• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.17 no.3
• /
• pp.186-190
• /
• 2014

Lymphocytic gastritis (LG) is a rare subtype of chronic gastritis. It is defined as dense proliferation of intraepithelial lymphocytes (IELs) more than 25 lymphocytes per 100 epithelial cells. The known major causes of LG are celiac disease and Helicobacter pylori infection. H. pylori associated LG (HpLG) has more enhanced cytotoxic and apoptotic tendencies than chronic H. pylori gastritis. A 12-year-old girl with postprandial epigastric pain was diagnosed HpLG on endoscopic biopsy. After the 1st eradication therapy, H. pylori bacilli were still found, and urea breathing test was positive. Although the endoscopic finding was partially improved, clinical symptoms and histologic finding were persisted. We could achieve the improvement of clinical symptoms and disappearance of IELs after the 2nd eradication. The discordant of histopathologic and endoscopic improvement occurred after the 1st eradication therapy of HpLG. Therefore the clinical and histopathologic evaluation should be considered as well as endoscopic findings.

• Parasites, Hosts and Diseases
• /
• v.40 no.3
• /
• pp.119-129
• /
• 2002

Although there are many reports on the splenic (systemic) T cell response after Toxoptasma gondii infection, little information is available regarding the local T cell responses of peritoneal exudate cells (PEC) and gut intraepithelial Iymphocytes (IEL) following peroral infection with bradyzoites. Mice were infected with 40 cysts of the 76K strain of T. gondii, and then sacrificed at days 0, 1, 4, 7 and 10 postinfection (PI). The cellular composition and T cell responses of PEC and IEL were analyzed. The total number of PEC and IEL per mouse increased after infection, but the ratio of increase was higher in IEL. Lymphocytes were the major component of both PEC and IEL. The relative percentages of PEC macrophages and neutrophils/eosinophils increased signiflcantly at day 1 and 4 PI, whereas those of IEL did not change significantly. The percentage of PEC NK1.1 and ${\gamma\delta}T$ cells peaked at day 4 PI (p < 0.0001), and CD4 and $CD8{\alpha}T$ cells increased continuously after infection. The percentages of IEL $CD8{\alpha}$ and ${\gamma\delta}T$ cells decreased slightly at first, and then increased. CD4 and NK1.1 T cells of IEL did not change significantly after infection. $IFN-{\gamma}-producing$ PEC NK1.1 T cells increased significantly from day 1 PI, but the other T cell subsets produced $IFN-{\gamma}$ abundantly thereafter. The proportion of IEL $IFN-{\gamma}-producing$ $CD8{\alpha}$ and ${\gamma\delta}T$ cells increased significantly after infection, while IEL NK1.1 T cells had similar $IFN-{\gamma}$ production patterns. Taken together, CD4 T cells were the major phenotype and the important $IFN-{\gamma}$ producing T cell subsets in PEC after oral infection with T. gondii whereas $CD8{\alpha}T$ cells had these roles in IEL. These results suggest that PEC and IEL comprise different cell differentials and T cell responses, and according to infection route these factors may contribute to the different cellular immune responses.

• Parasites, Hosts and Diseases
• /
• v.52 no.1
• /
• pp.27-33
• /
• 2014

Mucosal immune responses against Pygidiopsis summa (Trematoda: Heterophyidae) infection were studied in ICR mice. Experimental groups consisted of group 1 (uninfected controls), group 2 (infection with 200 metacercariae), and group 3 (immunosuppression with Depo-Medrol and infection with 200 metacercariae). Worms were recovered in the small intestine at days 1, 3, 5, and 7 post-infection (PI). Intestinal intraepithelial lymphocytes (IEL), mast cells, and goblet cells were counted in intestinal tissue sections stained with Giemsa, astra-blue, and periodic acid-Schiff, respectively. Mucosal IgA levels were measured by ELISA. Expulsion of P. summa from the mouse intestine began to occur from days 3-5 PI which sustained until day 7 PI. The worm expulsion was positively correlated with proliferation of IEL, mast cells, goblet cells, and increase of IgA, although in the case of mast cells significant increase was seen only at day 7 PI. Immunosuppression suppressed all these immune effectors and inhibited worm reduction in the intestine until day 7 PI. The results suggested that various immune effectors which include IEL, goblet cells, mast cells, and IgA play roles in regulating the intestinal mucosal immunity of ICR mice against P. summa infection.

