人巨细胞病毒先天性中枢神经系统感染小鼠模型的建立

将人巨细胞病毒（ＨＣＭＶ）接种至８￣１２周龄Ｂａｌｂ／ｃ雌雄小鼠腹腔后,交配。等雌鼠临产时剖腹取出胎鼠脑双侧大脑皮层,进行病毒分析、病理学检测及用地高辛标记的ＨＣＭＶ寡核苷酸探针对大脑皮层细胞压印片进行原位分子杂交检测。病理学研究结果证实,鼠脑为侵袭性脑膜脑炎性病理改变,并在神经细胞内发现病毒特性性的大的核内嗜碱性包涵体;原位杂交结果显示,病毒核酸存在于受染神经细胞及神经胶质细胞核内及胞浆内;在鼠     

病毒性皮肤疣小鼠模型的建立

目的 疣是因人乳头瘤病毒(HPV)感染导致的皮肤科疾病之一,常表现为寻常疣、尖锐湿疣等症状,治疗后易复发,目前尚无有效的小鼠模型.为研究皮肤疣的防治策略及产品,本研究拟建立病毒性皮肤疣小鼠模型.方法 免疫缺陷小鼠麻醉后,利用刀片轻轻刮擦小鼠尾部皮肤制造轻微创口,接种1.5×108 copies小鼠乳头瘤病毒,定期观察尾...     

小鼠脑潜伏巨细胞病毒激活模型的建立

目的:我们建立了小鼠脑潜伏巨细胞病毒激活模型,来实现小鼠脑内潜伏的巨细胞病毒(MCMV)的激活,并对潜伏MCMV激活时程进行分析,确定MCMV即刻早期蛋白基因1(ie1)基因转录,完成对ie1基因转录和活病毒产生量时程动力学的分析,以及为进一步阐明原始MCMV在脑中潜伏的细胞类型提供模型。方法:采用出生后两天的BALB/c幼鼠,经右侧耳和眼连线为底边的正三角形的中心将Smith Strain MCMV 500 PFU/5μL注射进入右侧脑室,培养至16周。之后,将脂多糖(LPS)依15μg/kg体重(接近致死量)分别经腹腔和侧脑室内注射,对照组注射生理盐水。于注射后的1日,2日,5日,7日,14日和21日分别在LPS组和对照组中选取5只小鼠取脑。应用反转录-聚合酶链式反应(RT-PCR)和高敏感性病毒空斑实验(结合病毒空斑实验和RT-PCR)测定MCMV即刻早期蛋白1(IE1)mRNA的表达以及活病毒产生定量分析。结果:LPS组中,可于14日和21日的脑内检测到IE1 mRNA的转录,敏感性病毒空斑实验只在14日和21日出现细胞病毒效应(CPE),病毒量约为4.29×104 PFU/μL和5.20×105PFU/μL,相应对应MEF细胞匀浆物的RT-PCR结果检测到7,14,21日有IE1 mRNA转录。结论:该实验成功建立了小鼠脑潜伏巨细胞病毒激活的模型,并证实和分析了即刻早期蛋白基因ie1在潜伏MCMV激活过程中的表达和时程。该模型的建立将为进一步阐明MCMV在脑中潜伏细胞类型以及MCMV在急性感染、潜伏和重激活过程中对中枢神经细胞的影响提供研究平台,并为人巨细胞病毒(HCMV)的临床研究提供实验依据。     

小鼠左肺原位移植模型的建立

目的通过显微外科技术建立小鼠原位肺移植模型,为肺移植研究提供动物模型。方法采用C57BL/6小鼠作为供、受体,行同基因小鼠原位左肺移植,使用Cuff套管法进行气管及血管吻合。术后7、14、21、28 d取移植肺及原肺,行HE染色,评价肺移植后效果。结果学习曲线后,共30例小鼠移植,手术成功率89%,小鼠成活率100%。供体手术时间:(35.2±9.81)min,受体手术时间:(24.6±7.42)min,冷缺血时间是:(46.6±8.92)min,热缺血时间是:(17.2±3.08)min。同基因移植物大体及病理无明显改变,病理显示与原肺无差别。结论本技术能够方便快捷建立小鼠肺移植模型,成功率高,可重复性强,符合原位肺移植临床生理,是研究肺移植发病机制和治疗的良好动物模型。     

