乙型流感病毒IgM ELISA免疫診斷試劑盒

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?乙型流感病毒IgM ELISA免疫診斷試劑盒

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【公司名稱】 廣州健侖生物科技有限公司
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痛風發作會在人體關節部位引發炎癥和劇烈疼痛，但過了一段時間后，炎癥通常會自動減弱，疼痛感也逐漸消失。這為何會發生?德國研究人員發現，原因在于一種人體免疫細胞的“抗原抗體式攻擊”。
痛風的病因是體內嘌呤物質新陳代謝紊亂，導致尿酸合成增加、排出減少，造成高尿酸血癥。血液中尿酸濃度過高時，尿酸會以微小的鈉鹽結晶(俗稱痛風石)形式析出，積累在關節、軟骨和腎臟中，引發炎癥。
德國埃爾朗根大學近日發表研究公報稱，其研究人員發現，人體免疫系統的嗜中性粒細胞在抗擊痛風引發的炎癥中發揮了關鍵作用。實驗顯示，這種免疫細胞會在關節等組織的炎癥部位聚集，然后破裂死亡，死亡細胞釋放的DNA和蛋白質等物質形成了一張緊密的網絡，包裹住痛風石。
炎癥反應越激烈，就會有越多的嗜中性粒細胞參與抗炎，形成的網絡會越緊密和復雜，能捕獲的痛風石晶體也越多。被這張網絡捕獲的痛風石晶體會逐漸分解，患者的痛風癥狀也就慢慢消失。
此外研究人員指出，嗜中性粒細胞的免疫機制在抑制囊腫性纖維化和系統性紅斑狼瘡中也扮演了重要的角色。他們希望這一發現將有助于在未來研發治療多種疾病的藥物。

Gout attacks can cause inflammation and severe pain at the joints of the body, but over time the inflammation usually weakens and the pain disappears. Why does this happen? German researchers found that the reason is that a human immune cells "antigen-antibody attack."
The cause of gout is the metabolism of purine substances in the body, resulting in increased uric acid synthesis, reduced emissions, resulting in hyperuricemia. Uric acid in the blood is too high, uric acid will be tiny sodium salt crystals (commonly known as tophi) precipitation, accumulation in the joints, cartilage and kidneys, trigger inflammation.
The University of Erlangen in Germany recently published a study bulletin said its researchers found that the immune system of human neutrophils play a key role in fighting gout-induced inflammation. Experiments have shown that such immune cells accumulate at the site of inflammation in joints and other tissues and then rupture and death. The DNA and proteins released by dead cells form a tight network that encapsulates tophus.
The more intense the inflammatory response is, the more neutrophils are involved in anti-inflammatory and the more compact and complex the network is and the more gouty stone crystals can be captured. Gout stone crystal captured by this network will be gradually decomposed, the patient's gout symptoms will gradually disappear.
In addition, researchers pointed out that neutrophil immune mechanisms also play an important role in the suppression of cystic fibrosis and systemic lupus erythematosus. They hope this finding will help to develop drugs for the treatment of multiple diseases in the future.