Contributions of the intestinal microbiome in lung immunity

The intestine is a critical site of immune cell development that not only controls intestinal immunity but extra‐intestinal immunity as well. Recent findings have highlighted important roles for gut microbiota in shaping lung inflammation. Here, we discuss interactions between the microbiota and immune system including T cells, protective effects of microbiota on lung infections, the role of diet in shaping the composition of gut microbiota and susceptibility to asthma, epidemiologic evidence implicating antibiotic use and microbiota in asthma and clinical trials investigating probiotics as potential treatments for atopy and asthma. The systemic effects of gut microbiota are partially attributed to their generating metabolites including short chain fatty acids, which can suppress lung inflammation through the activation of G protein‐coupled receptors. Thus, studying the interactions between microbiota and immune cells can lead to the identification of therapeutic targets for chronic lower respiratory diseases.     

Expression and characterization of αvβ5 integrin on intestinal macrophages

Macrophages play a crucial role in maintaining homeostasis in the intestine, but the underlying mechanisms have not yet been elucidated fully. Here, we show for the first time that mature intestinal macrophages in mouse intestine express high levels of αvβ5 integrin, which acts as a receptor for the uptake of apoptotic cells and can activate molecules involved in several aspects of tissue homeostasis such as angiogenesis and remodeling of the ECM. αvβ5 is not expressed by other immune cells in the intestine, is already present on intestinal macrophages soon after birth, and its expression is not dependent on the microbiota. In adults, αvβ5 is induced during the differentiation of monocytes in response to the local environment and it confers intestinal macrophages with the ability to promote engulfment of apoptotic cells via engagement of the bridging molecule milk fat globule EGF‐like molecule 8. In the absence of αvβ5, there are fewer monocytes in the mucosa and mature intestinal macrophages have decreased expression of metalloproteases and IL 10. Mice lacking αvβ5 on haematopoietic cells show increased susceptibility to chemical colitis and we conclude that αvβ5 contributes to the tissue repair by regulating the homeostatic properties of intestinal macrophages.     

γδ T cells restrain extrathymic development of Foxp3+‐inducible regulatory T cells via IFN‐γ

Inducible Treg (iTreg) cells generated from Ag‐stimulated naïve CD4⁺ T cells in the periphery play an important role in regulating immune responses. TGF‐β is a key cytokine that promotes this conversion process; however, how this process is regulated in vivo remains unclear. Here, we report that γδ T cells play a crucial role in controlling iTreg generation and suppressor function. Ag‐induced iTreg generation was significantly enhanced in C57BL/6 mice in the absence of γδ T cells. Inhibition of iTreg conversion was mediated by IFN‐γ produced by activated γδ T cells but not by activated CD4⁺ T cells. BM chimera experiments further confirmed γδ‐derived IFN‐γ‐dependent mechanism in regulating iTreg generation in vivo. Lastly, human peripheral blood γδ T cells also interfere with iTreg conversion via IFN‐γ. Our results suggest a novel function of γδ T cells in limiting the generation of iTreg cells, potentially balancing immunity and tolerance.     

双歧杆菌对内毒素损伤幼年大鼠肠道血管内皮细胞粘附分子－1的影响

目的：双歧杆菌是肠黏膜屏障中生物屏障的主要成分,参与了宿主的消化、营养、代谢、吸收、免疫及抗感染过程,然而其具体的作用机制目前还不清楚。该研究欲探讨双歧杆菌对内毒素损伤幼年大鼠血清和回肠组织的丙二醛（MDA）含量和小肠绒毛间质血管内皮细胞粘附分子-1（ICAM-1）表达的影响。方法：腹腔注射内毒素制造内毒素损伤动物模型（模型组,E组）,治疗组（T组）提前7 d给予双歧杆菌灌胃,同时设对照组（C组,腹腔注射生理盐水）,于不同时间点处死后检测血清和肠组织中MDA的含量,并用免疫组织化学和逆转录-聚合酶链反应（RT-PCR）方法检测小肠组织ICAM-1蛋白质和核酸水平的变化。结果：E组血清和小肠MDA含量较对照组增加,以6 h增加明显（肠组织：99.88±12.62 nmol/mg prot vs 84.25±12.96 nmol/mg prot,P<0.05;血清：1.67±0.30 nmol/mL vs 1.13±0.20 nmol/mL,P<0.05）;T组MDA含量（6 h：肠组织92.75±9.28 nmol/mg prot;血清1.17±0.23 nmol/mL）较E组下降;E组小肠组织ICAM-1蛋白质和核酸表达增加,分别以6 h和2 h为著,T组改变低于E组（P<0.05）。 结论：内毒素损伤幼鼠血清和小肠MDA含量增加,同时ICAM-1蛋白质和mRNA表达增加,外源性给予双歧杆菌能降低内毒素组MDA和ICAM-1的增加,表明双歧杆菌能通过抑制大鼠体内的MDA含量和ICAM-1的表达而起到一定的肠道保护作用。［中国当代儿科杂志,2007,9（4）：375-378］     

人体肠道生物力学特性的研究

为探讨人体肠道的生物力学特性，采用电子拉伸机对人体肠道进行一维拉伸试验。结果表明，人体肠道应力-应变关系为指数函数关系。人体肠道各段的指数系数a值接近，但材料常数C有一定的差异，说明肠道各段应力-应变趋势是一致的。在一定应力下，肠道各段轴向与环向的相对伸长率是不同的，表明人体肠道具有各向异性的特性。在一定应变下，肠道各段的增量弹性模量不同，结肠增量弹性模量相对较小，因而更容易发生变形。本研究为肠道内窥镜机器人的研制提供了理论基础。     