同种异体宫内移植小鼠嵌合模型的建立

干细胞宫内移植是一种很有前途的产前治疗方式。为深入研究干细胞移植后的细胞行为,采用宫内移植的方法建立同种异体的嵌合小鼠模型。将雄鼠骨髓单核细胞宫内注射到胎鼠腹腔,在受体鼠出生后检测雌性受体鼠外周血细胞。应用PCR检测外周血是否存在雄性鼠的DNA,并采用定量PCR技术确定其嵌合量;同时用荧光原位杂交（FISH）技术直观观察外周血中雄性来源的细胞。结果表明：共获得4只阳性外周血嵌合小鼠,其中3只稳定嵌合达到6个月以上。应用宫内移植成功建立了外周血中存在异源细胞的小鼠嵌合模型。     

MCMV不同途径感染免疫缺损性小鼠体内效应的研究

通过血管注射、腹下注射、唾液腺注射等3种不同途径将野生型小鼠巨细胞病毒(murine cytomegalovirus,MCMV)感染免疫缺损型小鼠CM17 SCID(sevele combined immunodeficiency,严重免疫缺损综合症),在感染后不同的时间内分别取唾液腺、脾、肝、肺和肾脏测定其病毒滴度,以及测定感染后SCID小鼠的死亡率．同时通过唾液腺注射RvM43突变株,测定病毒在唾液腺中的滴度．结果显示：经尾部血管途径注射的体内唾液腺、肺、脾、肝和肾脏的病毒滴度高峰期和SCID小鼠死亡时间均显著性早于经腹下注射、唾液腺注射途径、除唾液腺器官外,经唾液腺注射途径肺、脾、肝和肾脏的病毒的出现时间晚于经尾部血管和腹下注射途径．经唾液腺注射后,唾液腺中突变型RvM43在各时间点的病毒滴度及高峰出现时间与野生型相同．由此可知,从唾液腺感染小鼠后：MCMV病毒在唾液腺中的生长不受M43基因突变的影响,小鼠巨细胞病毒不同途径感染免疫缺损型小鼠CMl7 SCID的体内生物学效应有差异．因此有必要通过不同途径感染宿主来研究MCMV基因的体内功能．     

人巨细胞病毒中枢神经系统先天性感染小鼠模型的电镜研究

目的 应用人巨细胞病毒（ＨＣＭＶ）建立先天性中枢神经系统感染小鼠模型。以电镜研究探讨ＨＣＭＶ先天性感染对中枢神经系统损伤的机制和程度。方法 将ＨＣＭＶ腹腔内中纯系６－８周龄Ｂａｌｂ／ｃ雌雄小鼠成功后给予酱受孕,待雌鼠临产时取出胎鼠脑双侧大脑皮层,进行病毒分离、病理学检验和电镜研究。结果 在鼠脑组织上清液中分离出ＨＣＭＶ;病理学证实,鼠脑为侵袭性脑膜脑炎性病理改变;电镜下研究,在感染组子代鼠脑组织血     

建立小鼠心肌梗死模型的研究

目的建立心肌梗死小鼠模型。方法40只昆明小鼠,PTCA导丝逆行引导下气管插管,人工呼吸,采用开胸结扎左冠状动脉前降支方法造成心肌梗死。结果40只小鼠成功行左前降支结扎术;术后1天存活小鼠38只,术后2周存活32只。结论此方法可有效模拟心肌梗死的发生。     

小鼠溃疡性结肠炎模型的建立及病理组织学比较

目的建立乙酸,右旋葡聚糖硫酸钠（dextran sodium sulfate,DSS）,幽门螺杆菌（Helicobacter pyliri）小鼠溃疡性结肠炎（ulcerative colitis）动物模型,通过病理学对比观察,选择最佳的小鼠溃疡性结肠炎动物模型。方法将40只清洁级BALB/c小鼠随机分为4组,实验组中Ⅰ组采用乙酸刺激法诱发溃疡性结肠炎,Ⅱ组采用饮用3.5%DSS溶液诱发结肠炎,Ⅲ组采用幽门螺杆菌感染小鼠诱发溃疡性结肠炎,对照组饮用蒸馏水。观察小鼠每日的体重,大便性状和隐血情况,以及结肠大体形态和组织病理学改变。结果乙酸,右旋葡聚糖硫酸钠均可引起小鼠疡性结肠炎。结论 DSS诱发的小鼠溃疡性结肠炎是一种较理想的UC动物模型,可作为研究UC发病机制和药物治疗较理想的工具。     

