Recovery of viable bacteria from pelvic lymph nodes of patients with gynecologic tumors.
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Adult↗
Biomedical subjects
C L Wells
Publications and source records attributed to C L Wells.
Interactions of Escherichia coli and Proteus mirabilis with mouse mononuclear phagocytes.
Five strains of enterobacteria (three of Escherichia coli and two of Proteus mirabilis) were studied to assess and compare their phagocytic uptake and intracellular killing by mouse macrophages. Each strain was injected intraperitoneally into separate groups of mice and peritoneal exudate cells were harvested after 3 min for phagocytosis to occur in vivo. Acridine orange staining showed that there were approximately 10-fold fewer intracellular P. mirabilis than E. coli cells. The average numbers of viable intracellular bacteria per leucocyte were 0.03 and 0.02 for P. mirabilis strains M13 and H1, respectively, and 0.48, 0.45, and 0.28 for E. coli strains M14, A-D M5 and H40. Thus, both P. mirabilis strains were ingested less readily than any of the three E. coli strains (p less than 0.01). The rates of in-vitro intracellular killing were similar for all five strains of bacteria. The intracellular killing constants (Kk) for the three mouse isolates were 0.017, 0.016 and 0.020 min for E. coli M14 and A-D M5, and P. mirabilis M13, respectively; the Kks for the two human isolates were 0.026 and 0.029/min for E. coli H40 and P. mirabilis H1, respectively. The Kks for all five strains were not significantly different. Assuming that the numbers of viable intracellular bacteria at the beginning of the assay represented 100% viability, 6-17% of the intracellular bacteria remained viable after 2 h, reflecting log10 3.9-5.6 bacteria (6-8) x 10(6) peritoneal exudate cells. Intravenous injection of these five strains into separate groups of mice demonstrated that the P. mirabilis strains were more virulent than the E. coli strains. Injection of each P. mirabilis strain was associated with ruffled fur and death, whereas mice given any of the three E. coli strains remained visibly healthy and none died. Consistent with these observations, quantitation of viable bacteria in the liver and spleen showed that greater numbers of P. mirabilis M13 than of E. coli M14 or A-D M5 persisted in these organs; similarly greater numbers of P. mirabilis H1 than of E. coli H40 persisted in the liver and spleen. Because the rates of intracellular killing of these five strains were similar, the relative virulence of both strains of P. mirabilis appeared to be associated with decreased phagocytic uptake rather than differences in intracellular survival.
Animals↗
Mucosal protective activity of activated aluminum complex.
The antacid ES Riopan was acidified ex vivo to pH 2.5 to completely eliminate its buffering capacity and was then tested as a mucosal protective agent. The pH 2.5 acidified antacid solution was named activated aluminum complex. Activated aluminum complex was 8.2 times more potent than its parent antacid in protecting against acidified aspirin-induced gastric lesions in the rat. Activated aluminum complex had a duration of action greater than 10 h in the ethanol-induced gastric lesion model, while ES Riopan was active for 6 h. Activated aluminum complex was able to inhibit both acid- and nonacid-mediated ulcers in the stomach and intestine. Its mucosal protective activity was not blocked by pretreatment with indomethacin. These results demonstrate that the nonbuffering antacid activated aluminum complex exerted a more potent and longer-lasting mucosal protective activity than its parent antacid. The activity was probably due to the presence of a hexaaquoaluminum cation and supports the argument that antacids possess mucosal protective effects independent of their acid-neutralizing capacity.
Aluminum Hydroxide↗
Differences in epinephrine and substrate responses between arm and leg exercise.
