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PubMed1990

[Chronological observation of intestinal lesions of rats experimentally infected with Echinostoma hortense].

Intestinal histopathological changes due to infection with Echinostoma hortense (Trematoda) were studied in rats after experimental infection with the metacercariae. The metacercariae were obtained from the tadpoles of Rana nigromaculata, a second intermediate host infected in the laboratory. Total 18 albino rats (Sprague-Dawley) were given 200 matacercariae each and sacrificed on the day 1, 3, 7, 11, 22 or 44 post-infection (PI). Segments of the small intestine at 1, 3, 5, 8 and 30 cm posterior to the pylorus (PTP) were resected and studied histopathologically. 1. The flukes were seen to have intruded into the intervillous space in the upper small intestine at early stages (1-3 days PI), however, they were located mainly in the intestinal lumen at later stages (7-44 days PI). The flukes were sucking and destroying the epithelial layers of villi with their oral and ventral suckers. 2. Histopathological changes of the intestine were recognizable in as early as 1-3 days after infection, and the changes became severer as the infection progressed. 3. The intestinal mucosa was histopathologically characterized by villous atrophy and crypt hyperplasia throughout the infection period. Major villous changes were blunting, fusion, severe destruction and loss of epithelial layers of villi. Villous/crypt (V/C) height ratio was remarkably reduced from 3:1 in controls to 1:1 in severely infected animals. In the stroma of villi, inflammatory cell infiltrations, vascular congestion, edema, and/or fibrosis were recognized. The goblet cells were increased in number after 11 days PI.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

[Worm recovery rate and small intestinal lesions of albino rats coinfected with Fibricola seoulensis and Metagonimus yokogawai].

Worm recovery rates and pathologic changes in small intestine of albino rats were observed after concurrent and challenge infections with metacercariae (MC) of Fibricola seoulensis and Metagonimus yokogawai, and compared with those of single infection groups. Albino rats in concurrent infection group were killed 20 days after feeding with 1,000 MC of each fluke. Rats in challenge infection group were fed with 1,000 MC of F. seoulensis and challenged by 1,000 MC of M. yokogawai 10 days after primary infection, then killed 10 days thereafter. In concurrent infection group, mean number of F. seoulensis and M. yokogawai recovered, 250 and 118 respectively, were similar to those of single infection groups. However, more flukes were collected from the duodenum and less flukes were from the ileum than from single infection group. In challenge infection group, the recovery rate of F. seoulensis was similar to that of single infection group and the distribution of the flukes was similar to that of concurrent infection group. Mean number of M. yokogawai, 69, was significantly lower than that of single infection group. Its distribution, however, extended to the duodenum and most of the flukes were recovered from the jejunum. In concurrent infection group, villi of the duodenum were more markedly thickened, fused and shortened than those in F. seoulensis single infection group. The crypt epithelium appeared to be hyperplastic and inflammatory cell infiltration into the villous stroma was mild. Villous atrophy in the jejunum and ileum was milder than in M. yokogawai single infection group. In challenge infection group, the findings were similar to those of concurrent infection group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Mucosal mast cell responses to experimental Metagonimus yokogawai infection in rats.

Intestinal mucosal mast cell (MMC) responses were studied in rats experimentally infected with Metagonimus yokogawai (Digenea: Heterophyidae). Twenty Sprague-Dawley rats were fed each 2,500 metacercariae isolated from the sweetfish and sacrificed on the week 1, 2, 3 and 4 post-infection (PI). Recovery of worms was performed from the small intestine of each rat. To visualize the MMCs, duodenal and jejunal (upper, middle and lower) tissue sections were made and stained with alcian blue/safranine-0. The average worm recovery rates were 16.2% and 13.8% on the week 1 and week 2, respectively, but they decreased rapidly to 4.1% and 4.2% on the week 3 and week 4 PI, respectively, which indicate spontaneous worm expulsion after the week 2. The MMC number in the infected rats was, compared with uninfected controls, significantly increased in the whole small intestine, through the whole period of observation. The peak level of mastocytosis was observed on the week 3 PI. It is strongly suggested that MMCs might be involved in the expulsion process of flukes from the rat intestine.

Animals↗
PubMed1994

[Chronological observation on intestinal histopathology and intraepithelial lymphocytes in the intestine of rats infected with Metagonimus yokogawai].

