Caspase-11 mediated inflammasome activation in macrophages by systemic infection of A. actinomycetemcomitans exacerbates arthritis.

IF 10.8 1区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE International Journal of Oral Science Pub Date : 2024-08-15 DOI:10.1038/s41368-024-00315-x
Tokuju Okano, Hiroshi Ashida, Noriko Komatsu, Masayuki Tsukasaki, Tamako Iida, Marie Iwasawa, Yuto Takahashi, Yasuo Takeuchi, Takanori Iwata, Miwa Sasai, Masahiro Yamamoto, Hiroshi Takayanagi, Toshihiko Suzuki
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Abstract

Clinical studies have shown that Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) is associated with aggressive periodontitis and can potentially trigger or exacerbate rheumatoid arthritis (RA). However, the mechanism is poorly understood. Here, we show that systemic infection with A. actinomycetemcomitans triggers the progression of arthritis in mice anti-collagen antibody-induced arthritis (CAIA) model following IL-1β secretion and cell infiltration in paws in a manner that is dependent on caspase-11-mediated inflammasome activation in macrophages. The administration of polymyxin B (PMB), chloroquine, and anti-CD11b antibody suppressed inflammasome activation in macrophages and arthritis in mice, suggesting that the recognition of lipopolysaccharide (LPS) in the cytosol after bacterial degradation by lysosomes and invasion via CD11b are needed to trigger arthritis following inflammasome activation in macrophages. These data reveal that the inhibition of caspase-11-mediated inflammasome activation potentiates aggravation of RA induced by infection with A. actinomycetemcomitans. This work highlights how RA can be progressed by inflammasome activation as a result of periodontitis-associated bacterial infection and discusses the mechanism of inflammasome activation in response to infection with A. actinomycetemcomitans.

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放线菌全身感染导致巨噬细胞中的 Caspase-11 介导的炎性体激活会加重关节炎。
临床研究表明,放线杆菌(A. actinomycetemcomitans)与侵袭性牙周炎有关,并可能诱发或加重类风湿性关节炎(RA)。然而,人们对其机制知之甚少。在此,我们发现,在小鼠抗胶原抗体诱导的关节炎(CAIA)模型中,放线菌全身感染会诱发关节炎的恶化,而这种恶化是在IL-1β分泌和细胞浸润爪子之后发生的,其方式依赖于巨噬细胞中caspase-11介导的炎性体激活。服用多粘菌素 B(PMB)、氯喹和抗 CD11b 抗体可抑制巨噬细胞中的炎性体活化和小鼠的关节炎,这表明巨噬细胞中的炎性体活化后,需要溶酶体降解细菌后识别细胞膜中的脂多糖(LPS)并通过 CD11b 侵袭才能引发关节炎。这些数据揭示,抑制 caspase-11 介导的炎症小体活化会加剧放线菌感染诱发的 RA。这项研究强调了牙周炎相关细菌感染导致的炎性体活化可导致 RA 的恶化,并探讨了放线菌感染导致炎性体活化的机制。
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来源期刊
International Journal of Oral Science
International Journal of Oral Science DENTISTRY, ORAL SURGERY & MEDICINE-
CiteScore
31.80
自引率
1.30%
发文量
53
审稿时长
>12 weeks
期刊介绍: The International Journal of Oral Science covers various aspects of oral science and interdisciplinary fields, encompassing basic, applied, and clinical research. Topics include, but are not limited to: Oral microbiology Oral and maxillofacial oncology Cariology Oral inflammation and infection Dental stem cells and regenerative medicine Craniofacial surgery Dental material Oral biomechanics Oral, dental, and maxillofacial genetic and developmental diseases Craniofacial bone research Craniofacial-related biomaterials Temporomandibular joint disorder and osteoarthritis The journal publishes peer-reviewed Articles presenting new research results and Review Articles offering concise summaries of specific areas in oral science.
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