慢性非细菌性前列腺炎(CNP)是泌尿男科最常见的疾病之一,病因复杂,复发率高.中医药在治疗CNP中占据重要地位,可以通过多种机制发挥疗效.本文整理了近年来关于中医药治疗CNP的具体机制研究,包括抗感染、抗炎症、调节免疫、改善尿流动力学、调控内分泌、改善微循环和调节肠道菌群等,以期为临床应用和基础研究提供理论依据.

目的:探讨中青年脑卒中伴与不伴高同型半胱氨酸(Hey)血症患者肠道菌群特征的差异及临床意义.方法:选取2022年1月至2023年12月110例中青年脑卒中患者作为研究组,根据伴与不伴高Hey血症分为高Hey亚组与正常Hey亚组,另选取同期健康体检志愿者55例作为对照组.对比研究组与对照组、研究组不同亚组肠道菌群失调发生率、Alpha多样及相对丰度,分析肠道菌群与高Hey血症、脑卒中的关系,评价肠道菌群对脑卒中伴高Hey血症的预测价值.结果:研究组肠道菌群失调发生率 52.73％高于对照组 18.18％,Simpson 指数(417.61±66.51)高于对照组(668.39±91.08),Chaol 指数(0.96±0.06)、Shannon 指数(2.13±0.52)低于对照组(0.90±0.03)、(4.67±0.45)(x2=18.061,t=20.103、6.985、30.891,P均＜0.001);研究组厚壁菌门低于对照组,拟杆菌门、变形菌门相对丰度高于对照组(P＜0.05);研究组拟杆菌属相对丰度高于对照组,双歧杆菌属、粪杆菌属、柯林斯菌属相对丰度低于对照组(P＜0.05);高Hey亚组肠道菌群失调发生率80.00％高于正常Hey亚组33.85％,Simpson 指数(383.43±53.18)高于正常 Hey 亚组(441.27±65.39),Chaol 指数(0.99±0.05)、Shannon 指数(2.02±0.18)低于正常 Hey 亚组(0.94±0.03)、(2.21±0.25),(x2=22.725,t=4.913、6.545、4.371,P均＜0.001);高Hey亚组厚壁菌门低于正常Hey亚组,拟杆菌门、变形菌门相对丰度高于正常Hey亚组(P＜0.05);高Hey亚组拟杆菌属相对丰度高于正常Hey亚组,双歧杆菌属、粪杆菌属、柯林斯菌属相对丰度低于正常Hey亚组(P＜0.05);肠道菌群失调、Simpson指数与高Hcy血症、脑卒中及脑卒中伴高Hey血症呈正相关,Chaol指数、Shannon指数与高Hey血症、脑卒中及脑卒 中伴高Hey血症呈负相关(P＜0.05);肠道菌群失调、Simpson指数、Chaol指数、Shannon指数预测中青年脑卒中伴高Hey血症的AUC 为 0.731(95％CI:0.638～0.811)、0.809(95％CI:0.723～0.878)、0.782(95％CI:0.693～0.855)、0.822(95％CI:0.738～0.889),敏感度分别为 80.00％、86.67％、82.22％、75.56％,特异度为 66.15％、69.23％、61.54％、75.38％.结论:中青年脑卒中伴高Hey血症患者肠道菌群失调发生率较高,多样性下降,丰度也发生明显改变,可作为预测脑卒中伴高Hey血症的辅助指标,能为临床提供新的角度.

腹泻型肠易激综合征(IBS-D)是一种临床常见的功能性胃肠病,免疫失衡在其发病中起重要作用.相关免疫细胞包括固有免疫细胞和适应性免疫细胞,免疫细胞因子包括免疫球蛋白、干扰素、白介素、肿瘤坏死因子等.中药单体/化合物或复方可通过多通路、多靶点调节免疫治疗IBS-D.本文从免疫失衡与肠道感染、菌群失调、脑肠轴紊乱、内分泌紊乱的关系等方面,对中药单体/化合物和复方靶向免疫治疗IBS-D的相关文献进行了系统回顾与梳理,并同时印证了"脾为之卫"与免疫相通之处,以期为中医药通过免疫介导途径治疗IBS-D及相关疾病提供思路.