Role of Macrophages in Acute Murine Cytomegalovirus Infection

It has been recognized that macrophages play an important role in controlling virus infection in experimental animal models. To evaluate the role of macrophages in acute murine cytomegalovirus infection, macrophages in the spleen and the liver were eliminated by an intravenous injection of liposomes containing a cytolytic agent, dichloromethylene diphosphonate. The depletion of macrophages led to a significant increase of virus titer in the spleen and lungs in both susceptible BALB/c and resistant C57BL/6 mice during the first three days after intravenous infection. In the spleen, the increase of virus titer in macrophage-depleted BALB/c mice was much greater than that in NK cell-depleted mice. These results suggest that macrophages contribute to protection mainly by the mechanisms which are independent of NK cells during the first three days after infection. The increase of virus titer in macrophage-depleted C57BL/6 mice was as great as that in NK cell-depleted mice because of the high contribution of NK cells to protection in C57BL/6 mice. In the liver in both strains of mice, the effects of macrophage depletion on virus titer were not as much as those in the spleen and lungs. Furthermore, the local depletion of peritoneal macrophages resulted in a great increase of virus titer in the spleen at three days after intraperitoneal infection. We conclude that macrophages greatly contribute to decreasing the virus load in some organs possibly through either or both intrinsic and extrinsic mechanisms in the early phase of primary infection with murine cytomegalovirus.     

Early Atherosclerotic Plaques in the Aorta Following Cytomegalovirus Infection of Mice

We show here that BALB/c mice inoculated with murine cytomegalovirus (MCMV) express viral antigens in the endothelial and smooth muscle cells of the aortic wall, and that accumulation of inflammatory cells in the aortic lumen, similar to that seen in early atherosclerotic lesions in humans, colocalizes with the site of virus antigen expression. Immunosuppression of the mice at the time of virus infection increased the expression of viral antigens and the size of early atherosclerotic lesions in the intima. The percentage of the low-density lipoprotein cholesterol (LDL-C), the major lipid contributor to atherosclerotic plaques, was significantly increased in the serum of MCMV-infected mice, whether or not the mice were fed a high cholesterol diet. Human cytomegalovirus (HCMV) significantly increased the esterified cholesterol component of the total cholesterol in a human arterial smooth muscle cell line infected in vitro with HCMV. These results suggest that CMV infection is involved in two of the major mechanisms that lead to development of atherosclerosis, i.e., immune injury and high LDL-C.     

Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock

It is common knowledge that severe blood loss and traumatic injury can lead to a cascade of detrimental signaling events often resulting in mortality. ^{1, 2, 3, 4, 5} These signaling events can also lead to sepsis and/or multiple organ dysfunction (MOD). ^{6, 7, 8, 9} It is critical then to investigate the causes of suppressed immune function and detrimental signaling cascades in order to develop more effective ways to help patients who suffer from traumatic injuries. ¹⁰ This fixed pressure Hemorrhagic Shock (HS) procedure, although technically challenging, is an excellent resource for investigation of these pathophysiologic conditions. ^{11, 12, 13} Advances in the assessment of biological systems, i.e. Systems Biology have enabled the scientific community to further understand complex physiologic networks and cellular communication patterns. ¹⁴ Hemorrhagic Shock has proven to be a vital tool for unveiling these cellular communication patterns as they relate to immune function. ^{15, 16, 17, 18} This procedure can be mastered! This procedure can also be used as either a fixed volume or fixed pressure approach. We adapted this technique in the murine model to enhance research in innate and adaptive immune function. ^{19, 20, 21} Due to their small size HS in mice presents unique challenges. However due to the many available mouse strains, this species represents an unparalleled resource for the study of the biologic responses. The HS model is an important model for studying cellular communication patterns and the responses of systems such as hormonal and inflammatory mediator systems, and danger signals, i.e. DAMP and PAMP upregulation as it elicits distinct responses that differ from other forms of shock. ^{22, 23, 24, 25} The development of transgenic murine strains and the induction of biologic agents to inhibit specific signaling have presented valuable opportunities to further elucidate our understanding of the up and down regulation of signal transduction after severe blood loss, i.e. HS and trauma ^{26, 27, 28, 29, 30}. There are numerous resuscitation methods (R) in association with HS and trauma. ^{31, 32, 33, 34} A fixed volume resuscitation method of solely lactated ringer solution (LR), equal to three times the shed blood volume, is used in this model to study endogenous mechanisms such as remote organ injury and systemic inflammation. ^{35, 36, 38} This method of resuscitation is proven to be effective in evaluating the effects of HS and trauma ^{38, 39}.     