The purpose of this study was to determine epinephrine (EPI) and selected substrate responses during arm crank (AC) and leg cycle (LC) exercise at the same absolute and relative exercise intensity. Nine males performed 30 min AC and LC tests at 70% of ergometer-specific peak oxygen uptake (VO2), and a 30 min LC test eliciting a similar VO2 required during the AC test. Blood samples (30 ml) were collected via an indwelling arm catheter at rest, and at minutes 13 and 28 of exercise for determinations of plasma EPI, serum free fatty acid (FFA), serum glycerol (GLY), blood glucose (GLU), and blood lactate (LA) concentrations. At equivalent VO2, higher (P less than 0.05) EPI, LA, and respiratory exchange ratio (RER) responses were obtained during AC than LC exercise. However, these physiologic responses were similar during AC and LC exercise at the same relative intensity. No significant differences over time were observed for FFA, GLY, and GLU between AC and LC exercise at either the same absolute or relative intensity. The results support previous hypotheses that AC exercise is physiologically more stressful than LC exercise at the same VO2. The data further indicate that adrenomedullary activity (EPI response) and substrate utilization (LA and RER responses) are regulated by relative exercise intensity and not the exercising muscle mass.
Adult↗
Effect of oral dextran sulfate on the mouse intestinal tract.
Oral dextran sulfate is associated with adverse intestinal effects, including severe diarrhea, in some AIDS patients. We therefore investigated the intestinal flora and the intestinal histology of mice given drinking water supplemented with 8 mg/ml of dextran sulfate. There were no noticeable alterations in the major groups of intestinal bacteria in mice given oral dextran sulfate for 7 days. Likewise, there was no abnormal pathology in the ilea or colons of mice treated for 7 days with oral dextran sulfate. However, after 21 and 38 days, there was a noticeable overgrowth of facultative gram-negative bacilli in the colonic and cecal flora of dextran sulfate-treated mice. This overgrowth appeared to be due to bacterial species in the family Enterobacteriaceae, primarily Escherichia coli. Bacterial overgrowth was accompanied by mild histological alterations in the intestinal mucosa, i.e., blunting of ileal villi and colonic crypts, with mild epithelial cell dysplasia. Thus, oral dextran sulfate was associated with quantitative changes in the mouse intestinal flora, as well as histological changes in the intestinal mucosa.
Animals↗
Axenic culture and characterization of Giardia ardeae from the great blue heron (Ardea herodias).
Trophozoites of Giardia ardeae were obtained from the great blue heron (Ardea herodias) and established in axenic culture using the TYI-S-33 medium. The generation time in culture for G. ardeae was 22-25 hr, which was 3-fold longer than for Giardia duodenalis (WB strain). A morphological comparison of trophozoites in the original intestinal isolate to those grown in culture revealed that they were identical for the following characteristics: a pyriform-shaped body, a ventral adhesive disc with a deep notch in the posterior border, teardrop-shaped nuclei, pleomorphism in median body structure ranging from a round-oval appearance (Giardia muris type) to that of a clawhammer (G. duodenalis type), and a single caudal flagellum on the right side (as viewed dorsally) with the left one being rudimentary. Analysis of the chromosomal migration patterns was performed by orthogonal-field-alternation gel electrophoresis and demonstrated that the pattern for G. ardeae was distinctly different from that for G. duodenalis (Portland 1-CCW strain). Bacterial symbionts were seen attached to trophozoites in the original isolate but could not be detected in cultured trophozoites using scanning electron microscopy, fluorescence light microscopy using the Hoechst 33258 dye for DNA localization, or by standard microbiological techniques using nonselective media for growing aerobic or anaerobic bacteria. This study demonstrated that avian-derived Giardia could be grown in axenic culture; based on morphological criteria and chromosomal migration patterns, that G. ardeae should be considered a distinct species; and that rationale for determining Giardia spp., based on median body structure alone, should no longer be considered adequate for classification at the species level.
Animals↗
Effect of epidermal growth factor on non-steroidal anti-inflammatory drug-induced intestinal damage.
Epidermal growth factor (EGF, 10 micrograms/kg po, ip, or sc, BID, and 20 micrograms/kg iv) had no protective activity in the indomethacin-induced intestinal lesion model (6 h model). In the ethanol-induced gastric lesion model, EGF (10 micrograms/kg sc) reduced lesions by 52% and reduced gastric acid secretion by 68% (5 micrograms/kg iv). In the 24 h indomethacin-induced intestinal lesion model, pretreatment with EGF (10 micrograms/kg sc, BID; 1 day before and during indomethacin treatment) had no beneficial effects. Therefore, EGF had no protective effects against non-steroidal antiinflammatory drug (NSAID)-induced intestinal lesions at doses that protect against the necrotizing action of ethanol and that inhibit gastric acid secretion in the rat.
