Cells In Proximal Intestine Research Articles

Small Intestinal Bacterial Overgrowth (SIBO)

In the healthy human being, there are a variety of intrinsic defense mechanisms that control the number of bacteria and its composition in various parts of the gastrointestinal tract. These defense mechanism include gastric acid secretion, preserved gastrointestinal motility (particularly phase III of the migrating motor complex), normal bacterial microflora, pancreatic biliary secretion, and an intact ileocecal valve, all of which protect against bacterial overgrowth. Any disturbance or alteration in the inherent defense mechanisms can lead to small intestinal bacterial overgrowth (SIBO); therefore, we can define SIBO as an increase in the number and/or an alteration in the type of bacteria found in the small bowel. The etiology of SIBO is presumably multiefactorial and complex, including alternation of gastric acid secretion (primarily in the form of achlorhydria and pancreatic and biliary secretions insufficiency), chronic disease (e.g.renal failure, liver cirrhosis) and old age are among some of the different causes that result in competition between the host and overgrown bacteria for the ingested nutrients and catabolism of these nutrients which subsequently lead to release of toxic metabolites causing variable degree of injury to the proximal intestinal cells. The clinical features of SIBO are widely variable, including abdominal bloating, nausea, abdominal pain, chronic diarrhea, flatulence and weight loss; however, some patients have only subtle symptoms. For this reason, the diagnosis may often be overlooked. Although the diagnosis of SIBO is complex;, there are a few different approaches that may be used to help establish the diagnosis in patients with suspected SIBO. The gold standard for diagnosis remains microbial investigation of jejunal aspirate. Non-invasive, indirect methods include hydrogen and methane breath testing (using either glucose or lactulose as a substrate). A third approach is the empiric treatment in patients with suspected SIBO with a trial of antibiotics with subsequent evaluation of symptomatic response and normalization of breath testing. The underlying principles of treatment of SIBO are complex and typically treated with a course of antibiotics as first line therapy along with addressing the underlying defect. Additionally, probiotics, herbals, and certain diets may also play a significant role in the treatment of SIBO in the future.

Intestinal uptake of IgG in suckling rats: Distinction between jejunal and ileal epithelial cells demonstrated by simultaneous ultrastructural localization of IgG and acid phosphatase

During the suckling period, the proximal small intestine of neonatal rats absorbs maternal milk immunoglobulin G (IgG) into the circulation by a receptor-mediated mechanism. At the same time, milk IgG enters vacuoles in the distal small intestine unaided by a receptor and is degraded. To help define the distinction between the handling of IgG by the proximal and distal neonatal small intestine, we simultaneously localized IgG (by peroxidase-labeled antibodies) and acid phosphatase (by a lead phosphate technique) at the ultrastructural level. In the proximal small intestinal epithelial cells, IgG-containing vesicles were separate from acid phosphatase-containing structures, whereas in the distal intestinal epithelial cells, IgG was present together with acid phosphatase in large supranuclear vacuoles. These observations are consistent with the hypothesis that IgG avoids degradation in the proximal intestinal cells because vesicles in which it is transported do not fuse with lysosomes, whereas IgG in the distal small intestine is degraded in lysosomal enzyme-containing organelles.

Intestinal uptake of IgG in suckling rats

Abstract During the suckling period, the proximal small intestine of neonatal rats absorbs maternal milk immunoglobulin G (IgG) into the circulation by a receptor-mediated mechanism. At the same time, milk IgG enters vacuoles in the distal small intestine unaided by a receptor and is degraded. To help define the distinction between the handling of IgG by the proximal and distal neonatal small intestine, we simultaneously localized IgG (by peroxidase-labeled antibodies) and acid phosphatase (by a lead phosphate technique) at the ultrastructural level. In the proximal small intestinal epithelial cells, IgG-containing vesicles were separate from acid phosphatase-containing structures, whereas in the distal intestinal epithelial cells, IgG was present together with acid phosphatase in large supranuclear vacuoles. These observations are consistent with the hypothesis that IgG avoids degradation in the proximal intestinal cells because vesicles in which it is transported do not fuse with lysosomes, whereas IgG in the distal small intestine is degraded in lysosomal enzyme-containing organelles.

Development of villus absorptive cells in the human fetal small intestine: a morphological and morphometric study.

We describe the sequential ultrastructural changes in villus absorptive cells of human fetal small intestine between 9 and 22 weeks of gestation. In concert with villus formation at 9 to 10 weeks, a complex membranous system designated the apical tubular system appeared in the apical cytonous system designated the apical tubular system appeared in the apical cytoplasm of absorptive cells. The apical tubular system consisted of deep invaginations of plasma membrane and membrane-bounded vesicles and tubules. Some elements of this system were characterized by linear arrays of particles on the inner (luminal) membrane leaflet. After villus formation, many lysosomal elements designated "meconium corpuscles" also appeared in the apical cytoplasm. Modified morphometric studies suggested that both the apical tubular system and the lysosomal elements were more extensively developed in the distal than in the proximal intestine, were most abundant at 15 to 17 weeks, and decreased by 18 to 22 weeks. Morhpometry also showed an inverse relationship between the relative surface density of the apical tubular system and microvillus membrane, suggesting the possible derivation of elements of the former from the apical plasma membrane. Exposure of intestine to ferritin for 8 to 40 minutes in vitro revealed ferritin in elements of the apical tubular system of 12- to 20-week fetuses. There was no evidence of transport of ferritin across absorptive cells. Distinctive membranous bodies composed of convoluted membrane-bound cisternae separated by narrow channels of cytoplasmic matrix were seen in the Golgi region and apical cytoplasm of fetal absorptive cells between 14 and 22 weeks. In a single 22-week fetus, there was marked proliferation of smooth endoplasmic reticulum, a decrease in cytoplasmic glycogen and loss of most lysosomal and apical tubular elements in the proximal but not the distal intestine. Thus, by the end of the second trimester, the structure of absorptive cells in proximal intestine was remarkably similar to absorptive cells in adult intestine.