低功率CO2激光焊接鼠小肠的机制初探

目的比较激光焊接与传统缝合肠管吻合口的胶原和DNA含量在愈合过程中的变化。方法将60只SD大鼠分为两组,每组30只,分别为缝合组和激光组,每组再分为3小组:第3天组(n=10)、第7天组(n=10)和第14天(n=10)。肌肉注射10%水合氯醛0.5 mg/Kg。腹部正中切口,每只SD大鼠均完成一个吻合口,距回盲部10 cm的回肠处切除回肠约1.5 cm。分别于术后第3、7和14天取吻合口近远端各0.5 cm的小肠组织采用比色法和二苯胺法分别测定其羟脯氨酸和DNA含量。结果吻合口组织羟脯氨酸含量:术后3 d缝合组为(0.87±0.16)μg/mg pro,激光组为(0.70±0.18)μg/mg pro,差异有显著意义(P<0.05);术后7 d激光组含量为(1.00±0.19)μg/mg pro,缝合组为(0.94±0.21)μg/mg pro,差异无显著意义(P>0.05)。术后14 d缝合组为(1.05±0.18)μg/mg pro,激光组为(1.32±0.11)μg/mg pro,差异有非常显著意义P<0.001。吻合口DNA含量:缝合第3天术后组为1.85±0.34 mg/g,激光组为(1.55±0.45)mg/g,差异有显著意义(P<0.05)。第7天缝合组为(1.95±0.43)μg/g,激光组为(1.75±0.36)mg/g,差异无显著意义(P>0.05)。第14天缝合组为(2.04±0.38)μg/g,激光组为(2.95±0.53)μg/g差异有非常显著意义(P<0.001)。结论激光焊接可以造成胶原变性,激光焊接还具有促进组织增生、细胞增殖、加速愈合的作用。     

Extramedullary plasmacytoma of the small intestine: First case report of ileocolic fistula and review of the literature

Extramedullary plasmacytoma (EMP) of the small bowel is a rare entity previously reported as a cause of intestinal obstruction or bleeding. A case report of this disease entity presenting as an ileocolic fistula is reported. EMP is diagnosed by the following critiera: 1) absence of paraproteinemia; 2) absence of Bence Jones proteinuiria; 3) normal skeletal survey; and 4) normal bone marrow biopsy specimen. Gastrointestinal plasmacytoma often occurs as a manifestation of multiple myeloma. EMP of the gastrointestinal tract is a rare cases manifestation of the disease, accounting for 13 per cent of all cases of EMP. It is a slow-spreading, radiosensitive tumor with a high tendency toward local recurrence. Surgical excision combined with radiotherapy is the treatment of choice for EMP of the gastrointestinal tract.     

淤血后处理对大鼠小肠淤血再灌注损伤保护作用的实验研究

目的研究门静脉淤血后处理对小肠黏膜淤血再灌注损伤的保护作用。 方法将24只雄性SD大鼠随机分为假手术组（Sham组）、淤血损伤组（CR组）、淤血后处理组（CPO组）,各8只。Sham组仅行开关腹手术;CR组通过阻断门静脉45 min,再灌注60 min制作小肠淤血再灌注损伤模型;CPO组在再灌注时行开放30 s/夹闭30 s,3个循环淤血后处理。模型制作后60 min后抽取门静脉血检测血清肿瘤坏死因子α（TNF-α）及内毒素水平,取距回盲部约10 cm的近端小肠组织行病理组织学检查和水肿程度分析。 结果（1） Sham组、CR组、CPO组大鼠门静脉血清TNF-α质量浓度分别（31.37±2.39）、（114.75±7.46）、（89.37±5.83）μg/L,内毒素质量浓度分别为（0.64±0.16）、（5.04±0.28）、（4.00±0.31）EU/ml,三组血清TNF-α、内毒素的质量浓度比较,CR组较Sham组显著增高,CPO组较CR组显著降低,差异均有统计学意义（F=404.84、680.85,均P<0.01）。（2） CR组的小肠组织病理损伤邱氏评分为4.01±0.35,显著高于Sham组的0.43±0.21和CPO组的3.58±0.34（Z=6.18、4.25,均P<0.01）。（3） CR组的小肠组织湿干比为5.29±0.36,显著高于Sham组的3.34±0.23和CPO组的4.26±0.26 （F=2.03、0.44,P=0.003、0.012）。 结论淤血后处理对小肠黏膜的淤血再灌注损伤具有保护作用,其保护机制可能是延缓并减少炎性介质释放。     

小肠淋巴管扩张症一例及其文献复习

目的通过1例小肠淋巴管扩张症患者及文献复习,探讨小肠淋巴管扩张症的临床表现、诊断及治疗等。方法 1例小肠淋巴管扩张症患者除一般的血清学、腹部B超、胃镜检查并取黏膜行病理活检外,同时做胶囊内镜、小肠淋巴管造影检查。结果患者59岁发病,因反复腹胀、乏力、胸水及顽固低蛋白血症入院,小肠淋巴管造影及胶囊内镜疑为小肠淋巴管扩张症,胃镜下见十二指肠黏膜弥漫性白色粟米样改变,病理示：十二指肠黏膜淋巴管扩张。本例患者通过中链三酰甘油乳剂治疗后,症状缓解。结论小肠淋巴管扩张症较少见。对于反复腹胀、浆膜腔积液及低蛋白血症的患者要警惕小肠淋巴管扩张症的可能,应尽早行内镜及病理活检,并通过特殊的饮食控制疾病。     

消化道磁共振检查技术与诊断

随着MR技术的快速发展,胃肠道MR检查成为现实。本文将讨论最佳MR胃肠成像所需诊断技术要求及与已有的X线检查方法相比MR所处的位置。当前这一新的检查方法在食道、小肠、结肠中都有报道。这些发展显示胃肠道MR检查可能将由科学研究向常规的临床应用转变。