The small intestinal mucosa in dermatitis herpetiformis. II. Relationship of the small intestinal lesion to gluten.
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Adult↗
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The effects of fat feeding on apolipoprotein AI secretion from rat small intestinal epithelium.
The small intestine is known to be an important synthetic site for certain apolipoproteins, which are subsequently secreted from the enterocyte into the mesenteric lymph. We have studied apolipoprotein AI and CIII content of the enterocyte during the course of fat feeding in order to determine their relative synthetic and secretory rates. Rat intestinal enterocytes were isolated from the entire jejunal villus after fat feeding in vivo. The apo AI content fell 50% as determined by RIA one and two hours after fat feeding. By four hours, the intracellular cellular levels had returned to prefeeding levels. These changes in apolipoprotein AI levels were not seen in the terminal ileum. Apolipoprotein CIII levels remained unchanged afer fat feeding. To determine the effect of free fatty acids on apolipoprotein AI secretion, organ culture explants were incubated for four hours in the presence and absence of 360 microM oleic acid bound to albumin. Apolipoprotein AI detected in the incubation media reflected release from the lamina propria (which was not colchicine sensitive), and secretion from the enterocyte (which was inhibited by colchicine). In the absence of oleic acid, enterocyte secretion of apolipoprotein AI accounted for about half of the apo AI recovered in the medium. In the presence of oleic acid, the total apolipoprotein AI content of the tissue increased by 50 percent. A similar increase in colchicine sensitive secretion was observed. The secretion of apolipoprotein AI from explants was more rapid in the presence of oleic acid and began without the half hour lag noted when oleic acid was absent. The mid intestine was most active in the secretion of apolipoprotein AI. These data are consistent with the hypothesis that in the first few hours after feeding the rate of secretion of apolipoprotein AI exceeds the synthetic capacity of the small intestinal epithelium.
Animals↗
Effect of transplantation on tissue levels of substance P, vasoactive intestinal polypeptide, and serotonin in rat small intestine.
Denervation of the gut, resulting in altered bowel function, has been viewed as an impediment to the clinical success of small intestinal transplantation. This study examined the effect of complete extrinsic denervation of the jejunum and ileum on tissue levels of VIP, SP, and 5-HT in a rat model of small intestinal transplantation. Orthotopic total small bowel isograft transplants were performed in 18 Lewis inbred rats. Sham operations consisted of occluding the superior mesenteric artery of 18 Lewis rats for 10 minutes to provide comparable degrees of ischemia. Six rats from each group were sacrificed 1, 2, and 4 weeks following transplantation or sham operation. The jejunum and ileum were removed and extracted in acid for measurement of VIP, SP, and 5-HT by radioimmunoassay. There were no statistically significant differences in the jejunal or ileal content of VIP or 5-HT or the jejunal content of SP between the transplant and sham groups. An initial decrease in ileal SP content at 1 week following transplantation was no longer evident by the fourth week. We conclude that the extrinsic denervation of small intestinal transplantation has minimal effects on the intestinal content of VIP, SP, and 5-HT and should not significantly affect physiologic function controlled by these gastrointestinal hormones.
Animals↗
The large intestine compensates for insufficient calcium absorption in the small intestine in rats.
