Sepsis is characterized by a profound dysregulation of the immune response, which typically evolves through overlapping phases of hyper-inflammation and immune suppression rather than a simple linear progression.
敗血症的核心病理並非單純的感染，而是免疫反應的嚴重失衡，通常同時呈現高炎症反應與免疫抑制兩種狀態，而非線性依序發生。
During the hyper-inflammatory phase, bacterial products such as lipopolysaccharide (LPS) and other pathogen-associated molecular patterns activate innate immune receptors and trigger intracellular inflammatory signaling pathways including NF-κB and STAT. This activation can drive a systemic “cytokine storm,” with excessive release of pro-inflammatory mediators such as TNF-α, IL-6, and IL-1β.
在高炎症階段，細菌產物（如脂多醣 LPS）與其他病原相關分子會啟動先天免疫受器，進而活化 NF-κB、STAT 等細胞內發炎訊號路徑。此過程可能推動全身性的「細胞激素風暴」，並伴隨 TNF-α、IL-6、IL-1β 等促發炎因子過量釋放。
Hyper-inflammation is closely intertwined with oxidative stress and cellular energy failure. Sepsis can induce excessive reactive oxygen species (ROS), increased lipid peroxidation (often discussed with markers such as MDA), and reduced antioxidant defenses (commonly including SOD). In parallel, mitochondrial injury is described through Ca2+ overload, nitric oxide (NO)-related damage, and loss of mitochondrial membrane potential, leading to insufficient energy production and progressive multi-organ dysfunction.
高炎症反應也與氧化壓力及細胞能量失衡緊密相連。敗血症可造成 ROS 過量、脂質過氧化升高（常以 MDA 等指標討論）、以及抗氧化防禦下降（常包含 SOD）。同時，粒線體損傷可表現為 Ca2+ 過載、NO 相關傷害與粒線體膜電位降低，導致能量產生不足，進一步推動多器官功能障礙。
Neutrophils contribute to hyper-inflammation through the release of neutrophil extracellular traps (NETs). While NETs can support host defense, they can also promote endothelial injury, intravascular coagulation, and microcirculatory disturbance.
中性球可透過釋放 NETs（中性球胞外捕捉網）參與高炎症反應。NETs 雖可協助防禦感染，但也可能加劇內皮損傷、血管內凝血與微循環障礙。
In sepsis, inflammation and coagulation amplify each other. Cytokines promote tissue factor expression and activate extrinsic and intrinsic coagulation, while coagulation factors and fibrin can further induce pro-inflammatory responses. NET components also participate in coagulation. Unchecked activation can lead to coagulation imbalance and disseminated intravascular coagulation (DIC), contributing to organ failure.
在敗血症中，炎症與凝血會彼此放大。細胞激素促進組織因子表現並活化外源性與內源性凝血；同時凝血因子與纖維蛋白也可反向促進發炎反應。NETs 成分亦可參與凝血。若失控，可能導致凝血失衡與DIC，進一步造成器官衰竭。
In parallel with, or following hyper-inflammation, many patients develop a state of immune suppression. This phase is associated with functional exhaustion and apoptosis of immune cells, including CD4+ and CD8+ T cells, B cells, NK cells, and dendritic cells (DCs). At the same time, immunosuppressive populations such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) may expand and inhibit effective antimicrobial immunity.
與高炎症反應並行或隨後，許多患者會進入免疫抑制狀態。此階段常見免疫細胞功能衰竭與凋亡增加，包含 CD4+、CD8+ T 細胞、B 細胞、NK 細胞與樹突細胞（DC）。同時，Treg 與 MDSCs 等免疫抑制細胞群可能上升，抑制有效的抗感染免疫反應。
Monocytes and macrophages can be reprogrammed into an immunotolerant phenotype, often described as “LPS tolerance,” with reduced antigen presentation (including decreased MHC class II expression) and diminished cytokine production after ex vivo stimulation. Immune checkpoint regulation also becomes prominent; programmed death protein 1 (PD-1) is upregulated on activated T cells and is associated with T-cell exhaustion, impaired proliferation, increased IL-10, higher rates of secondary/nosocomial infections, and mortality risk in septic shock.