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 Metagonimus yokogawai. Fifteen Sprague-Dawley rats were orally infected each with 3,000 metacecariae, 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 cm and 70 cm posterior to the pylorus 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/crypt 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. yokogawai infection should be closely related to the progression and recovery of the intestinal histopathology.

Animals↗
PubMed1995

The effect of reinfection with Neodiplostomum seoulensis on the histopathology and activities of brush border membrane bound enzymes in the rat small intestine.

Neodiplostomum seoulensis, one of the human intestinal trematodes, was reinfected to albino rats, and worm recovery rates, histopathology and activity changes of the intestinal brush border membrane bound enzymes were observed. The experimental groups were three; uninfected, primary infection and reinfection. The worm recovery rate in the reinfection group was much lower than in the primary infection group 14 days after infection. The duodenal histopathology showed villous atrophy during the first and second week in the primary infection group. In the reinfection group, however, villous changes occurred as early as 3 days after the infection, and the lesion was found healed 7 days after infection. The activities of alkaline phosphatase and sucrase in the duodenum of primary infection rats decreased nearly half of the controls 2 weeks after infection, whereas the activities were unchanged in the reinfection group. However, no changes in the activities were observed in the proximal jejunum between the experimental groups. These findings suggested that a secondary infection of N. seoulensis in rats should make less damage on the intestinal mucosa than a primary infection.

Alkaline Phosphatase↗
PubMed1995

IgA response in mice infected with Neodiplostomum seoulensis.

To observe the production of IgA in Balb/c mice with neodiplostomiasis, 20 mice were infected with each 200 metacercariae of Neodiplostomum seoulenis. Sera and the duodenums were obtained 3, 7, 14, 28 days post-infection (PI) from five mice each group. Neodiplostomum specific IgA in serum by the enzyme-linked immunosorbent assay increased from 7 days PI and persisted till 28 days PI. Immunohistochemistry for IgA was done with sections of the duodenum. The IgA-positive reaction was generally seen in the lamina propria and submucosa. Some of epithelial cells were positive at 7 and 14 days PI. The present finding showed that Neodiplostomun specific IgA antibody increased in serum and that there was local reaction of IgA in the mucosa and submucosa of the duodenum but not directly related with worm expulsion.

Animals↗
PubMed1997

Expression patterns of proliferating cell nuclear antigen in the small intestine of mice infected with Metagonimus yokogawai and Metagonimus Miyata type.

Genus Metagonimus has been a subject of taxonomic debates for several years. In morphological aspects, M. yokogawai has been thought to have three subtypes, namely Yokogawa type (M. yokogawai in strict sense), Miyata type and Koga type, But differences in the intestinal pathology induced by these subtypes have not been studied yet. In this study we compared the pathological reactions induced by M. yokogawai and Metagonimus Miyata type using proliferating cell nuclear antigen (PCNA) index. Metacercariae (Mc) of M. yokogawai were collected by artificial digestion of Plecoglossus altivelis and Mc of Metagonimus Miyata type were collected from Zacco platypus. Three hundreds Mc of each species were infected orally to ICR mice. The mice were sacrificed at 3, 6, 10, 16 and 23 days after infection and the small intestines were resected into three portions (proximal, middle, and distal). Immunohistochemical staining for PCNA was done using PC-10 (DAKO-PCNA, CA, USA). The PCNA indices in M. yokogawai infected group on the 6th and 23rd day after infection were lower than in the control and Miyata type infected groups (p < 0.05) from all of the three intestinal regions. On the other hand, the control group and Metagonimus Miyata type infected group did not make any differences in PCNA indices. The villus/crypt (V/C) ratio was also decreased significantly in M. yokogawai infected mice but not in Metagonimus Miyata type infected ones. It is suggested that M. yokogawai induce villous atrophy through a decrease in the cell proliferation at the crypt. The results of this study suggested that M. yokogawai induce more serious intestinal pathology than Metagonimus Miyata type.

Animals↗
PubMed1998

Intestinal mastocytosis and goblet cell hyperplasia in BALB/c and C3H mice infected with Neodiplostomum seoulense.