A Novel Clinically Relevant Animal Model for Studying Galectin-3 and Its Ligands During Colon Carcinogenesis

Galectin-3 (Gal-3) is a multifunctional protein that plays different roles in cancer biology. To better understand the role of Gal-3 and its ligands during colon carcinogenesis, we studied its expression in tumors induced in rats treated with 1,2-dimethylhydrazine (DMH) and in human tissues. Normal colon from untreated rats showed no staining using two specific monoclonal antibodies. In contrast, morphologically normal colon from DMH-treated rats and dysplastic aberrant crypt foci were strongly stained, indicating that increased Gal-3 expression is an early event during the neoplastic transformation in colon cells. Gal-3 was weakly expressed in adenocarcinomas. Overall, the Gal-3 expression pattern observed in the DMH rat model closely resembles that displayed by human colon stained with the same antibodies. We also found that Gal-3 phosphorylation diminishes in serines while increasing in tyrosines during rat colon carcinogenesis. Finally, we showed that Gal-3–ligands expression is strikingly similar in rat and human malignant colon and in non-malignant tissues. In conclusion, the DMH-induced rat colon cancer model displays expression patterns of Gal-3 and its ligands very similar to those observed in human samples. This animal model should contribute to clarifying the role of Gal-3 in colon carcinogenesis and also to finding effective preventive cancer agents based on Gal-3 targeting. (J Histochem Cytochem 58:553–565, 2010)     

Therapeutic Potential of 6-Gingerol in Prevention of Colon Cancer Induced by Azoxymethane through the Modulation of Antioxidant Potential and Inflammation

A polyphenolic component of ginger, 6-gingerol, is widely reported to possess antioxidant, anti-inflammatory and anticancer activities. In the current study, it was aimed to investigate the anticancer effects of 6-gingerol (6-Gin) on azoxymethane (AOM)-induced colon cancer in rats. The results reveal that 6-Gin treatment significantly improves the antioxidant status disturbed by AOM intoxication. The 6-Gin treatment animal group showed enhanced activity of catalase (CAT) (46.6 ± 6.4 vs. 23.3 ± 4.3 U/mg protein), superoxide dismutase (SOD) (81.3 ± 7.6 vs. 60.4 ± 3.5 U/mg protein) and glutathione-S-transferase (GST) (90.3 ± 9.4 vs. 53.8 ± 10 mU/mg protein) (p < 0.05) as compared to the disease control group. Furthermore, the results reveal that AOM significantly enhances the inflammatory response and 6-gingerol potentially attenuates this response, estimated by markers, such as tumor necrosis factor-α (TNF-α) (1346 ± 67 vs. 1023 ± 58 pg/g), C-reactive protein (CRP) (1.12 ± 0.08 vs. 0.92 ± 0.7 ng/mL) and interleukin-6 (IL-6) (945 ± 67 vs. 653 ± 33 pg/g). In addition, the lipid peroxidation estimated in terms of malondialdehyde (MDA) provoked by AOM exposure is significantly reduced by 6-gingerol treatment (167 ± 7.5 vs. 128.3 nmol/g). Furthermore, 6-gingerol significantly maintains the colon tissue architecture disturbed by the AOM treatment. Loss of tumor suppressor protein, phosphatase and tensin homolog (PTEN) expression was noticed in the AOM treated group, whereas in the animals treated with 6-gingerol, the positivity of PTEN expression was high. In conclusion, the current findings advocate the health-promoting effects of 6-gingerol on colon cancer, which might be due to its antioxidant and anti-inflammatory potential.     