單核球與巨噬細胞可能被重新編程為免疫耐受表型，常被描述為 「LPS tolerance」：抗原呈現能力下降（包含 MHC II 表現降低），且在體外再刺激時促發炎細胞激素產生能力減弱。免疫檢查點調控也變得突出；PD-1 在活化 T 細胞上升，與 T 細胞耗竭、增殖受損、IL-10 增加、續發／院內感染比例提高與死亡風險相關。
Across reviewed studies, Zusanli (ST36) appears as the central node of electroacupuncture protocols for sepsis. For uncomplicated sepsis, ST36 is frequently used as a single point, and a commonly reported combination is ST36 + Tianshu (ST25) + Shangjuxu (ST37).
在整理的研究中，足三里（ST36）幾乎是電針介入敗血症的核心穴位。單純敗血症常以 ST36 單穴為主，亦常見 ST36 + 天樞（ST25）+ 上巨虛（ST37） 的組合。
When sepsis is complicated by gastrointestinal injury, frequently used acupoints include ST36, Guanyuan (RN4/CV4), and ST25. Common prescriptions include ST36 + RN4/CV4, and broader combinations such as ST36 + ST25 + ST37 + Xiajuxu (ST39).
合併胃腸道損傷時，常見穴位包含 ST36、關元（RN4／CV4）與 ST25；常見處方包括 ST36 + RN4/CV4，以及更完整的 ST36 + ST25 + ST37 + 下巨虛（ST39）。
For sepsis-associated acute lung injury (ALI), a reported prescription is ST36 + Chize (LU5). For myocardial injury, studies report multi-point protocols including PC6 (Neiguan) + ST36 + HT7 (Shenmen) + LR3 (Taichong) + SP10 (Xuehai) + BL17 (Geshu) + SP6 (Sanyinjiao) + LI4 (Hegu).
合併肺損傷（ALI）時，有研究使用 ST36 + 尺澤（LU5）。合併心肌損傷時，則有研究採用較多穴位的方案，例如 PC6（內關）+ ST36 + HT7（神門）+ LR3（太衝）+ SP10（血海）+ BL17（膈俞）+ SP6（三陰交）+ LI4（合谷）。
For sepsis-associated encephalopathy or brain injury, one reported protocol uses GV20 (Baihui) + DU26 (Shuigou). In oxidative stress / neuroprotection discussions, additional combinations include GV20 + LI11 (Quchi) + ST36 and ST36 + GV20, including animal-model contexts related to mitochondrial and hippocampal injury.
合併腦病變時，有研究使用 GV20（百會）+ DU26（水溝）。在氧化壓力／神經保護的討論中，也提到 GV20 + LI11（曲池）+ ST36 以及 ST36 + GV20（含粒線體／海馬損傷相關的動物研究脈絡）。
In mechanistic pathway discussions, ST36 + BL13 (Feishuxue) appears in relation to STING and NF-κB signaling. In clinical contexts discussing immune checkpoint regulation, a reported protocol is ST36 + CV4 + CV6 (Qihai).
在路徑機制討論中，ST36 + BL13（肺俞穴／Feishuxue）出現在與 STING、NF-κB 相關的敘述段落。與免疫檢查點調控（PD-1）相關的臨床脈絡中，則出現 ST36 + CV4 + CV6（氣海） 的處方。
Quick view: all acupoints mentioned / 全部出現穴位一覽
Current evidence suggests that electroacupuncture (EA) may exert immunomodulatory effects through multiple interacting mechanisms rather than a single pathway. These mechanisms are discussed at several levels, including neuro-immune reflexes, intracellular inflammatory signaling, oxidative stress and mitochondrial function, inflammation–coagulation interactions, and immune suppression checkpoints.