Mucosal mast cell (MMC) and goblet cell (GC) responses were observed in the small intestine of two strains of mice (BALB/c and C3H) infected with Neodiplostamum seoulense, and their roles in the host defense and worm expulsion were studied. From day 3 to 28 post-infection (PI) with 200 metacercariae, the worm recovery rate from BALB/c mice was consistently and remarkably higher than that from C3H mice. In the duodenum of both strains of mice, the main habitat of the flukes, mastocytosis was pronounced on day 7 PI but quickly diminished thereafter. Similar kinetics were observed in the jejunum and ileum, although the extent of mastocytosis was lesser in the ileum than other two areas. These MMC kinetics were not different between the two strains of mice. Moreover, the extent of mastocytosis was stronger in BALB/c mice than in C3H mice. GC hyperplasia was remarkable in the duodenum of BALB/c mice throughout the course of infection except day 14 PI, whereas it was recognizable only in the jejunum and ileum of C3H mice on day 7 PI. Mucin activation was evidently demonstrated in both strains of mice throughout the course of infection, but more marked in BALB/c than in C3H mice. The results strongly suggest that mastocytosis and GC hyperplasia are local immune responses against N. seoulense, however, they play a minor role in the host defense and worm expulsion.

Animals↗
PubMed1999

An incidental case of human Heterophyes nocens infection diagnosed by sectional morphology in a biopsy specimen of the small intestine.

A case of human infection with Heterophyes nocens (Heterophyidae) was incidentally found in a biopsy specimen of the Meckel's diverticulum at the upper part of the small intestine. The patient was a 58-year-old man living in a rural area of Talsonggun, Kyongsangbuk-do. He had gastrointestinal symptoms such as epigastric pain, indigestion, and abdominal discomfort for 3 months, and severe diarrhea, abdominal pain, and vomiting for about 1 month before hospitalization. Endoscopy of the upper part of the small intestine revealed a Meckel's diverticulum, and it was excised and histopathologically examined. Three adult flukes were incidentally found sectioned in the mucosa, and they were identified as H. nocens. The patient had a history of eating raw mullets at a fish market in Pusan 6 months ago, and the mullets were presumed to be the source of infection. This case brings a considerable interest in that specific diagnosis of heterophyid infections could be done by sectional morphology of the worms.

Animals↗
PubMed2000

Mucosal mast cell responses in the small intestine of rats infected with Echinostoma hortense.

Mucosal mast cell (MMC) responses and worm recovery rates in rats infected with Echinostoma hortense were investigated from day 3 to day 56 post-infection (p.i.). Experimental infected group showed apparently higher number of MMC in each part of the small intestine than that of the control group. The number of MMC in the duodenum increased gradually after the infection and reached a peak on day 35 p.i. Thereafter, the number of MMC continued to decrease at a slow pace. The kinetics of MMC responses in the upper and lower jejunum were similar to that of the duodenum, but the number of MMC in the jejunum was lower. The worm recovery rate decreased with respect to time of which it was markedly reduced on day 49 and 56 p.i. The duration in which a high number of MMC appeared was similar to that in which a low rate in worm recovery was recorded. These results indicate that intestinal mastocytosis may play an important role in the expulsion of E. hortense.

Animals↗
PubMed2001

Intestinal histopathology and in situ postures of Gymnophalloides seoi in experimentally infected mice.

The intestinal histopathology and in situ postures of Gymnophalloides seoi (Digenea: Gymnophallidae) were studied using C3H/HeN and C57BL/6 mice as experimental hosts; the effects of immunosuppression were also observed. The metacercariae isolated from naturally infected oysters, 300 or 1,000 in number, were infected orally to each mouse, and the mice were killed at days 3-21 post-infection (PI). In immunocompetent (IC) mice, only a small number of flukes were found in the mucosa of the duodenum and jejunum during days 3-7 PI, with their large oral suckers pinching and sucking the root of villi. The intestinal mucosa showed mild villous atrophy, crypt hyperplasia, and inflammations in the villous stroma and crypt, with remarkable goblet cell hyperplasia. These mucosal changes were almost restored after days 14-21 PI. In immunosuppressed (IS) mice, displacement as well as complete loss of villi adjacent to the flukes was frequently encountered, otherwise the histopathology was generally mild, with minimal goblet cell hyperplasia. In these mice, numerous flukes were found, and it seemed that they were actively moving and rotating in situ. Several flukes were found to have invaded into the submucosa, almost facing the serosa. These results indicate that in IC mice the intestinal histopathology caused by G. seoi is generally mild, and the flukes do not penetrate beyond the mucosa, however, in IS mice, the flukes can cause severe destruction of neighboring villi, and some of them invade into the submucosa.