A Population-Based Epidemiologic Study of Helicobacter Pylori Infection and its Association with Systemic Inflammation

Background:  Infection with Helicobacter pylori is associated with a variety of non-gastrointestinal sequelae. These may be mediated by an increase in systemic inflammation. We assessed if serologic evidence of infection with H. pylori is associated with increased serum C-reactive protein (CRP) levels.
Methods:  The study design consisted of a randomly selected, cross-sectional population-based study of 2633 individuals phenotyped in 1991, of whom 2361 participants provided serum samples to permit measurement of H. pylori 's serologic status and CRP levels.
Results:  Male gender (odds ratio (OR): 1.65; 95% confidence interval (CI): 1.23–2.21), age (OR per year: 1.05; 95% CI: 1.04–1.06), height (OR per meter: 0.05; 95% CI: 0.01–0.24), current smoking habit (compared with never smokers, OR: 1.46; 95% CI: 1.13–1.88), and less affluent socioeconomic status were associated with increased odds of being seropositive for H. pylori . Helicobacter pylori infection was associated with increased risk of having an elevated serum CRP (above 3 mg/L) after adjustment for gender, age, height, smoking status, and socioeconomic status (OR: 1.32; 95% CI: 1.05–1.67). Similar associations were seen using a threshold for elevated serum CRP of greater than 1 mg/L.
Conclusions:  Our data suggest that infection with H. pylori is associated with increased systemic inflammation. This suggests one potential mechanism to explain the extra-gastrointestinal conditions associated with H. pylori infection.     

滴鼻途径建立鼠结核病模型的探讨

目的 探讨滴鼻途径建立BALB/C小鼠结核分枝杆菌感染的模型的可行性.方法 人型Mtb H_(37)Rv标准株经腹腔接种小鼠,取小鼠腹腔冲洗液100 μl接种改良罗-琴氏培养基.刮取上述培养基上生长4周已恢复毒力的结核分枝杆菌H_(37)Rv标准株,加0.05%Tween80生理盐水磨菌制成悬液,菌落计数,计数后稀释悬液为5×10~3 CFU/50 μl、5×10~4 CFU/50 μl、5×10~5 CFU/50 μl及50 μl生理盐水分别感染4组Balb/c小鼠,制作结核分枝杆菌感染模型.结果 滴鼻感染小鼠4周后,所有小鼠肺、脾组织中均可见抗酸阳性菌,在感染小鼠肺、脾组织匀浆均培养出Mtb.肺组织病理改变明显,正常肺泡结构消失,以充血实变、淋巴细胞、巨噬细胞浸润为主,增生性改变不明显,未见明显的组织坏死.脾组织病理改变主要是巨噬细胞和淋巴细胞增生.结论 滴鼻感染途径建立小鼠结核病模型简便、可行,为进一步研究开发重组BCG疫苗对鼠结核病的防治打下良好的基础. 0~4 CFU/50 μl、5×10~5 CFU/50 μl及50 μl生理盐水分别感染4组Balb/c小鼠,制作结核分枝杆菌感染模型.结果 滴鼻感染小鼠 周后,所有小鼠肺、脾组织中均可见抗酸阳性菌,在感染小鼠肺、脾组织匀浆均培养出Mtb.肺组织病理改变明显,正常肺泡结构消失,以充血实变、淋巴细胞、巨噬细胞浸润为主,增生性改变不明显,未见明显的组织坏死.脾组织病理改变主要是巨噬细胞和淋巴细胞增生.结论 滴鼻感染途径建立小鼠结核病模型简便、可行,为进一步研究开发重组BCG疫苗对鼠结核病的防治打下良好的基础. 0~4 CFU/50 μl、5×10~5 CFU/50 μl及50 μl生理盐水分别感染4组Balb/c     

Murine Cytomegalovirus Immediate-Early 1 Gene Expression Correlates with Increased GVHD after Allogeneic Hematopoietic Cell Transplantation in Recipients Reactivating from Latent Infection

The success of allogeneic (allo) hematopoietic cell transplantation (HCT) is limited by its treatment related complications, mostly graft versus host disease (GVHD) and fungal and viral infections. CMV reactivation after HCT has been associated with increased morbidity and mortality, and a causal relation between GVHD, immunosuppressive therapy and vice versa has been postulated. Using a low GVHD severity murine HCT model, we assessed the role of MCMV reactivation and GVHD development. BALB/c mice were infected with either murine CMV (MCMV) or mock and monitored for 25 weeks to establish latency, followed by sublethal irradiation conditioning and infusion of bone marrow plus splenocytes from either syngeneic (syn) BALB/c or allo B10.D2 donors. Engraftment of allo donor cells was confirmed by PCR for D2Mit265 gene product size. Day+100 mortality and overall GVHD severity in allo MCMV pre-infected recipients was higher than in allo mock controls. Pathologic changes of lung and liver GVHD in immediate-early gene 1 (IE1) positive recipients were significantly increased compared to mock controls, and were only slightly increased in IE1 negative. No significant gut injury was seen in any group. Aggravated lung injury in IE1 positive recipients correlated with higher BAL cell counts both for total cells and for CD4+ T cells when compared with mock controls, and also with protein expression of lung IFN-gamma and liver TNF. No evidence for CMV specific morphologic changes was seen on histopathology in any organ of IE1 positive recipients, suggesting that CMV reactivation is related to increased GVHD severity but does not require active CMV disease, strengthening the concept of a reciprocal relationship between CMV and GVHD.     

