Host PTX3 Protein and Bacterial Capsule Coordinately Regulate the Inflammatory Response during Streptococcus suis Infection.
Host PTX3 Protein and Bacterial Capsule Coordinately Regulate the Inflammatory Response during Streptococcus suis Infection.
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DOI：
10.3390/vetsci10030239
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发表时间：
2023-03-22
影响因子：
2.4
通讯作者：
Ma J
中科院分区：
文献类型：
--
作者：
Bai Q;Fan R;Zhong N;Liu J;Pan X;Yao H;Ma J
猪链球菌2型（Streptococcussuisserotype 2，SS 2）是一种重要的人畜共患病病原体，给养猪业造成了巨大的经济损失，并严重威胁人类健康。在这项研究中，五聚蛋白3（PTX 3）在SS 2感染过程中的作用进行了探索，以验证其作为一种新的和有效的生物制剂，可以部分解决SS 2所带来的问题的潜力。研究结果表明，PTX 3促进巨噬细胞Ana-1对SS 2菌株HA 9801的吞噬，并促进小鼠气囊中炎症细胞的募集和细胞因子IL-6的释放，从而有助于SS 2感染期间的细菌清除。SS 2的荚膜多糖（CPS 2）的存在被鉴定为PTX 3触发炎性活化所需;在SS 2感染期间宿主先天免疫应答的这种协调调节进一步表明PTX 3是用于预防和治疗由SS 2引起的链球菌病的潜在生物制剂。然而，必须进一步评估PTX 3的推荐剂量，以避免过度的炎症反应。猪链球菌2型（Streptococcussuisserotype 2，SS 2）是一种重要的人畜共患病原菌，给养猪业造成了巨大的经济损失，也严重威胁着人类的健康。正五聚蛋白3（PTX 3）是对细菌病原体的先天免疫应答的重要调节剂;然而，其在SS 2感染期间的作用尚未完全了解。在这项研究中，我们发现SS 2菌株HA 9801在小鼠气囊模型中诱导了显著的炎症反应;就炎症细胞募集和促炎细胞因子IL-6产生的结果而言，这种反应同时通过外源性PTX 3的治疗而放大。此外，PTX 3促进巨噬细胞Ana-1对SS 2菌株HA 9801的吞噬作用。与单独HA 9801感染的样品相比，外源性PTX 3的补充以剂量依赖性方式显著降低了SS 2感染小鼠的肺、肝和血液中的细菌载量;这一发现表明PTX 3可能通过增强SS 2感染期间的宿主炎症反应来促进细菌清除。PTX 3和SS 2芙膜多糖（CPS 2）都是强有力的炎症反应所需的，这意味着宿主PTX 3蛋白和SS 2表面CPS 2共同调节宿主先天免疫反应。所有这些结果表明，PTX 3是一种潜在的新型生物制剂的SS 2感染;然而，PTX 3的推荐剂量必须严格评估，以避免诱导过度的炎症反应，可导致严重的组织损伤和动物死亡。
Streptococcus suis serotype 2 (SS2) is a noteworthy zoonotic pathogen that has been responsible for substantial economic losses to the swine industry and a great threat to human health. In this study, the role of Pentraxin 3 (PTX3) during SS2 infection is explored to verify its potential as a new and effective biological agent that could partially resolve the problems posed by SS2. The study’s results showed that PTX3 facilitated the phagocytosis of macrophage Ana-1 against SS2 strain HA9801, and contributed to inflammatory cell recruitment and cytokine IL-6 release in the mouse air pouch; thus, it was conductive to bacterial clearance during the SS2 infection. The presence of capsular polysaccharide of SS2 (CPS2) was identified as being required for PTX3 to trigger the inflammatory activation; this coordinating modulation of the host’s innate immune response during the SS2 infection further suggested that PTX3 is a potential biological agent for the prevention and treatment of streptococcosis caused by SS2. However, the recommended dose of PTX3 must be further evaluated to avoid an excessive inflammatory response. Streptococcus suis serotype 2 (SS2) is a noteworthy zoonotic pathogen that has been responsible for large economic losses in pig production and a great threat to human health. Pentraxin 3 (PTX3) is an essential regulator of the innate immune response to bacterial pathogens; however, its role during SS2 infection is not fully understood. In this study, we found that the SS2 strain HA9801 induced a significant inflammatory response in the mouse air pouch model; this response was amplified by the treatment of exogenous PTX3 simultaneously in terms of the results of inflammatory cell recruitment and proinflammatory cytokine IL-6 production. In addition, PTX3 facilitated the phagocytosis of macrophage Ana-1 against SS2 strain HA9801. The supplementation of exogenous PTX3 significantly reduced the bacterial loads in a dose-dependent manner in lungs, livers and bloods of SS2-infected mice compared to the samples with HA9801 infection alone; this finding indicated that PTX3 may facilitate the bacterial clearance through enhancing the host inflammatory response during SS2 infection. Both PTX3 and SS2 capsular polysaccharide (CPS2) were required for the robust inflammatory response, implying that the host PTX3 protein and SS2 surface CPS2 modulate the host innate immune response in concert. All of these results suggested that PTX3 is a potential novel biological agent for the SS2 infection; however, the recommended dose of PTX3 must be evaluated strictly to avoid inducing an excessive inflammatory response that can cause serious tissue injury and animal death.
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