目前整理的證據顯示，電針（EA）的免疫調節並非單一路徑，而是多層次的交互作用：包含神經－免疫反射、細胞內發炎訊號、氧化壓力與粒線體功能、炎症－凝血互相放大、以及免疫抑制期的檢查點調控等。
The cholinergic anti-inflammatory pathway (CAP) is discussed as a mechanism by which neural signaling downregulates systemic inflammatory mediators. A related concept is the vagal-adrenal axis, which can inhibit systemic inflammation; this framework is often used to explain why low-intensity EA at ST36 is especially highlighted for anti-inflammatory effects that may be safer and easier to manage.
膽鹼能抗發炎路徑（CAP）被用來描述：透過神經訊號下調全身性發炎介質。與此相關的概念是 迷走－腎上腺軸，其啟動可能抑制系統性發炎；這也常被用來解釋為何 低強度 ST36 電針在抗發炎效果與可操作性上特別受到關注。
EA is summarized as being able to influence core inflammatory signaling, especially NF-κB and the upstream TLR4/MyD88/NF-κB axis, with reported associations to reduced TNF-α, IL-6, and IL-1β, which in turn is discussed alongside improvements in tissue inflammation and organ injury outcomes.
EA 被整理為可能影響核心發炎訊號，尤其是 NF-κB 以及其上游 TLR4/MyD88/NF-κB 軸線；並被報告與 TNF-α、IL-6、IL-1β 等發炎因子下降相關，進而與器官損傷改善的討論相連結。
In some experimental contexts, EA is described as downregulating JAK/STAT (or STAT3) signaling. This is discussed in relation to decreased inflammatory mediator release and potential improvements in complications such as lung injury.
在部分實驗研究脈絡中，EA 被描述可下調 JAK/STAT（或 STAT3）訊號，並與發炎介質下降、以及如肺損傷等併發症改善的討論相連。
Sepsis is described with ROS↑, MDA↑, SOD↓, loss of mitochondrial membrane potential, and energy failure that contributes to organ dysfunction. EA is summarized as enhancing antioxidant enzyme systems, reducing lipid peroxidation, and improving brain/hippocampal injury, with the HO-1 and Nrf2/HO-1 axis frequently discussed as an important antioxidant framework.
敗血症常被描述為 ROS↑、MDA↑、SOD↓、粒線體膜電位下降與能量失衡，進而造成器官功能障礙。EA 被整理為可提升抗氧化酶系統、降低脂質過氧化並改善腦部／海馬損傷；其中 HO-1 與 Nrf2/HO-1 軸線常被作為重要的抗氧化機制框架。
In sepsis, coagulation activation and impaired anticoagulation can contribute to DIC and microcirculatory failure. Reviewed work reports that EA may improve some coagulation/fibrinolytic indicators such as D-dimer, PAI-1, and AT-III, suggesting a possible role in modulating the inflammation–coagulation amplification loop.
敗血症中凝血被活化且抗凝下降，可促成 DIC 與微循環失衡。文獻整理指出 EA 在部分研究中被報告可改善 D-dimer、PAI-1、AT-III 等指標，提示其可能參與調節炎症－凝血的放大迴路。
Late-stage sepsis is framed around immune cell apoptosis, expansion of Tregs/MDSCs, impaired antigen presentation, and immune checkpoint upregulation such as PD-1. EA is summarized in some studies as improving CD4/CD8 ratios, increasing NK and lymphocyte proportions, and showing reported regulatory effects on the PD-1 pathway, particularly in clinical contexts using ST36 + CV4 + CV6.
敗血症晚期常以免疫細胞凋亡、Treg/MDSCs 上升、抗原呈現受損與 PD-1 等免疫檢查點上調作為關鍵框架。部分研究整理指出 EA 可能改善 CD4/CD8 比例、提升 NK 與淋巴球比例，並在使用 ST36 + CV4 + CV6 的臨床脈絡中被報告具有 PD-1 路徑調節效果。
Electroacupuncture targeting the immune system to alleviate sepsis
https://journals.lww.com/ahm/fulltext/2024/03000/electroacupuncture_targeting_the_immune_system_to.5.aspx
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