• Asian-Australasian Journal of Animal Sciences
• /
• v.18 no.9
• /
• pp.1320-1325
• /
• 2005

A 2${\times}$3 factorial arrangement of treatments was used to determine the effects of olaquindox and cyadox on immune response of Landrace${\times}$Large-White geld piglets that had been orally given 10$^{10}$ CFU of Escherichia coli (E. coli, O$_{139}$:K$_{88}$). Factors included (1) E. coli inoculation or control, and (2) no antimicrobials, 100 mg/kg olaquindox and 100 mg/kg cyadox in the basal diet respectively. E. coli inoculums were orally administered 7 days after the diets were supplemented with olaquindox and cyadox. The effects of the two antimicrobials were assessed in terms of: (1) average daily gain (ADG), (2) systemic immune response (the number of white blood cells and lymphocytes, leukocyte bactericidal capacity, lymphocyte proliferation response to PHA, immunoglobulin concentrations, and total serous hemolytic complement activity), and (3) intestinal mucosal immunity including the number of intraepithelial lymphocytes (IELs) and immunoglobulin A secreting cells (ASCs) in the intestinal lamina propria. E. coli inoculation reduced ADG (p<0.05) during the period of d 0 to d 14 after the challenge while the antimicrobial supplementations improved ADG (p<0.01) during the experiment. ADG in cyadox-supplemented pigs was higher (p<0.05) than that in olaquindox-supplemented pigs. The antimicrobials decreased IEL and ASC counts in the jejunum and ileum (p<0.01) while E. coli inoculation caused them to increase (p<0.01). Jejunal ASCs in the cyadox-supplemented pigs were lower (p<0.05) than those in the olaquindox-supplemented. E. coli elicited increase (p<0.05) in white blood cell counts, leukocyte bactericidal capacity, lymphocyte proliferation rate, serous IgA concentrations, and serous hemolytic complement activity. The antimicrobials decreased the measured systemic immune parameters, but not significantly (p>0.05). The data suggest that olaquindox and cyadox suppress E. coli-induced immune activation, especially intestinal mucosal immune activation, which may be involved in the observed growth promotion.

• Parasites, Hosts and Diseases
• /
• v.27 no.2
• /
• pp.87-100
• /
• 1989

Eimeria tenella, an intracellular protozoan parasite infecting the epithelial cells of the ceca of chickens, causes severe diarrhea and bleeding that can lead its host to death. It is of interest that 2. tenezla first penetrate into the mucosal intraepithelial Iymphocytes (IEL) before they parasitize crypt or villous epithelial cells. This in vitro study was undertaken to know whether the penetration of E. tenella into such a lymphoid cell is a beneficial step for the parasite survival and development. Three sequential experiments were performed. First, the in vitro established bovine kidney cell line, MDBK cells, were evaluated for use as host cells for E. tenella, through morphological observation. Second, the degree of parasite development and multiplication in MDBK cells was quantitatively assayed using radioisotope labelled uracil ($^3H-uracil$) . Third, the E. tenella sporozoites viability was assayed after preincubation of them with thicken spleen cells. E. tenella oocysts obtained from the ceca of the infected chickens were used for the source of the sporozoites. Spleen cells (I) obtained from normal chickens (FP strain) were preincubated with the sporozoites (T) at the E:T ratio of 100:1, 50:1 or 25:1 for 4 or 12 hours, and then the mixture was inoculated into the MDBK cell monolayer. Morphologically the infected MDBK cells revealed active schisogonic cycle of E. tenella in 3~4 days, which was characterized by the appearance of trophozoites, and immature and mature schizonts containing merogoites. The 3H-uracil uptake by E. tenella increased gradually in the MDBK cells, which made a plateau after 48~60 hours, and decreased thereafter. The uptake amount of $^3H-uracil$ depended not only upon the inoculum sixte of the sporozoites but also on the degree of time delay (preincubation; sporozoites only) from excystation to inoculation into MDBK cells. The 3H-uracil uptake became lower as the preincubation time was prolonged. In comparison, after preincubation of sporozoites with spleen cells for 4 or 12 hours, the 3H-uracil uptake was significantly increased compared with that of control group. From the results, it was inferred that, although the penetration of E. tenella sporozoites into the lymphoid cells such as IEL is not an essential step, it should be at least a beneficial one for the survival and development of sporozoites in the chicken intestine.

