• Biomedical Science Letters
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• v.5 no.1
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• pp.109-118
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• 1999

The relationship between the intestinal histopathology and number and position of intraepithelial lymphocytes (IEL) was observed chronologically in the small intestine of rats experimentally infected with Echinostoma hortense. Sprague-Dawley rats were orally infected with 200 metacercariae obtained from Misgurnus anguillicaudatus. The rats each were sacrificed on the week 1, 2, 4, 6, 8 post-infection (PI) and samples of the intestine in the part of duodenum and jejunum were taken. The samples were stained with Hematoxylin-eosin and Giemsa. The intestinal histopathology was the severest after the week 1 PI and characterized by villous atrophy, crypt hyperplasia and decrease of villus/crypt(v/c) ratio, which continued until the week 8 Pl. The number of IEL dramatically decreased during the week 1 PI, but increased gradually thereafter with a slight decrease on the week 8 PI. In control rats, the great majority of the IEL were located at the basal region of the epithelium. During the early stage of infection, however, we found a considerable proportion of IEL to moved to the intermediate or apical regions of the epithelium. From the above results, it is sugested that the change of IEL number and position during the course of E. hortense infection should be closely related to the progression and recovery of the intestinal histopathology.

• Parasites, Hosts and Diseases
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• v.40 no.3
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• pp.119-129
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• 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
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• v.32 no.4
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• pp.215-222
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• 1994

The relationship between the intestinal histopathology and number and position of' intraepithelial Iymphocytes(IEL) was observed chronologically in the small intestine of rats experimentally infected wiH Metagonimw vokogawci. Fifteen Sprague-Dawley rats were orally infected each with 3,000 metacercariae, and 3 were kept uninfected for controls. Three rats each were sacrificed on the day 5, 10, 15, 24 and 70 post-infection (PI) and samples of the small intestine, 5 cm, 10 cm, 20 cia and 70 cm posterior to the pylonls were taken. The samples were processed routinely and stained with Giemsa. The intestinal histopathology was severe during the day 5-15 PI and characterized by villous atrophy, crypt hyperplasia, and decrease of villus/ciypt height ratio. After the day 24 PI, the intestinal lesions showed some tendency of recovery The number of IEL increased at the early stage of infection, but decreased thereafter to a lower level than that of controls, with progression of the pathological changes. Then, the IEL number began to increase again after the day 24 PI. In control rats, the great majority of the IEL were located at the basal region of the epithelium. During the early stage of infection, however, a considerable proportion of IEL was found to have moved to the intermediate or apical region of the epithelium. From the above results, it is suggested that the change of IEL number and position during the course of M. yokogowoi infection should be closely related to the progression and recovery of the intestinal histopathology.

• BMB Reports
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• v.49 no.1
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• pp.11-17
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• 2016

The gastrointestinal tract forms the largest surface in our body with constantly being exposed to various antigens, which provides unique microenvironment for the immune system in the intestine. Accordingly, the gut epithelium harbors the most T lymphocytes in the body as intraepithelial lymphocytes (IELs), which are phenotypically and functionally heterogeneous populations, distinct from the conventional mature T cells in the periphery. IELs arise either from pre-committed thymic precursors (natural IELs) or from conventional CD4 or CD8αβ T cells in response to peripheral antigens (induced IELs), both of which commonly express CD8α homodimers (CD8αα). Although lineage commitment to either conventional CD4 T helper (Th) or cytotoxic CD8αβ T cells as well as their respective co-receptor expression are mutually exclusive and irreversible process, CD4 T cells can be redirected to the CD8 IELs with high cytolytic activity upon migration to the gut epithelium. Recent reports show that master transcription factors for CD4 and CD8 T cells, ThPOK (Th-inducing BTB/POZ-Kruppel-like factor) and Runx3 (Runt related transcription factor 3), respectively, are the key regulators for re-programming of CD4 T cells to CD8 lineage in the intestinal epithelium. This review will focus on the unique differentiation process of IELs, particularly lineage re-commitment of CD4 IELs. [BMB Reports 2016; 49(1): 11-17]

• Parasites, Hosts and Diseases
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• v.52 no.1
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• pp.27-33
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• 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
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• v.18 no.9
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• pp.1320-1325
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• 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.