Animals↗
PubMed2000

IL-10 is required for prevention of necrosis in the small intestine and mortality in both genetically resistant BALB/c and susceptible C57BL/6 mice following peroral infection with Toxoplasma gondii.

The role for IL-10 in the immunopathogenesis of acute toxoplasmosis following peroral infection was examined in both genetically susceptible C57BL/6 and resistant BALB/c mice. C57BL/6-background IL-10-targeted mutant (IL-10-/-) mice all died in 2 wk after infection with 20 cysts of the ME49 strain, whereas only 20% of control mice succumbed. Histological studies revealed necrosis in the small and large intestines and livers of infected IL-10-/- mice. The necrosis in the small intestine was the most severe pathologic response and was not observed in control mice. Treatment of infected IL-10-/- mice with either anti-CD4 or anti-IFN-gamma mAb prevented intestinal pathology and significantly prolonged time to death. Treatment of these animals with anti-IL-12 mAb also prevented the pathology. Significantly greater amounts of IFN-gamma mRNA were detected in the lamina propria lymphocytes obtained from the small intestine of infected IL-10-/- mice than those from infected control mice. In common with C57BL/6-background IL-10-/- mice, BALB/c-background IL-10-/- mice all died developing intestinal pathology after infection. Control BALB/c mice all survived even after infection with 100 cysts and did not develop the intestinal lesions. Treatment with anti-IFN-gamma mAb prevented the pathology and prolonged time to death of the infected IL-10-/- mice. These results strongly suggest that IL-10 plays a critical role in down-regulating IFN-gamma production in the small intestine following sublethal peroral infection with Toxoplasma gondii and that this down-regulatory effect of IL-10 is required for prevention of development of IFN-gamma-mediated intestinal pathology and mortality in both genetically resistant BALB/c and susceptible C57BL/6 mice.

Administration, Oral↗
PubMed2000

A role of mast cell glycosaminoglycans for the immunological expulsion of intestinal nematode, Strongyloides venezuelensis.

We examined effects of mast cell glycosaminoglycans on the establishment of the intestinal nematode, Strongyloides venezuelensis, in the mouse small intestine. When intestinal mastocytosis occurred, surgically implanted adult worms could not invade and establish in the intestinal mucosa. In mast cell-deficient W/Wv mice, inhibition of adult worm invasion was not evident as compared with littermate +/+ control mice. Mucosal mastocytosis and inhibition of S. venezuelensis adult worm mucosal invasion was tightly correlated. To determine effector molecules for the invasion inhibition, adult worms were implanted with various sulfated carbohydrates including mast cell glycosaminoglycans. Among sulfated carbohydrates tested, chondroitin sulfate (ChS)-A, ChS-E, heparin, and dextran sulfate inhibited invasion of adult worms into intestinal mucosa in vivo. No significant inhibition was observed with ChS-C, desulfated chondroitin, and dextran. ChS-E, heparin, and dextran sulfate inhibited adhesion of S. venezuelensis adult worms to plastic surfaces in vitro. Furthermore, binding of intestinal epithelial cells to adhesion substances of S. venezuelensis, which have been implicated in mucosal invasion, was inhibited by ChS-E, heparin, and dextran sulfate. Because adult worms of S. venezuelensis were actively moving in the intestinal mucosa, probably exiting and reentering during infection, the possible expulsion mechanism for S. venezuelensis is inhibition by mast cell glycosaminoglycans of attachment and subsequent invasion of adult worms into intestinal epithelium.

Animals↗
PubMed2000

Enteric infection acts as an adjuvant for the response to a model food antigen.

Oral administration of soluble protein Ags typically induces Ag-specific systemic nonresponsiveness. However, we have found that feeding a model food protein, OVA, to helminth-infected mice primes for a systemic OVA-specific Th2 response. In this report we show that, in addition to creating a Th2-priming cytokine environment, helminth infection up-regulates costimulatory molecule expression on mucosal, but not peripheral, APCs. To examine the consequences of mucosal infection for the T cell response to orally administered Ag, we adoptively transferred transgenic, OVA-specific, T cells into normal mice. We found that helminth infection enhances the expansion and survival of transgenic T cells induced by Ag feeding. Transfer of 5,6-carboxyfluorescein diacetate succinimidyl ester-labeled donor cells showed that T cell proliferation in response to Ag feeding takes place primarily in the mesenteric lymph nodes. Upon subsequent peripheral exposure to Ag in adjuvant, the proliferative capacity of the transferred transgenic T cells was reduced in noninfected mice that had been fed OVA. Helminth infection abrogated this reduction in proliferative capacity. Our data suggests that enteric infection can act as an adjuvant for the response to dietary Ags and has implications for allergic responses to food and the efficacy of oral vaccination.