• Asian-Australasian Journal of Animal Sciences
• /
• v.25 no.3
• /
• pp.382-392
• /
• 2012

This study evaluated the effects of dietary anticoccidial drugs plus antibiotic growth promoters (AGPs) on parameters of immunity in commercial broiler chickens. Day-old chicks were raised on used litter from a farm with endemic gangrenous dermatitis to simulate natural pathogen exposure and provided with diets containing decoquinate (DECX) or monensin (COBN) as anticoccidials plus bacitracin methylene disalicylate and roxarsone as AGPs. As a negative control, the chickens were fed with a non-supplemented diet. Immune parameters examined were concanavalin A (ConA)-stimulated spleen cell proliferation, intestine intraepithelial lymphocyte (IEL) and spleen cell subpopulations, and cytokine/chemokine mRNA levels in IELs and spleen cells. ConA-induced proliferation was decreased at 14 d post-hatch in DECX-treated chickens, and increased at 25 and 43 d in COBN-treated animals, compared with untreated controls. In DECX-treated birds, increased percentages of $MHC2^+$ and $CD4^+$ IELS were detected at 14 d, but decreased percentages of these cells were seen at 43 d, compared with untreated controls, while increased $TCR2^+$ IELs were evident at the latter time. Dietary COBN was associated with decreased fractions of $MHC2^+$ and $CD4^+$ IELs and reduced percentages of $MHC2^+$, $BU1^+$, and $TCR1^+$ spleen cells compared with controls. The levels of transcripts for interleukin-4 (IL-4), IL-6, IL-17F, IL-13, CXCLi2, interferon-${\gamma}$ (IFN-${\gamma}$), and transforming growth factor${\beta}$4 were elevated in IELs, and those for IL-13, IL-17D, CXCLi2, and IFN-${\gamma}$ were increased in spleen cells, of DECX- and/or COBN-treated chickens compared with untreated controls. By contrast, IL-2 and IL-12 mRNAs in IELs, and IL-4, IL-12, and IL-17F transcripts in spleen cells, were decreased in DECX- and/or COBN-treated chickens compared with controls. These results suggest that DECX or COBN, in combination with bacitracin and roxarsone, modulate the development of the chicken post-hatch immune system.

• Animal Bioscience
• /
• v.35 no.8
• /
• pp.1235-1249
• /
• 2022

Objective: The purpose of this study was to evaluate the protection of glutamate (GLU) against the impairment in intestinal barrier function induced by lipopolysaccharide (LPS) stress in weaned pigs. Methods: Twenty-four weaned pigs were divided into four treatments containing: i) non-challenged control, ii) LPS-challenged control, iii) LPS+1.0% GLU, and iv) LPS+2.0% GLU. On day 28, pigs were treated with LPS or saline. Blood samples were collected at 0, 2, and 4 h post-injection. After blood samples collection at 4 h, all pigs were slaughtered, and spleen, mesenteric lymph nodes, liver and intestinal samples were obtained. Results: Dietary GLU supplementation inhibited the LPS-induced oxidative stress in pigs, as demonstrated by reduced malondialdehyde level and increased glutathione level in jejunum. Diets supplemented with GLU enhanced villus height, villus height/crypt depth and claudin-1 expression, attenuated intestinal histology and ultrastructure impairment induced by LPS. Moreover, GLU supplementation reversed intestinal intraepithelial lymphocyte number decrease and mast cell number increase induced by LPS stress. GLU reduced serum cortisol concentration at 4 h after LPS stress and downregulated the mRNA expression of intestinal corticotropin-releasing factor signal (corticotrophin-releasing factor [CRF], CRF receptor 1 [CRFR1], glucocorticoid receptor, tryptase, nerve growth factor, tyrosine kinase receptor A), and prevented mast cell activation. GLU upregulated the mRNA expression of intestinal transforming growth factor β. Conclusion: These findings indicate that GLU attenuates LPS-induced intestinal mucosal barrier injury, which is associated with modulating CRF signaling pathway.

