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R D Berg

Publications and source records attributed to R D Berg.

At least 55 records · Page 3Linked to original sources
PubMed1986

Translocation of indigenous bacteria from the gastrointestinal tract of mice after oral ricinoleic acid treatment.

A single dose of ricinoleic acid, the active component of castor oil, administered intragastrically to specific pathogen-free mice produced significant alterations in the proximal small intestinal mucosa. Two hours after drug administration, the duodenal villi were markedly shortened with massive exfoliation of columnar and goblet cells. This disruption of the mucosal barrier resulted in continuity between the intestinal lumen and the lamina propria of the villi. Because of the loss of the mucosal barrier, bacteria of the indigenous gastrointestinal flora translocated from the gastrointestinal lumen to the mesenteric lymph nodes, spleen, and liver. The peak incidence of bacterial translocation occurred 4 days after the ricinoleic acid treatment. Strictly anaerobic bacteria, which normally colonize the gastrointestinal tract at greater levels than aerobic or facultatively anaerobic bacteria, were translocated at a greater incidence to the mesenteric lymph nodes than were the other indigenous bacteria. The mucosa began regenerating within 4 h after the ricinoleic acid treatment and viable translocated bacteria were no longer cultured from the mesenteric lymph nodes by 7 days after treatment.

Animals↗
PubMed1985

Increased translocation of bacteria from the gastrointestinal tracts of tumor-bearing mice.

Aerobic gram-negative bacilli and other indigenous gastrointestinal (GI) bacteria are important opportunistic pathogens in immunosuppressed cancer patients. These same bacteria frequently translocate from the GI tracts of mice immunosuppressed by single injections of certain anticancer drugs or by T-lymphocyte impairments. Since similar cellular and humoral immune deficiencies may be present in the tumor-bearing host, we sought to determine if progressive growth of a tumor alone would be sufficient to enhance the translocation of indigenous bacteria from the murine GI tract. Pathogen-free DBA/2 mice were injected intraperitoneally with 10(6) viable sarcoma 180 (S-180) cells or 0.5 ml of sterile buffer. Mesenteric lymph nodes, livers, spleens, and kidneys were tested for the presence of translocated aerobic GI bacteria on various days after tumor injection. Immunity was assessed by measuring footpad delayed-type hypersensitivity and serum hemagglutinins to sheep erythrocytes. Overall, translocated aerobic GI bacteria infected 33 of 92 S-180-bearing mice (36%) and only 9 of 99 control mice (9%) (P less than 10(-6)). Cumulatively, 50 of 460 sites (10.9%) in S-180-bearing mice were infected with translocated GI bacteria as opposed to only 9 of 485 sites (1.9%) in control animals (P less than 10(-7)). GI bacteria often translocated to infect more than one site in tumor-bearing mice, but not in controls. Aerobic gram-negative bacilli translocated 11 times in tumor-bearing mice, but only once in controls, even though the mean cecal population levels of these bacteria were relatively low (range, 4.33 to 5.28 log10 bacteria per g). The population levels of cecal aerobic bacteria were similar in S-180 and control mice throughout the period of observation. S-180 mice had significantly suppressed (P less than 0.04) delayed-type hypersensitivity and serum hemagglutinin responses when sensitized 4 or 8 days after S-180 injection. S-180 growth was associated with a neutrophilic leukocytosis and a slight drop in platelet counts; no bleeding was detected. Thus, the translocation of gram-negative bacilli and other indigenous aerobic bacteria from the GI tract to the mesenteric lymph nodes and other organs was increased in immunosuppressed S-180-bearing mice, and this increase was not caused by bacterial overgrowth in the intestines or by neutropenia.

Animals↗
PubMed1985

Bacterial translocation from the intestines.

Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal (GI) tract through the mucosal epithelium to other sites, such as the mesenteric lymph nodes, spleen, liver and blood. This paper reviews results from animal models utilized to obtain information concerning the defense mechanisms operating in the healthy host to confine bacteria to the GI tract. Gnotobiotic and antibiotic-decontaminated mice colonized with particular bacteria demonstrated that the indigenous GI flora maintains an ecologic equilibrium to prevent intestinal bacterial overgrowth and translocation from the GI tract. Studies with athymic (nu/nu) mice, thymus-grafted (nu/nu) mice, neonatally thymectomized mice, and mice injected with immunosuppressive agents demonstrated that the host immune system is another defense mechanism inhibiting bacterial translocation from the GI tract. Ricinoleic acid given orally to mice disrupted the intestinal epithelial barrier allowing indigenous bacteria to translocate from the GI tract. Thus, bacterial translocation from the GI tract of healthy adult mice is inhibited by: (a) an intact intestinal epithelial barrier, (b) the host immune defense system, and (c) an indigenous GI flora maintaining ecological equilibrium to prevent bacterial overgrowth. Deficiencies in host defense mechanisms act synergistically to promote bacterial translocation from the GI tract as demonstrated by animal models with multiple alterations in host defenses. Bacterial translocation occurred to a greater degree in mice with streptozotocin-induced diabetes, mice receiving nonlethal thermal injury, and mice receiving the combination of an immunosuppressive agent plus an oral antibiotic than in mice with only a primary alteration in host defenses. The study of bacterial translocation in these complex models suggests that opportunistic infections from the GI tract occur in discrete stages. In the healthy adult animal, bacterial translocation from the GI tract either does not occur or occurs at a very low level and the host immune defenses eliminate the translocating bacteria. Bacterial translocation does take place if one of the host defense mechanisms is compromised, such as a deficiency in the immune response, bacterial overgrowth in the intestines, or an increase in the permeability of the intestinal barrier. In this first stage, the bacteria usually translocate in low numbers to the mesenteric lymph node, and sometimes spleen or liver, but do not multiply and spread systemically.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Bacterial translocation from the gastrointestinal tracts of rats receiving thermal injury.

Rats receiving nonlethal thermal burns over 20 or 40% of their total body surface area were tested at various intervals for the translocation of indigenous bacteria from their gastrointestinal tracts to their mesenteric lymph nodes, peritoneal cavities, and bloodstreams. No indigenous bacteria were cultured from these organs of control rats or from rats receiving 20% burns. However, 44% of the rats receiving 40% burns exhibited viable Escherichia coli, Proteus mirabilis, Staphylococcus sp. and Clostridium sp. in their mesenteric lymph nodes 2 days after thermal injury. Bacterial translocation after burn stress also was tested in antibiotic-decontaminated rats monoassociated with E. coli. E. coli attained population levels in these animals of 10(8) to 10(9) per g cecum. E. coli translocated to 100% of the mesenteric lymph nodes of both the control and 40% burned rats. However, E. coli translocated at a greater incidence to the spleens, livers, and peritoneal cavities of the burned rats compared with translocation to these organs in control rats. The numbers of E. coli translocating to the mesenteric lymph nodes, spleens, and livers also were greater in the 40% burned rats than in control rats. By 14 days after thermal injury, the rats were able to clear E. coli from their spleens and livers, and the infection remained localized in the mesenteric lymph nodes. These results support the concept that the indigenous gastrointestinal flora or exogenous organisms colonizing the gastrointestinal tract are potential sources of septicemia after thermal injury.

Animals↗
PubMed1984

Use of a purified outer membrane protein F (porin) preparation of Pseudomonas aeruginosa as a protective vaccine in mice.

The outer membrane protein F (porin) from the PAO1 strain of Pseudomonas aeruginosa was purified by two different methods. One procedure involved separation by column chromatography of proteins extracted from isolated outer membranes, whereas the other involved extraction from gels after slab polyacrylamide gel electrophoresis of proteins extracted from cell envelopes. Both procedures yielded protein F preparations which successfully immunized mice from subsequent challenge with the PAO1 strain. The protein F preparations contained small quantities of lipopolysaccharide (LPS). This level of LPS contamination protected immunized mice from challenge with the homologous LPS serotype strain. However, immunization of mice with protein F preparations from the PAO1 strain also afforded protection against challenge with two different LPS serotype strains. This protective ability was lost when the protein F preparation was treated with papain before use as a vaccine. These observations support the conclusion that protein F has protective ability, which is not due to LPS contamination, when given as a vaccine. After immunization with the protein F preparation, mice showed an increase in antibody titer to the purified protein F preparation by enzyme-linked immunosorbent assay. Mice were protected passively by administration of rabbit antisera raised to the protein F preparation. These results indicate that the protein F preparation elicits a specific humoral antibody response in immunized animals. Our results suggest that purified protein F has potential as an effective vaccine for P. aeruginosa.

Animals↗
PubMed1984

Assessment of mouse strain on bacterial translocation from the gastrointestinal tract.

