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Biomedical subjects

R D Berg

Publications and source records attributed to R D Berg.

60 records · Page 4Linked to original sources
PubMed1975

Immune responses of specific pathogen-free and gnotobiotic mice to antigens of indigenous and nonindigenous microorganisms.

Strains of indigenous Escherichia coli, Bacteroides, and Lactobacillus were isolated from the gastrointestinal tracts of specific pathogen-free (SPF) mice. Nonvaccinated SPF mice exhibited in their spleens low numbers of plaque-forming cells (PFC) and rosette-forming cells reacting with antigens of these andigenous bacteria. PFC reacting with these bacterial antigens were not detected in infant SPF mice until 7 days after birth. Compared with nonvaccinated controls, SPF mice vaccinated parenterally with indigenous E. coli or Bacteroides produced a moderate increase in the numbers of specific PFC. Thus, the SPF mouse is capable of responding immunologically after vaccination with microbes indigenous to its intestinal tract. However, more PFC reacting with homologous vaccine antigens were detected after parenteral vaccination of SPF mice with nonindigenous E. coli O127:B8, E.coli O14, or B. fragilis than after parenteral vaccination with indigenous E. coli or Bacteroides. Gnotobiotic mice orally monoassociated with these nonindigenous bacteria exhibited greater immune responses to antigens of the bacteria used to monoassociation than did gnotobiotes monoassociated with the indigenous microbes. The results are consistent with the hypothesis that mice are more responsive immunologically to antigens of nonindigenous bacteria than they are to antigens of certain microbes indigenous to their gastrointestinal tracts.

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PubMedDate not supplied

The Caco-2 cell monolayer system as an in vitro model for studying bacterial-enterocyte interactions and bacterial translocation.

Partly because of inherent limitations of in vivo models, the cellular mechanisms underlying the process of bacterial translocation across the intestinal epithelial barrier are incompletely understood. We therefore used the Caco-2 intestinal cell line as an in vitro model to examine the bacterial translocation process under controlled conditions. Caco-2 cells were grown on porous membranes in the upper compartment of a two-compartment system. Caco-2 cells were cultured for 7, 14, 21, or 28 days. Cellular confluence and tight junction integrity were verified by measurements of dextran permeability and transepithelial electrical resistance. Bacterial translocation was measured by culturing the bacteria (E. coli C25) that were able to cross the Caco-2 cell monolayer. The passage of E. coli C-25 and dextran across the Caco-2 monolayer was higher and the transepithelial electrical resistance lower after 7 days of culture than after 14 or 21 days of culture. The Caco-2 cells became impermeable to dextran blue after 14 days of culture with an average transepithelial electrical resistance of 173.1 +/- 9.24 ohms.cm2. When increasing doses of (10(2)-10(9) colony-forming units) of E. coli were tested in 14-day-old Caco-2 monolayers, bacterial translocation occurred in a time- and dose-dependent fashion. Once cellular confluence and tight junction integrity have been established, bacterial translocation across Caco-2 cells appears to be a time- and dose-dependent process.

Cell Movement↗
PubMedDate not supplied

Effects of protein malnutrition and endotoxin on the intestinal mucosal barrier to the translocation of indigenous flora in mice.

Since protein malnourished or endotoxemic patients are at increased risk of developing nosocomial infections with enteric organisms, we investigated the effects of these risk factors alone and in combination on the intestinal mucosal barrier to bacteria. Protein malnutrition resulted in severe ileal atrophy that was directly related to the length of time the mice were protein malnourished. Although protein malnutrition did not promote bacterial translocation from the gut to systemic organs, the protein-malnourished mice were more susceptible to endotoxin-induced bacterial translocation than normally nourished mice (p less than 0.01). Since the gross epithelial damage documented after endotoxin administration in normally nourished mice was diminished after protein malnutrition, there was no correlation between the gross appearance of the epithelial mucosal barrier and the extent of endotoxin-induced bacterial translocation. These results suggest that the synergistic effect of endotoxin plus protein malnutrition on bacterial translocation is not primarily related to failure of the gut mucosal barrier. Nonetheless, it appears that protein-malnourished mice are less able to clear translocating bacteria than normally nourished mice.

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PubMedDate not supplied

Bulk prevents bacterial translocation induced by the oral administration of total parenteral nutrition solution.

The effects of a fat and glutamine-free orally administered total parenteral nutrition (TPN) solution on intestinal mucosal mass, morphology, barrier function, and cecal bacterial population levels were measured in CD-1 mice. Ileal mucosal protein content decreased by 63% (p less than 0.01) in the oral TPN-fed mice, although they gained weight on this diet. These TPN-fed mice also exhibited changes in mucosal structure and the normal ecology of their cecal microflora was disrupted leading to overgrowth with Gram-negative enteric bacilli. These changes in intestinal mucosal mass, morphology, and gut bacterial ecology were associated with an increased incidence of bacterial translocation (BT) (TPN group 70% BT vs control group 15% BT: p less than 0.01). The administration of cellulose fiber or kaolin (bulk-forming agents), but not of citrus-pectin (a fully-fermentable, nonresidue fiber) reduced the incidence of BT in the TPN-fed mice to control levels. The beneficial effects of these bulk-forming agents appeared to be due to their ability to prevent TPN-induced disruption of the intestinal microflora and alterations in intestinal morphology, even though they did not prevent ileal mucosal protein levels from decreasing. These results suggest that the administration of bulk forming agents will prevent the loss of intestinal barrier function against luminal bacteria that occurs in mice fed an oral TPN solution.

Administration, Oral↗
PubMedDate not supplied

Protein malnutrition alone and in combination with endotoxin impairs systemic and gut-associated immunity.

Because protein-malnourished or endotoxemic patients are at an increased risk of developing nosocomial infections, this study was performed to investigate the effects of protein malnutrition and endotoxemia, alone and in combination, on systemic and intestinal immunity. Protein malnutrition was created by feeding the animals a solid diet containing 0.03% protein. Subgroups of these protein-malnourished mice were killed after being challenged with saline or endotoxin on days 0, 7, 14, or 21. At death, the animals were weighed, tissues were harvested for histologic analysis (ileum, mesenteric lymph node [MLN], liver, and spleen), mitogen responsiveness (MLN, Peyer's patches, and spleen), and xanthine oxidase measurements (ileum and cecum). Separate groups were evaluated for survival. Both the saline and endotoxin-challenged mice had lost about 30% of their body weight after 21 days on the low-protein diet. The protein-malnourished mice were more susceptible to endotoxin-induced mortality (70% at 21 days) than the normally nourished mice (0%) (p less than .001). The mitogen responsiveness of the protein-malnourished mice to the T-cell mitogens (PHA and Con-A) progressively decreased the longer the mice were protein malnourished, and this decreased in blastogenic responsiveness was associated with histologic evidence of lymphoid atrophy. In contrast, the blastogenic response to the primarily B-cell mitogen, PWM, was largely preserved. The endotoxin challenge further depressed the immune state of mice tested after 0, 7, or 14 (but not 21) days of protein malnutrition. Thus, both protein malnutrition and endotoxin impaired systemic and gut-associated immune responsiveness to mitogens. However, in the protein-malnourished mice, the degree of immune suppression did not correlate with endotoxin-induced mortality.

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