• Journal of Veterinary Science
• /
• v.21 no.2
• /
• pp.26.1-26.14
• /
• 2020

Pancreatic ductal adenocarcinoma is a lethal cancer type that is associated with multiple gene mutations in somatic cells. Genetically engineered mouse is hardly applicable for developing a pancreatic cancer model, and the xenograft model poses a limitation in the reflection of early stage pancreatic cancer. Thus, in vivo somatic cell gene engineering with clustered regularly interspaced short palindromic repeats is drawing increasing attention for generating an animal model of pancreatic cancer. In this study, we selected Kras, Trp53, Ink4a, Smad4, and Brca2 as target genes, and applied Campylobacter jejuni Cas9 (CjCas9) and Streptococcus pyogens Cas9 (SpCas9) for developing pancreatic cancer using adeno associated virus (AAV) transduction. After confirming multifocal and diffuse transduction of AAV2, we generated SpCas9 overexpression mice, which exhibited high double-strand DNA breakage (DSB) in target genes and pancreatic intraepithelial neoplasia (PanIN) lesions with two AAV transductions; however, wild-type (WT) mice with three AAV transductions did not develop PanIN. Furthermore, small-sized Cjcas9 was applied to WT mice with two AAV system, which, in addition, developed high extensive DSB and PanIN lesions. Histological changes and expression of cancer markers such as Ki67, cytokeratin, Mucin5a, alpha smooth muscle actin in duct and islet cells were observed. In addition, the study revealed several findings such as 1) multiple DSB potential of AAV-CjCas9, 2) peri-ductal lymphocyte infiltration, 3) multi-focal cancer marker expression, and 4) requirement of > 12 months for initiation of PanIN in AAV mediated targeting. In this study, we present a useful tool for in vivo cancer modeling that would be applicable for other disease models as well.

• Clinical and Experimental Pediatrics
• /
• v.51 no.5
• /
• pp.492-499
• /
• 2008

Purpose : Helicobacter pylori infection is one of the most common gastrointestinal infections worldwide; it almost invariably causes chronic gastritis. Pediatric studies may provide important insights into the mucosal immune response of H. pylori-infection, as children are not submitted to environmental factors such as alcohol, tobacco and anti-inflammatory medication. The aim of the present study was to investigate the mucosal immune response against H. pylori in clinically well-defined groups: H. pylori-positive (divided into peptic ulcer disease and gastritis) and H. pylori-negative control. Methods : Antral biopsies were obtained from 45 children undergoing an upper GI endoscopy for dyspeptic symptoms. T cells (CD3+, CD4+, CD8+) and B cells (CD20+) were analyzed by quantitative immunohistochemistry. The correlation of lymphocyte subsets of gastric mucosa with histology was evaluated. Results : T cells (CD3+, CD4+, CD8+) and B cells (CD20+) were significantly increased in the lamina propria of H. pylori-positive group (P<0.01). CD8+ T cells were significantly increased in the lamina propria of the H. pylori-positive peptic ulcer disease (P<0.01). Within the epithelium, only CD4+ T cells were significantly increased in the H. pylori-positive group (P<0.01). Gastric histological parameters had a closer correlation with lymphocytes in the lamina propria than intraepithelial lymphocytes. Conclusion : This study suggests that both T cells and B cells in the lamina propria play important roles in the local immune response of H. pylori-infected children. Furthermore, it remains to be elucidated whether CD8+ T cells in the lamina propria may contribute to peptic ulcer formation in H. pylori-infected children.