Adjuvants, Immunologic↗
PubMed2001

The role of IL-4 in Heligmosomoides polygyrus-induced alterations in murine intestinal epithelial cell function.

IL-4 and IL-13 promote gastrointestinal worm expulsion, at least in part, through effects on nonlymphoid cells, such as intestinal epithelial cells. The role of IL-4/IL-13 in the regulation of intestinal epithelial function during Heligmosomoides polygyrus (Hp) infection was investigated in BALB/c mice infected with Hp or treated with a long-lasting formulation of recombinant mouse IL-4/alphaIL-4 complexes (IL-4C) for 7 days. Separate groups of BALB/c mice were drug-cured of initial infection and later reinfected and treated with anti-IL-4R mAb, an antagonist of IL-4 and IL-13 receptor binding, or with a control mAb. Segments of jejunum were mounted in Ussing chambers, and short circuit current responses to acetylcholine, histamine, serotonin, PGE2, and glucose were determined. Although only modest changes in epithelial cell function were observed during primary Hp infection, IL-4C or a secondary Hp infection each induced more dramatic changes, including increased mucosal permeability, reduced sodium-linked glucose absorption, and increased Cl- secretory response to PGE2. Some, but not all, effects of IL-4C and Hp infection were dependent on enteric nerves. Hp-induced changes in epithelial function were attenuated or prevented by anti-IL-4R mAb. Thus, IL-4/IL-13 mediate many of the effects of Hp infection on intestinal epithelial cell function and do so both through direct effects on epithelial cells and through indirect, enteric nerve-mediated prosecretory effects. These immune system-independent effector functions of IL-4/IL-13 may be important for host protection against gastrointestinal nematodes.

Animals↗
PubMed2003

Absence of CC chemokine ligand 2 results in an altered Th1/Th2 cytokine balance and failure to expel Trichuris muris infection.

Despite a growing understanding of the role of cytokines in immunity to intestinal helminth infections, the importance of chemokines has been neglected. As a chemokine with both chemoattractive properties and an ability to shape the quality of the adaptive immune response, CC chemokine ligand 2 (CCL2) was investigated as an attractive candidate for controlling resistance to these types of infection, which require highly polarized Th cell responses. We show here for the first time that CCL2 plays an important role in the development of resistance to infection by the gastrointestinal nematode Trichuris muris. Thus, in the absence of CCL2, worm expulsion does not occur, and the lymph node draining the site of infection becomes a Th1-promoting environment. Elevated levels of IL-12 are produced by polarizing APCs, and the composition of the APC environment itself is perturbed, with reduced numbers of macrophages.

Animals↗
PubMed2004

Enteric nematodes induce stereotypic STAT6-dependent alterations in intestinal epithelial cell function.

Infection with gastrointestinal nematodes exerts profound effects on both the immune and physiological responses of the host. We showed previously that the Th2 cytokines, IL-4 and IL-13, induce STAT6-dependent changes in intestinal epithelial cell permeability, absorption, and secretion that are similar to those observed in a secondary infection with Heligmosomoides polygyrus. In the current study we investigated whether nematode-induced effects on epithelial cell function were 1) generic, 2) dependent upon STAT6, and 3) attributable to direct effects on the epithelial cells themselves or mediated by effects on enteric nerves. Our results demonstrate that infection of BALB/c mice with three different gastrointestinal nematodes (H. polygyrus, Nippostrongylus brasiliensis, and Trichinella spiralis) alters intestinal epithelial cell function by decreasing resistance, glucose absorption, and secretory responses to 5-hydroxytryptamine and acetylcholine, two critical mediators in the submucosal reflex pathway. These modified responses are dependent on STAT6 and are the result of both direct effects and indirect effects mediated through enteric nerves.

Animals↗