肠道微生物在维持宿主体内代谢稳态及宿主代谢性疾病发生发展过程中发挥重要作用，其通过代谢物与宿主相互作用，对机体代谢和免疫调节等生理病理过程产生影响。早期流产是常见妊娠并发症之一，占所有临床妊娠的10%~15%。既往研究表明，肠道微生物群在妊娠并发症的病理生理过程中发挥着重要的作用，有望成为早期自然流产临床预防和治疗的新候选者。早期自然流产与肠道微生物之间的相关性得到越来越多的关注，但肠道微生物群影响早期自然流产的机制需要进一步研究。本文综述了肠道微生物群与早期自然流产发病原因的相关性，显示其可能通过调节人体内分泌、免疫功能、子宫环境参与了早期自然流产的发生发展，希望能够为临床诊治及研究提供新的思路。

Background::Preeclampsia (PE) is a serious complication that affects maternal and perinatal outcomes. However, the mechanisms have not been fully explained. This study was designed to analyze longitudinal gut microbiota alterations in pregnant women with and without PE in the second (T2) and third trimesters (T3).Methods::In this nested case-control study, which was conducted at Nanjing Maternity and Child Health Care Hospital, fecal samples from 25 PE patients (25 fecal samples obtained in T2 and 15 fecal samples obtained in T3) and 25 matched healthy controls (25 fecal samples obtained in T2 and 22 fecal samples obtained in T3) were collected, and the microbiota were analyzed using 16S rRNA gene sequencing. The diversity and composition of the microbiota of PE cases and controls were compared.Results::No significant differences in diversity were found between the PE and control groups ( P > 0.05). In the control group, from T2 to T3, the relative abundances of Proteobacteria (median [Q1, Q3]: 2.25% [1.24%, 3.30%] vs. 0.64% [0.20%, 1.20%], Z = -3.880, P < 0.05), and Tenericutes (median [Q1, Q3]: 0.12% [0.03%, 3.10%] vs. 0.03% [0.02%, 0.17%], Z= -2.369, P < 0.05) decreased significantly. In the PE group, the relative abundance of Bacteroidetes in T2 was lower than in T3 (median [Q1, Q3]: 18.16% [12.99%, 30.46%] vs. 31.09% [19.89%, 46.06%], Z= -2.417, P < 0.05). In T2, the relative abundances of mircrobiota showed no significant differences between the PE group and the control group. However, in T3, the relative abundance of Firmicutes was significantly lower in the PE group than in the control group (mean ± standard deviation: 60.62% ± 15.17% vs. 75.57% ± 11.53%, t= -3.405, P < 0.05). The relative abundances of Bacteroidetes, Proteobacteria, and Enterobacteriaceae were significantly higher in the PE group than in the control group (median [Q1, Q3]: 31.09% [19.89%, 46.06%] vs. 18.24% [12.90%, 32.04%], Z=-2.537, P < 0.05; 1.52% [1.05%, 2.61%] vs. 0.64% [0.20%, 1.20%], Z=-3.310, P < 0.05; 0.75% [0.20%, 1.00%] vs. 0.01% [0.004%, 0.023%], Z = -4.152, P < 0.05). Linear discriminant analysis combined effect size measurements analysis showed that the relative abundances of the phylum Bacteroidetes, class Bacteroidia and order Bacteroidales were increased in the PE group, while those of the phylum Firmicutes, the class Clostridia, the order Clostridiales, and the genus unidentified Lachnospiraceae were decreased in the PE group; and these differences were identified as taxonomic biomarkers of PE in T3. Conclusion::From T2 to T3, there was an obvious alteration in the gut microbiota. The gut microbiota of PE patients in T3 was significantly different from that of the control group.

Colorectal cancer (CRC) is one of the most prevalent, most lethal cancers in the world. Increasing evidence suggests that the intestinal microbiota is closely related to the pathogenesis and prognosis of CRC. The normal microbiota plays an essential role in maintaining gut barrier function and the immune microenvironment. Recent studies have identified carcinogenic bacteria such as enterotoxigenic Bacteroides fragilis ( ETBF) and Streptococcus gallolyticus ( S. gallolyticus), as well as protective bacterial such as Akkermansia muciniphila ( A. muciniphila), as potential targets of CRC treatment. Gut microbiota modulation aims to restore gut dysbiosis, regulate the intestinal immune system and prevent from pathogen invasion, all of which are beneficial for CRC prevention and prognosis. The utility of probiotics, prebiotics, postbiotics, fecal microbiota transplantation and dietary inventions to treat CRC makes them novel microbe-based management tools. In this review, we describe the mechanisms involved in bacteria-derived colorectal carcinogenesis and summarized novel bacteria-related therapies for CRC. In summary, we hope to facilitate clinical applications of intestinal bacteria for preventing and treating CRC.

