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.

We report a case of performing a 4-stage operations, including TEVAR through the descending aorta as an access route, for multiple aortic aneurysms complicated by severe COPD. The patient was a 71-year-old woman. A chest X-ray suggested a thoracic aortic aneurysm (TAA). CT scans revealed significant aortic tortuosity and six aortic aneurysms, including a TAA with a maximum diameter of 65 mm. However, due to severe mixed ventilatory impairment with an FEV1 of 39% and a %VC of 64%, a multi-stage surgery including TEVAR was chosen from the perspective of surgical tolerance. Additionally, due to severe calcification and stenosis extending from both iliac arteries to the femoral arteries and significant aortic tortuosity, careful planning for endovascular access was necessary. In the first stage, TEVAR was performed through the descending aorta as the access route for the TAA. In the second stage, a prosthetic graft replacement (abdominal four-branched reconstruction) was performed for the thoracoabdominal aortic aneurysm. In the third stage, TEVAR was performed using a prosthetic graft branch as the access route for the remaining TAA. In the fourth stage, additional TEVAR was performed for the endoleak, and EVAR was performed for the abdominal aortic aneurysm and common iliac artery aneurysm, completing the treatment in four stages. By carefully designing treatment strategies, such as access routes for endovascular stent-graft insertion with a focus on minimal invasiveness, severe postoperative complications, including respiratory issues, were successfully avoided.