We previously demonstrated that the large intestine compensated for decreased calcium (Ca) absorption caused by renal failure in rats fed a highly fermentable dietary fiber. In this study, we examined whether the large intestine compensated for insufficient Ca absorption in the rat small intestine without ingestion of a fermentable dietary fiber. Rats were fed one of four test diets containing either insoluble (carbonate) or soluble (gluconate, lactate, or citrate) Ca sources. The dietary Ca level was 2.0 g/kg, which is lower than the minimum requirement for rats (3.0 g/kg), to conduct the present study under a condition in which rats can maximally absorb Ca. To prevent Ca absorption in the small intestine, we replaced a primary phosphate (KH2PO4) with secondary phosphates (K2HPO4 and Na2HPO4) in diets. The apparent Ca absorption in the small intestine was estimated by adding chromic oxide (Cr2O3) as an insoluble and an unabsorbed marker to test diets and by measuring the ratio of Ca:Cr in the cecal content. The apparent Ca absorption in the whole intestine was estimated by the intake and fecal excretion of Ca. The apparent Ca absorption in the small intestine was significantly lower from the Ca carbonate diet than from the Ca gluconate, lactate, or citrate diets. The apparent Ca absorption in the whole intestine was not significantly different among the four groups, and the values were similar to the absorption rates in the small intestines of rats fed diets containing soluble Ca sources. These results show the following: (a) In rats fed 0.2% Ca diets containing soluble Ca salts, Ca is mostly absorbed in the small intestine, even in secondary phosphate intakes; (b) In contrast, in rats fed a 0.2% Ca diet containing an insoluble Ca salt (carbonate), Ca is not sufficiently absorbed in the small intestine. However, the large intestine compensates for the small intestinal Ca absorption decreased by dietary secondary phosphates.
Animals↗
[Data on alkaline and acid phosphatase in the small intestine. V. Relationship between glucose absorption and alkaline phosphatase, acid phosphatase, and hexokinase activities in the rat small intestine].
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Acid Phosphatase↗
STUDIES ON SMALL INTESTINAL CRYPT EPITHELIUM. II. EVIDENCE FOR THE MECHANISMS OF SECRETORY ACTIVITY BY UNDIFFERENTIATED CRYPT CELLS OF THE HUMAN SMALL INTESTINE.
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Cell Biology↗
Rac1 mutations produce aberrant epithelial differentiation in the developing and adult mouse small intestine.
The mouse small intestinal epithelium undergoes continuous renewal throughout life. Previous studies suggest that differentiation of this epithelium is regulated by instructions that are received as cells migrate along crypt-villus units. The nature of the instructions and their intracellular processing remain largely undefined. In this report, we have used genetic mosaic analysis to examine the role of Rac1 GTPase-mediated signaling in controlling differentiation. A constitutively active mutation (Rac1Leu61) or a dominant negative mutation (Rac1Asn17) was expressed in the 129/Sv embryonic stem cell-derived component of the small intestine of C57Bl/6-ROSA26<->129/Sv mice. Rac1Leu61 induces precocious differentiation of members of the Paneth cell and enterocytic lineages in the proliferative compartment of the fetal gut, without suppressing cell division. Forced expression of the dominant negative mutation inhibits epithelial differentiation, without affecting cell division, and slows enterocytic migration along crypt-villus units. The effects produced by Rac1Leu61 or Rac1Asn17 in the 129/Sv epithelium do not spread to adjacent normal C57Bl/6 epithelial cells. These results provide in vivo evidence that Rac1 is involved in the import and intracellular processing of signals that control differentiation of a mammalian epithelium.
Aging↗
Control mechanisms of crypt cell production in the small intestinal epithelium.
The small intestinal epithelium constitutes the cell renewing system with the largest turnover activity in the body. It is influenced by numerous factors, and has a great potential for adaptation. The control mechanisms responsible for the balance between cell production and cell loss in this system are still largely unknown. In this paper we present the hypothesis for two control mechanisms of crypt cell production. The first mechanism, the feedback control mechanism of crypt cell production by the functional villus cell population, regulates the relative size of the proliferative cell compartment in the crypt (i.e. the growth fraction), and it is a strictly local control mechanism. The second mechanism, the adaptive control mechanism of crypt cell reduction, regulates the total size of the crypt without changing the relative size of the proliferative cell compartment in the crypt. This control mechanism may act in a local as well as in a systemic way. Some of the problems encountered in studies on the control of crypt cell production in the small intestinal epithelium, are briefly discussed.
Animals↗
Semi-invasive laser-Doppler flowmetry technique. New application for recordings of hemodynamics in combination with manometry of human small intestine.
