Mechanical signaling regulates NLRP3 activation in macrophages

作者
Hemant P. Joshi,Alison Almgren‐Bell,Anvitha Addanki,Elizabeth M. Todd,Sharon Celeste Morley
出处
期刊:Journal of Immunology [American Association of Immunologists]
卷期号:210 (Supplement_1): 167.20-167.20 被引量:1
标识
DOI:10.4049/jimmunol.210.supp.167.20
摘要

Abstract Macrophage controls infection and inflammation via releasing pro-inflammatory cytokine IL-1β. NLRP3 inflammasomes assembly triggers a signaling cascade to process pro-IL-1β in the active form via activating caspase-1. In the lungs, dysregulated NLRP3 activation escalates inflammatory diseases such as acute lung injury (ALI), ventilator-induced lung injury (VILI), and idiopathic pulmonary fibrosis (IPF). These inflammatory disorders are associated with changing tissue compliance/stiffness due to accumulated extracellular matrix (ECM). Tissue-resident macrophages interaction with ECM via integrins transduce “mechanotransduction” signaling. However, the molecular mechanism of how mechanotransduction cross-talks with NLRP3 pathways and inflammatory response is not clear yet. We are examining NLRP3 activation in lung resident alveolar macrophages (AMs) during mechanical stress. For that, we culture macrophages on collagen-coated surfaces with altered stiffness (elastic modulus of 0.2 to 64 Kilo Pascals (kPa)). We observed that the NLRP3 inflammasome pathway is responsive to surface stiffness and IL-1β processing suppressed by a stiffer surface (64 kPa) when compared to a softer surface (0.2 kPa). Similarly, culture surface stiffness also regulates monocyte-to-macrophage differentiation. AMs show altered transcriptome signatures with changing the stiffness and favored activated macrophage phenotype at 0.2 kPa. Further, activation of the integrin-induced signaling also reduced the NLRP3-induced IL-1β release. Future examination of adhesion-based integrin-induced mechanical signaling and NLRP3 pathway will reveal the therapeutic potential in associated inflammatory diseases such as ALI/fibrosis. National Institutes of Health grants R01- AI104732, R21EB030171, R01 AI118719, HL148033, R01AI139540, and R56 AI104732, National Science Foundation grants CBET-1900277 and CMMI1548571, American Lung Association grant ETRA 736343, Washington University in Saint Louis Children’s Discovery Institute grants CDI-CORE-2019-813 and CDI-CORE-2015-505, Foundation for Barnes-JewishHospital grants 3770 and 4642, American Association of Immunologists AAICareers in immunology fellowship.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
1秒前
上官若男的应助被白岛采纳,获得50
1秒前
1秒前
芸芸发布了新的文献求助10
1秒前
852的应助被科研通管家采纳,获得10
1秒前
1秒前
null的应助被科研通管家采纳,获得10
1秒前
CarryLJR的应助被科研通管家采纳,获得30
1秒前
思源的应助被科研通管家采纳,获得10
2秒前
共享精神的应助被科研通管家采纳,获得10
2秒前
yl完成签到,获得积分10
2秒前
2秒前
NexusExplorer的应助被科研通管家采纳,获得10
2秒前
2秒前
aajhajkahna的应助被科研通管家采纳,获得10
2秒前
华仔的应助被科研通管家采纳,获得10
2秒前
2秒前
情怀的应助被科研通管家采纳,获得10
2秒前
3秒前
脑洞疼的应助被科研通管家采纳,获得10
3秒前
情怀的应助被科研通管家采纳,获得10
3秒前
Xiaohuyan发布了新的文献求助10
3秒前
lc719的应助被科研通管家采纳,获得10
3秒前
李雷完成签到,获得积分10
3秒前
null的应助被科研通管家采纳,获得10
3秒前
传奇3的应助被科研通管家采纳,获得10
3秒前
jjk的应助被科研通管家采纳,获得10
3秒前
打打的应助被科研通管家采纳,获得10
4秒前
orixero的应助被科研通管家采纳,获得10
4秒前
顾矜的应助被科研通管家采纳,获得10
4秒前
NexusExplorer的应助被科研通管家采纳,获得10
4秒前
4秒前
4秒前
4秒前
脑洞疼的应助被科研通管家采纳,获得10
4秒前
在水一方的应助被turnsole采纳,获得10
4秒前
4秒前
群青完成签到,获得积分10
5秒前
doctor_loong发布了新的文献求助10
5秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Energie-Contracting 1500
Klimaschutzrecht durch den Energiesektor im Mehrebenensystem – Ein Rechtsvergleich 1000
Stochastic Models in Operations Research,Vol. 2 600
Critical Bildung: Hegel and the Logic of Diremption 500
桑白皮エキスの実験的, 臨床的育毛効果について 500
Qualitative Methodologies in Tourism Studies: Disrupting and Co-creating Critical Research 350
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 计算机科学 工程类 有机化学 化学工程 生物化学 物理 复合材料 内科学 催化作用 光电子学 人工智能 细胞生物学 无机化学 物理化学 数学
热门帖子
关注 科研通微信公众号,转发送积分 8038421
求助须知:如何正确求助?哪些是违规求助? 9473545
关于积分的说明 21266611
捐赠科研通 7607495
什么是DOI,文献DOI怎么找? 3390659
关于科研通互助平台的介绍 2522250
邀请新用户注册赠送积分活动 2428130