The translocation of indigenous bacteria from the gastrointestinal tract to the mesenteric lymphnodes was compared in ten strains of mice. Indigenous Escherichia coli were cultured from the mesenteric lymphnodes of only two of the six mouse strains examined. Thus, spontaneous translocation of indigenous enteric bacteria across the intestinal barrier did not occur to any significant extent in any of the mouse strains examined. Since bacterial overgrowth in the gastrointestinal tract promotes bacterial translocation, bacterial translocation was tested in ten mouse strains including B10 series after antibiotic-decontaminated and subsequent colonization with streptomycin-resistant E. coli C25. E. coli C25 populated the ceca of the mice at levels of 10(8) to 10(9) per gram and translocated to 90-100% of the mesenteric lymphnodes with mean of 10(1.13) to 10(1.86) per mesenteric lymphnode. However, there were no significant differences between mouse strains as to the translocation incidence or the numbers of viable E. coli C25 per mesenteric lymphnode. Thus, genetic differences between mouse strains did not influence bacterial translocation from the gastrointestinal tract to the mesenteric lymphnodes.

Animals↗
PubMed1983

Kinetic analysis of bacterial clearance in mice using the ESTRIPc and KINET microcomputer programs.

Two BASIC microcomputer programs, ESTRIPc and KINET, were used to analyze the kinetics of bacterial clearance from the blood and mesenteric lymph nodes of mice. Because of the similarities between the clearance of bacteria and the clearance of drugs from tissue, blood pharmacokinetic techniques were applied to the analysis of bacterial clearance data. The ESTRIPc program, developed for pharmacokinetic analysis and modified for the study of bacterial clearance, was employed to fit the experimental data of bacterial survival versus time to a polyexponential equation with 1, 2, or 3 terms. The KINET program, written specifically for kinetic analysis of bacterial clearance, uses the biexponential equation constants derived with ESTRIPc to calculate half-life values, rate constants, and other useful kinetic parameters. The combined use of these programs permits precise comparisons of the clearance rates of different bacterial species from the blood or tissues of experimental animals.

Animals↗
PubMed1983

Relationship between cecal population levels of indigenous bacteria and translocation to the mesenteric lymph nodes.

Translocation is defined as the passage of viable bacteria from the gastrointestinal tract to the mesenteric lymph nodes (MLN) and other organs. The extent of translocation of certain indigenous, oxygen-tolerant bacteria from the cecum to the MLN, spleen, liver, kidney, and peritoneal cavity were determined in diassociated or triassociated gnotobiotic mice. Minimal bacterial translocation occurred to the spleen, liver, kidney, or peritoneal cavity. However, most bacterial strains readily translocated to the MLN. The percentage of the total population of each bacterial strain in the ceca was compared with the percentage of the total population of that strain in the MLN. There was a direct relationship between the numbers of a particular bacterial strain populating the ceca of diassociated or triassociated mice and the numbers of viable bacteria of this strain present in the MLN. Thus, the cecal population level of a particular bacterial strain determined the numbers of viable bacteria of this strain translocating to the MLN. The translocation of these bacterial strains from the gastrointestinal tract is an important first step in the pathogenesis of infection caused by members of the normal intestinal microflora.

Animals↗
PubMed1981

Derivation of a breeding colony of germ-free athymic mice by cesarean section and foster nursing.

Germ-free athymic mice were obtained by removing the uterus by cesarean section from a gravid heterozygous (nu/+) female at precisely full term. The uterus was transferred into a germ-free flexible isolator containing two germ-free CD-1 mice that were communally nursing their recently delivered litters. These germ-free CD-1 mice served as foster mothers for the newborn germ-free athymic mice.

Animals↗
PubMed1981

Promotion of the translocation of enteric bacteria from the gastrointestinal tracts of mice by oral treatment with penicillin, clindamycin, or metronidazole.

Specific pathogen-free mice were treated orally with antibiotics to determine whether the resulting disruption of the normal flora ecology would allow certain gram-negative enteric bacteria to overpopulate the ceca, thereby promoting the translocation of these bacteria from the gastrointestinal tract. The mice were treated orally with penicillin, clindamycin, or metronidazole for 4 days, and then the antibiotic was discontinued. The mice were tested at various intervals for viable enteric bacilli translocating from the gastrointestinal tract to the mesenteric lymph nodes. Penicillin treatment decreased the total anaerobe population levels in the ceca an average of 1,000-fold, whereas clindamycin treatment decreased these anaerobe levels only 10-fold, and metronidazole treatment slightly increased the anaerobe levels. Penicillin or metronidazole treatment slightly increased the anaerobe levels. Penicillin or metronidazole treatment increased the enteric bacilli populations in the ceca an average of 1,000-fold, whereas clindamycin treatment increased the enteric bacilli populations 100,000-fold. The peak incidence of translocation of the enteric bacilli to the mesenteric lymph nodes averaged 100% after penicillin treatment, 97% after clindamycin treatment, and 62% after metronidazole treatment. Thus, oral treatment of mice with penicillin, clindamycin, or metronidazole for only 4 days disrupts the normal flora ecology, allowing an overgrowth in the ceca of the gram-negative enteric bacilli and promoting their translocation to the mesenteric lymph nodes.