A small-bowel manometry tube was supplied with two single-fiber microprobes, which recorded blood flow in the proximal small intestine by the laser-Doppler flowmetry (LDF) technique. In all experiments, saline was infused intravenously as control during the first migrating motor complex (MMC) cycle, and a drug or another saline control given intravenously during the second MMC cycle. Recordings were performed during phase 1 of MMC, i.e. when motor pattern showed quiescence. Adrenaline increased blood perfusion values by 140% in proximal duodenum and 95% in distal duodenum. The alpha 2-adrenoceptor agonist clonidine decreased the corresponding values by 34 and 25%, respectively, while oxymetazoline decreased perfusion by 33 and 44% at the same levels. The beta-adrenoceptor agonist isoprenaline increased blood perfusion values by 172% in the proximal duodenum and 194% in the distal duodenum, whereas the antagonist propranolol decreased the corresponding values by 45 and 52%, respectively. In a separate group of subjects, propranolol was given after adrenaline. The increase in blood perfusion regularly seen after adrenaline was blocked after propranolol administration. In conclusion, our findings validate semi-invasive LDF technique for studies of hemodynamics in human small intestine under basal motor conditions and in drug-induced blood flow changes.
Adrenergic alpha-Agonists↗
A case of intestinal hemorrhage due to small intestinal metastases from primary lung cancer.
Although intestinal metastases from lung cancer are not rare at postmortem studies, the development of clinically significant symptoms from the gastrointestinal metastases is very unusual. We report a case of small intestinal hemorrhage leading to intestinal perforation secondary to metastases from a large cell carcinoma of the lung in a 31-year-old man along with a review of the literature.
Adult↗
JNK (c-Jun NH2 terminal kinase) and p38 during ischemia reperfusion injury in the small intestine.
BACKGROUND: In small intestinal ischemia reperfusion injury, we investigated the pathophysiological role of c-Jun NH2 terminal kinase (JNK) and p38 in order to determine whether the dual inhibition of JNK and p38 was beneficial. METHODS: Ischemia reperfusion injury was induced by clamping the superior mesenteric artery for 30 min in Wistar male rats. The inhibition of JNK and p38 was achieved with LL-Z1640-2 as a novel JNK and p38 dual inhibitor in vivo. Between the non-treatment group (Control group) and the LL-Z1640-2 treatment group (LL-Z group), the following findings were compared; histological damage by hematoxylin and eosin (H. E.) staining, JNK and p38 activation by a kinase assay, the localization of apoptosis using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method, the localization of activated JNK and activated p38 based on immunohistochemistry. RESULTS: The activation of JNK and p38 increased remarkably after reperfusion according to a kinase assay. In immunohistochemistry for activated JNK and activated p38, a remarkable degree of positive staining was revealed in the nucleus of the detached epithelial cells from the tip of villi after reperfusion. In addition, many TUNEL positive cells were observed in the detached epithelial cells where JNK and p38 were activated. Pretreatment of LL-Z1640-2 inhibited the activation of JNK and p38, and also significantly improved the histological damage. CONCLUSIONS: These results suggest that JNK and p38 both play a key role during small intestinal ischemia reperfusion injury through a proapoptotic action on the tip of villi.
Animals↗
Intestinal malrotation: the role of small intestinal dysmotility in the cause of persistent symptoms.
To investigate the possibility that small intestinal dysmotility is a cause of long-standing and persistent symptoms in patients with malrotation, we retrospectively reviewed 94 patients operated on for intestinal malrotation. In 50 patients operated on during the neonatal period, associated abnormalities were common (24%) and all presented with obstructive symptoms; only three (6%) had continuing mild symptoms the postneonatal period (aged 1 month to 1 year), five of whom (22%) had other abnormalities. Recurrent vomiting was the most common presentation (11/23); only 5 patients (21%) had acute obstruction. Response to operation was good in 18 (78%) and two had persistant symptoms; both died. Twenty-one patients presented beyond infancy (aged greater than 1 year), only 19 of whom had symptoms of less than 2 months' duration. Eight (47%) of those with long-standing symptoms had no relief from operation. Small bowel motility was recorded manometrically in 4 patients with long-standing symptoms. The findings suggest that small intestinal dysmotility may be common in patients with malrotation and persistant symptoms.