Incomplete immune reconstitution remains a global challenge for human immunodeficiency virus (HIV) treatment in the present era of potent antiretroviral therapy (ART), especially for those individuals referred to as immunological non-responders (INRs), who exhibit dramatically low CD4 + T-cell counts despite the use of effective antiretroviral therapy, with long-term inhibition of viral replication. In this review, we provide a critical overview of the concept of ART-treated HIV-positive immunological non-response, and also explain the known mechanisms which could potentially account for the emergence of immunological non-response in some HIV-infected individuals treated with appropriate and effective ART. We found that immune cell exhaustion, combined with chronic inflammation and the HIV-associated dysbiosis syndrome, may represent strategic aspects of the immune response that may be fundamental to incomplete immune recovery. Interestingly, we noted from the literature that metformin exhibits properties and characteristics that may potentially be useful to specifically target immune cell exhaustion, chronic inflammation, and HIV-associated gut dysbiosis syndrome, mechanisms which are now recognized for their critically important complicity in HIV disease-related incomplete immune recovery. In light of evidence discussed in this review, it can be seen that metformin may be of particularly favorable use if utilized as adjunctive treatment in INRs to potentially enhance immune reconstitution. The approach described herein may represent a promising area of therapeutic intervention, aiding in significantly reducing the risk of HIV disease progression and mortality in a particularly vulnerable subgroup of HIV-positive individuals.

Background::We previously found that the intestinal epithelial chemokine (C-C motif) ligand 7 (CCL7) plays an important role in the development of toxin-induced acute liver damage. The detailed effects of intestinal epithelial CCL7 on chronic diseases; however, are still unclear. Here, we aimed to investigate the impact of intestinal epithelial CCL7 overexpression on high-fat diet (HFD)-induced obesity and steatohepatitis in mice.Methods::Intestinal epithelial CCL7 overexpression (CCL7 tgIEC) mice and their wild-type (WT) littermates were fed with normal chow or HFD for 16 weeks to induce obesity and non-alcoholic fatty liver disease. Body weight gain, as well as adipose tissue index were assessed. Liver injury was monitored by histological analysis and real time polymerase chain reaction. Gut microbial composition was analyzed by 16S rRNA gene sequencing. Results::We found that the CCL7 tgIEC mice on a HFD had markedly decreased weight gain (8.9 vs. 17.0 g, P < 0.05) and a lower adipose tissue index that include mesenteric fat (1.0% vs. 1.76%, P < 0.05), gonadal fat (2.1% vs. 6.1%, P < 0.05), subcutaneous fat (1.0% vs. 2.8%, P < 0.05) compared to WT animals. HFD-induced glucose intolerance and insulin resistance were also significantly improved in CCL7 tgIEC mice compared to WT. Furthermore, HFD-fed CCL7 tgIEC mice displayed less hepatic lipid accumulation and lower expression of inflammatory factors than WT mice. 16S rRNA gene sequencing demonstrated that CCL7 overexpression in intestinal epithelial cells improved HFD-induced gut microbial dysbiosis. Conclusions::Our study revealed that CCL7 overexpression in the intestinal epithelium protects mice against the progression of diet-induced obesity, hepatic steatosis, and enteric dysbiosis.

感染是导致外科重症监护病房中危重患者死亡的主要病因之一。越来越多的证据表明，外科重症患者的感染多来源于肠道中机会致病菌易位。肠道菌群作为人体共生的部分，其代谢产物被人体摄取利用后会影响患者机体的生理病理代谢改变。危重症患者在入住外科重症监护病房期间往往由于外科手术、原发疾病、继发感染以及临床治疗措施的使用，很大程度上引起肠道微生态失调。本文以外科重症患者为焦点，深入回顾外科重症监护病房中患者临床治疗期间肠道微生态的变化特点与肠道微生物影响外科重症感染性疾病发生发展及其预后转归关系的相关研究，作一综述。