Administration, Oral↗
PubMed1980

Bacterial translocation from the gastrointestinal tract of athymic (nu/nu) mice.

The immune system may be one host defense mechanism preventing viable indigenous bacteria from translocating from the mouse gastrointestinal lumen to the mesenteric lymph nodes, spleen, liver, or kidney. The role of T-cell-dependent immunity in preventing bacteria from translocating from the gastrointestinal tract was tested with congenitally athymic nude (nu/nu) mice, heterozygous (nu/+) mice, and thymus-grafted nude (nu/nu) mice. Viable bacteria were cultured from 50% of the mesenteric lymph nodes, spleens, livers, and kidneys of athymic (nu/nu) mice, whereas heterozygous (nu/+) mice exhibited viable bacteria in only 5.2% of these organs. Both aerobic and strictly anaerobic bacteria were cultured from these organs with Escherichia coli and Lactobacillus predominanting. Grafting thymuses to the athymic (nu/nu) mice restored their immunological responses to sheep erythrocyte antigens. The incidence of bacterial translocation from the gastrointestinal tract was reduced from 50% in the athymic (nu/nu) mice to 7.8% in the thymus-grafted (nu/nu) mice. Thus, T-cell-dependent immunity restored by thymic grafts inhibited the translocation of certain indigenous bacteria from the gastrointestinal tract to the spleen, liver, and kidney in nu/nu mice.

Animals↗
PubMed1980

Inhibition of Escherichia coli translocation from the gastrointestinal tract by normal cecal flora in gnotobiotic or antibiotic-decontaminated mice.

Escherichia coli C25 maintained population levels of 10(9) to 10(10) per g of cecum and translocated to 100% of the middle mesenteric lymph nodes in gnotobiotic mice monoassociated with E. coli C25. Intragastric inoculation of these mice with the cecal contents from specific-pathogen-free mice reduced the population levels of E. coli C25 to 10(6) per g of cecum and completely inhibited translocation to the mesenteric lymph nodes. Intragastric inoculation with heat-treated, Formalintreated, or filtered cecal contents did not reduce the population levels of E. coli C25 or reduce the incidence of translocation of E. coli C25 to the mesenteric lymph nodes. Thus, viable bacteria apparently are required in the cecal contents inocula to reduce the population levels and the incidence of translocation of E. coli C25. Treatment with streptomycin plus bacitracin decreased the anaerobic bacterial levels in these gnotobiotic mice, allowing increased population levels of E. coli C25 and increased translocation to the mesenteric lymph nodes. E. coli C25 also translocated to the mesenteric lymph nodes of specific-pathogen-free mice treated with streptomycin and bacitracin before colonization with E. coli C25. The high cecal population levels of E. coli C25 in these antibiotic-decontaminated specific-pathogen-free mice apparently overwhelm any barrier to translocation exerted by the immunologically developed lamina propria of the specific-pathogen-free mice. Inoculation of gnotobiotic mice with a cecal flora also reduced the population levels of an indigenous strain of E. coli with a concomitant inhibition of translocation of the indigenous E. coli to the mesenteric lymph nodes. Thus, bacterial antagonism of the gastrointestinal population levels of certain indigenous bacteria, such as E. coli, by other members of the normal bacterial flora appears to be an important defense mechanism confining bacteria to the gastrointestinal tract.

Animals↗
PubMed1980

Translocation of Escherichia coli from the gastrointestinal tract to the mesenteric lymph nodes in gnotobiotic mice receiving Escherichia coli vaccines before colonization.

Germfree mice were immunized orally or intraperitoneally for 6 weeks with heat-killed vaccines of indigenous Escherichia coli or nonindigenous E. coli O 127: B8 before colonization with these strains. The mice exhibited increases in specific serum antibodies and intestinal immunoglobulin A reacting with the E coli antigens. Prior immunization did not reduce the gastrointestinal population levels of the E. coli strains attained 3 and 7 days after colonization. Neither oral nor intraperitoneal immunization with the E. coli strains before colonization decreased the incidence of bacterial translocation to the mesenteric lymph nodes or reduced the number of viable E. coli cells per mesenteric lymph node. There also was no relation in individual mice between serum antibody titers and the numbers of viable E. coli cells translocating to the mesenteric lymph nodes. Thus, prior vaccination with E. coli in this study did not decrease the incidence or reduce the numbers of viable E. coli translocating to the mesenteric lymph nodes in gnotobiotic mice monoassociated with E. coli.

