotoxins, such as lipopolysaccharide (LPS). Many recent studies have investigated LPS tolerance, but the molecular mechanism for Pam3CSK4-tolerance in mouse macrophage is poorly understood. Pam3CSK4 binds to TLR1/2 and regulates several downstream signaling pathways, including NF-κB and MAPK pathways. In this study, pretreatment with Pam3CSK4 inhibited TNF-α and IL-6 production after secondary Pam3CSK4 challenge in a time- and dose-dependent manner without cell cytotoxicity. Nontolerized RAW 264.7 cells responded to Pam3CSK4 challenge with the degradation of IκBα and phosphorylation of p38, ERK and JNK. On the other hand, activation of IκBα and MAPKs was diminished in Pam3CSK4-tolerized cells. We also investigated whether pretreatment with Pam3CSK4 regulates the expression of signaling inhibitors TNFAIP3, SOCS1 and SOCS3. Compared with the nontolerized macrophages, the expression of A20, SOCS1 and SOCS3 was increased in Pam3CSK4-tolerized macrophages. These results indicate that am3CSK4-tolerized macrophages suppress pro-inflammatory responses and induce the expression of signaling inhibitors of TLR mechanism.

목차

서 론(Introduction)

실험 방법(Experimental Methods)

결과 및 고찰(Results and discussion)

결 론(Conclusion)

Conflict of Interests

감사의 말씀(Acknowledgments)

References

키워드

tolerance Pam3CSK4 TNF-α inducible protein 3 suppressor of cytokine signaling 1/3