Adolescent↗
Experimental studies on fluid pathophysiology in small intestinal obstruction in the rat. VI. Effects of intraluminal hyperosmolality and simultaneous intravenous infusions on the experimentally obstructed small intestine of the rat.
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Animals↗
[A roentgenological study on the small intestinal lesions in 3 cases of amyloidosis --with special reference to the double contrast study of the upper small intestine (author's transl)].
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Amyloidosis↗
An overview of adenocarcinoma of the small intestine.
Even though the small intestine contains 90% of the gastrointestinal tract mucosa and is located between the stomach and large intestine, two organs with a high cancer incidence, adenocarcinoma of the small intestine is 1/50th as common as adenocarcinoma of the large bowel. In several other respects, small-intestinal adenocarcinoma resembles large bowel adenocarcinoma; eg, it arises from adenomatous polyps, co-occurs in the same individuals, and has a similar pattern of incidence rates by country. Small-intestinal adenocarcinoma is diagnosed prior to surgery in only about 50% of cases and often occurs in conjunction with small bowel obstruction. The mainstay of treatment is surgery; prognosis depends on stage at presentation. Little is known about the use of radiotherapy and chemotherapy in this malignancy, but most physicians utilize therapeutic strategies modeled on the management of large-intestinal adenocarcinoma. Clarification of the reason for the low incidence of small-intestinal adenocarcinoma could lead to new interventions for the prevention of colorectal cancer.
Adenocarcinoma↗
Pathogenic importance of intestinal hypermotility in NSAID-induced small intestinal damage in rats.
BACKGROUND/AIM: Nonsteroidal anti-inflammatory drugs (NSAIDs) such as indomethacin produce damage in the small intestine as a major adverse reaction. We examined the effect of various NSAIDs on intestinal motility and investigated the pathogenic importance of motility changes in the intestinal ulcerogenic response to indomethacin in rats. METHODS: Animals without fasting were given various NSAIDs (indomethacin 10 mg/kg, diclofenac 40 mg/kg, flurbiprofen 20 mg/kg, naproxen 40 mg/kg) s.c., and in the case of indomethacin, the following parameters were examined in the small intestine 24 h later; the lesion score, the number of enterobacteria and myeloperoxidase (MPO) as well as inducible nitric oxide (iNOS) activity. Intestinal motility was monitored as intraluminal pressure recordings using a balloon under anesthesia. RESULTS: All NSAIDs tested decreased mucosal PGE(2) levels and produced hemorrhagic lesions in the small intestine, accompanied by intestinal hypermotility. As representative of NSAIDs, indomethacin also increased the extent of enterobacterial invasion and MPO as well as iNOS activity before the occurrence of intestinal damage, and the hypermotility response was observed earlier than the onset of any other event caused by this agent. The intestinal lesions induced by indomethacin were prevented by either supplementation with dmPGE(2), inhibition of bacterial invasion with ampicillin or inhibition of iNOS activity with aminoguanidine, while the hypermotility response was prevented by dmPGE(2) only. In addition, the observed effects of dmPGE(2) were all mimicked by atropine when the intestinal hypermotility was suppressed by this agent. CONCLUSION: These results suggest the pathogenic importance of intestinal hypermotility in the intestinal ulcerogenic response to NSAIDs in rats and show that this event is critical for the occurrence of enterobacterial invasion under PG deficiency, followed by various inflammatory changes and damage in the mucosa. This study also suggests that the antispasmodic drug is protective against NSAID-induced intestinal lesions.
Animals↗
Experimental assessment of small intestinal submucosa as a small bowel graft in a rat model.