Investigating Intestinal Inflammation in DSS-induced Model of IBD

Inflammatory bowel disease (IBD) encompasses a range of intestinal pathologies, the most common of which are ulcerative colitis (UC) and Crohn''s Disease (CD). Both UC and CD, when present in the colon, generate a similar symptom profile which can include diarrhea, rectal bleeding, abdominal pain, and weight loss.¹ Although the pathogenesis of IBD remains unknown, it is described as a multifactorial disease that involves both genetic and environmental components.²There are numerous and variable animal models of colonic inflammation that resemble several features of IBD. Animal models of colitis range from those arising spontaneously in susceptible strains of certain species to those requiring administration of specific concentrations of colitis-inducing chemicals, such as dextran sulphate sodium (DSS). Chemical-induced models of gut inflammation are the most commonly used and best described models of IBD. Administration of DSS in drinking water produces acute or chronic colitis depending on the administration protocol.³ Animals given DSS exhibit weight loss and signs of loose stool or diarrhea, sometimes with evidence of rectal bleeding.^4,5 Here, we describe the methods by which colitis development and the resulting inflammatory response can be characterized following administration of DSS. These methods include histological analysis of hematoxylin/eosin stained colon sections, measurement of pro-inflammatory cytokines, and determination of myeloperoxidase (MPO) activity, which can be used as a surrogate marker of inflammation.⁶The extent of the inflammatory response in disease state can be assessed by the presence of clinical symptoms or by alteration in histology in mucosal tissue. Colonic histological damage is assessed by using a scoring system that considers loss of crypt architecture, inflammatory cell infiltration, muscle thickening, goblet cell depletion, and crypt abscess.⁷ Quantitatively, levels of pro-inflammatory cytokines with acute inflammatory properties, such as interleukin (IL)-1β, IL-6 and tumour necrosis factor (TNF)-α,can be determined using conventional ELISA methods. In addition, MPO activity can be measured using a colorimetric assay and used as an index of inflammation.⁸In experimental colitis, disease severity is often correlated with an increase in MPO activity and higher levels of pro-inflammatory cytokines. Colitis severity and inflammation-associated damage can be assessed by examining stool consistency and bleeding, in addition to assessing the histopathological state of the intestine using hematoxylin/eosin stained colonic tissue sections. Colonic tissue fragments can be used to determine MPO activity and cytokine production. Taken together, these measures can be used to evaluate the intestinal inflammatory response in animal models of experimental colitis.     

Trichuris muris Infection: A Model of Type 2 Immunity and Inflammation in the Gut

Trichuris muris is a natural pathogen of mice and is biologically and antigenically similar to species of Trichuris that infect humans and livestock¹. Infective eggs are given by oral gavage, hatch in the distal small intestine, invade the intestinal epithelial cells (IECs) that line the crypts of the cecum and proximal colon and upon maturation the worms release eggs into the environment¹. This model is a powerful tool to examine factors that control CD4⁺ T helper (Th) cell activation as well as changes in the intestinal epithelium. The immune response that occurs in resistant inbred strains, such as C57BL/6 and BALB/c, is characterized by Th2 polarized cytokines (IL-4, IL-5 and IL-13) and expulsion of worms while Th1-associated cytokines (IL-12, IL-18, IFN-γ) promote chronic infections in genetically susceptible AKR/J mice^2-6. Th2 cytokines promote physiological changes in the intestinal microenvironment including rapid turnover of IECs, goblet cell differentiation, recruitment and changes in epithelial permeability and smooth muscle contraction, all of which have been implicated in worm expulsion^7-15. Here we detail a protocol for propagating Trichuris muris eggs which can be used in subsequent experiments. We also provide a sample experimental harvest with suggestions for post-infection analysis. Overall, this protocol will provide researchers with the basic tools to perform a Trichuris muris mouse infection model which can be used to address questions pertaining to Th proclivity in the gastrointestinal tract as well as immune effector functions of IECs.