Administration, Oral↗
PubMed1979

Translocation of certain indigenous bacteria from the gastrointestinal tract to the mesenteric lymph nodes and other organs in a gnotobiotic mouse model.

Viable bacteria were not cultured from the mesenteric lymph nodes, spleens, or livers of specific-pathogen-free (SPF) mice. Viable enteric bacteria, primarily indigenous Escherichia coli and lactobacilli, were present in the mesenteric lymph nodes of gnotobiotic mice inoculated intragastrically with the whole cecal microflora from SPF mice but not in the nodes of control SPF mice similarly inoculated. These indigenous E. coli also were cultured from the mesenteric lymph nodes of 96% of gnotobiotic mice monoassociated with E. coli but from none of the mesenteric lymph nodes of SPF mice inoculated with the E. coli. Furthermore, viable E. coli were detected in the mesenteric lymph nodes of these monoassociated gnotobiotes for as long as 112 days after inoculation. Indigenous Lactobacillus acidophilus also translocated to the mesenteric lymph nodes of gnotobiotic mice monoassociated with L. acidophilus. Apparently, there are mechanisms active in SPF mice inhibiting translocation of indigenous bacteria from the gastrointestinal tract to the mesenteric lymph nodes, spleens, and livers, whereas these mechanisms are either absent or reduced in gnotobiotic mice. Indigenous E. coli maintained higher population levels in the gastrointestinal tracts of the gnotobiotes compared with their population levels in SPF mice, suggesting that high bacterial population levels might promote translocation of certain bacteria from the gastrointestinal lumen to the mesenteric lymph nodes. Gnotobiotic and SPF mice, therefore, provide experimental models for determining the nature of the mechanisms operating to confine indigenous bacteria to the gastrointestinal tract in normal, healthy animals.

Animals↗
PubMed1979

Inhibition of translocation of viable Escherichia coli from the gastrointestinal tract of mice by bacterial antagonism.

The incidence of translocation of viable Escherichia coli C25 from the gastrointestinal tract to the mesenteric lymph nodes was compared in gnotobiotic mice colonized with only E. coli C25 and in gnotobiotic mice colonized with E. coli C25 plus the whole cecal flora from specific pathogen-free mice. The population levels of E. coli C25 in the ilea and ceca of these mice also were compared. E. coli C25 maintained high population levels in the gastrointestinal tracts of the monoassociated gnotobiotes, and the incidence of translocation to the mesenteric lymph nodes was 100%. The gastrointestinal population levels of E. coli C25 were reduced drastically in the gnotobiotes associated with both E. coli C25 and a cecal flora with concomitant reduction in the incidence of translocation of E. coli C25 from 100 to 0%. A decrease in the numbers of viable E. coli C25 per mesenteric lymph node also accompanied the decrease in C. coli C25 population levels in the gastrointestinal tracts of these mice. Thus, high population levels of E. coli C25 in the gastrointestinal tracts of monoassociated gnotobiotic mice appear to promote translocation of viable E. coli C25 to the mesenteric lymph nodes. Bacterial antagonism of E. coli population levels in conventional mice, therefore, could be one mechanism whereby viable E. coli are confined to the gastrointestinal tract.

Animals↗
PubMed1978

Antagonism among the normal anaerobic bacteria of the mouse gastrointestinal tract determined by immunofluorescence.

Strictly anaerobic Bacteroides sp., Eubacterium sp., and Fusobacterium sp. were isolated from the cecum of a conventional mouse. An immunofluorescent method utilizing rabbit antisera specific for each of these three strains was developed to determine their population levels in the gastrointestinal tracts of gnotobiotic mice. Population levels of these anaerobes in groups of gnotobiotic mice colonized with either Bacteroides, Eubacterium, or Fusobacterium were compared with those of gnotobiotes colonized with all three strains. Bacteroides population levels in gnotobiotes colonized with all three strains were 100-fold less than the Bacteroides population level in gnotobiotes colonized with only the Bacteroides strain. Eubacterium or Fusobacterium population levels were not reduced by the presence of the other anaerobic strains. Thus, strictly anaerobic Eubacterium sp. and Fusobacterium sp. that colonized gnotobiotic mice caused a reduction in the in vivo population levels of a strictly anaerobic Bacteroides sp.

Anaerobiosis↗