BACKGROUND/PURPOSE: Small intestinal submucosa (SIS) is an extracellular matrix used in tissue engineering. The purpose of this study is to evaluate the feasibility of using SIS as a scafford for small bowel regeneration in a rat model. METHODS: A 2-cm length tubular SIS graft from donor Sprague Dawley rats was interposed with bilateral anastomosis in the median tract of an isolated ileal loop of Lewis rats used to construct an ileostomy. The grafts were harvested and analyzed at each of the time-points ranging from 2 weeks to 24 weeks after operation using histology and immunohistochemistry. RESULTS: Macroscopic examination found no adhesion in the surrounding area of neointestine by 24 weeks, and no stenosis was visible. The shrinkage of neointestine was indicated from 20% to 40%. Histologic and immunohistochemical evaluation showed that SIS grafts were colonized by numerous inflammation cells by 2 weeks. Neovascularization was evident, but the luminal surface was not epithelized. By 4 weeks, transitional mucosal epithelial layer began to line the luminal surface of the graft, and nearly 70% luminal surface of the graft had been covered by mucosal epithelium at 8 weeks. By 12 weeks, the luminal surface was covered completely by a mucosal layer with distinct bundles of smooth muscle cells in the neointestine. At 24 weeks, the neointestine wall showed 3 layers of mucosa, smooth muscle, and serosa. CONCLUSIONS: The preliminary study suggested that SIS allow rapid regeneration of mucosa and smooth muscle and might be a viable material for the creation of neointestine.
Absorbable Implants↗
Human small intestinal mucosa harbours a small population of cytolytically active CD8+ alphabeta T lymphocytes.
Intraepithelial lymphocytes (IEL) in normal human small intestine exhibit cytotoxicity. This study was undertaken to characterize the effector cells and their mode of action. Freshly isolated jejunal IEL and lamina propria lymphocytes (LPL), as well as IEL and LPL depleted of CD4+, CD8+ and T-cell receptor (TCR)-gammadelta+ cells were used as effector cells in anti-CD3-mediated redirected cytotoxicity against a murine FcgammaR-expressing cell line. Effector cell frequencies were estimated by effector to target cell titration and limiting dilution. The capacity of IEL and LPL to kill a Fas-expressing human T-cell line was also analysed. T-cell subsets were analysed for perforin, granzyme B, Fas-ligand (FasL), tumour necrosis factor-alpha (TNF-alpha) and TNF-related apoptosis inducing ligand (TRAIL) mRNA expression by reverse transcription-polymerase chain reaction (RT-PCR). Frequencies of IEL expressing the perforin and FasL proteins were determined by immunomorphometry. Both IEL and LPL exhibited significant Ca2+-dependent, anti-CD3-mediated cytotoxicity, approximately 30% specific lysis at the effector to target cell ratio 100. The cytotoxic cells constituted, however, only a small fraction of IEL and LPL ( approximately 0.01%). CD8+ TCR-alphabeta+ cells accounted for virtually all the cytotoxicity and expressed mRNA for all five cytotoxic proteins. The frequency of granzyme B-expressing samples was higher in CD8+ cells than in CD4+ cells (P<0.05 and <0.01 for IEL and LPL, respectively). In addition, both IEL and LPL exhibited significant spontaneous anti-CD3-independent cytotoxicity against Fas-expressing human T cells. This killing was mediated by Fas-FasL interaction. On average, 2-3% of the IEL expressed perforin and FasL. We speculate that CD8+ memory cells accumulate in the jejunal mucosa and that the CD8+ TCR-alphabeta+ lymphocytes executing TCR/CD3-mediated, Ca2+-dependent cytotoxicity are classical cytotoxic T lymphocytes 'caught in the act' of eliminating infected epithelial cells through perforin/granzyme exocytosis. The observed Fas/FasL-mediated cytotoxicity may be a reflection of ongoing down-regulation of local immune responses by 'activation-induced cell death'.
Adult↗