Animals↗
Effects of low- and moderate-intensity training in spinal cord-injured persons.
This study examined the applicability of exercise prescription guidelines established for the able-bodied to spinal cord-injured (SCI) persons. Two SCI groups performed wheelchair ergometry (WCE) 20 min three times per week for 8 wk. Low-intensity (LI, N = 6) and moderate-intensity (MI, N = 5) groups trained at 50-60% and 70-80% maximal heart rate reserve (HRR), respectively. The subjects completed an incremental discontinuous maximal WCE test to exhaustion pre- and post-training. A submaximal WCE test consisting of 4-min exercise stages at power outputs of 5, 10, and 15 W was also performed pre- and post-training. Blood samples were collected before and after training and analyzed for total cholesterol (TC), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C). The TC/HDL-C ratio was calculated. Both groups exhibited no significant changes (P greater than 0.10) in VO2max, HRmax, POmax, lactate (La)max, and VO2 at 4 mmol [La]. No pre- to post-training differences were recorded in the LI group for submaximal VO2, HR, VE, La, and ratings of perceived exertion (RPE). The MI group had significantly lower (P less than or equal to 0.10) post-training submaximal HR, La, and RPE and no changes in VO2 or VE. Blood lipid levels remained unaltered in the LI group, while the MI group exhibited significant increases in HDL-C and decreases in TG, LDL-C, and the TC/HDL-C ratio. The maximal test data revealed that 8 wk of LI and MI wheelchair ergometry training did not improve VO2max in SCI persons.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Somatotypes of premenarcheal athletes and non-athletes.
One-hundred thirty-four premenarcheal girls between the ages of 7 and 15 years were somatotyped according to the Health-Carter technique. Sexual maturation was determined by self-assessed Tanner stages. Statistical analysis was completed on 50 athletes (representing seven sports) and 29 non-athletes over the age of 10 years. The mean somatotype for the athletes was calculated to be 2.4-3.6-3.9 and for the non-athletes 3.7-3.7-3.6. Single component ANOVA's revealed that the athletes were significantly less endomorphic (p less than 0.01) than the non-athletes. The overall somatotype ratings and the equality of dispersion about the means were significantly different between the athletes and non-athletes. The single highest category for the athletes was mesomorph-ectomorph and for the non-athletes, mesomorphic-endomorph. Significant negative correlations were obtained between mesomorphy and breast development (-0.33, p less than 0.05) and mesomorphy and pubic hair development (-0.44, p less than 0.01) for the athletes. Significant positive correlations were obtained between endomorphy and breast development (0.55, p less than 0.01) and endomorphy and pubic hair development (0.45, p less than 0.05) for the non-athletes. The mean somatotype for the gymnasts was 2.1-3.9-3.6 and for the swimmers 2.5-3.4-4.1. These two groups were significantly different from each other on each separate component and overall somatotype, but not in equality of dispersion. The results support the conclusion that premenarcheal athletes are morphologically different from non-athletes despite their youth and from each other based on sport specificity.
Adolescent↗
Nutrient intakes and iron status in female long-distance runners during training.
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Adult↗
Role of intestinal anaerobic bacteria in colonization resistance.
The purpose of this study was to clarify the role of the intestinal anaerobe bacteria in colonization resistance. Germfree mice were associated with Escherichia coli C25 and either (a) no other species; (b) enterococcus; (c) Escherichia coli M14 and Proteus mirabilis, or (d) Bacteroides fragilis and Bacteroides vulgatus. All species colonized the cecum in high numbers, but only enterococcus significantly limited the translocation of Escherichia coli C25 to mesenteric lymph nodes. However, the overall translocation rates were similar in all groups and ranged from 60% to 100%, due to translocation of other intestinal flora in addition to Escherichia coli C25. Conventionally reared mice were given either streptomycin, bacitracin/streptomycin or metronidazole which selectively eliminated facultative gram-negative bacteria, nearly all bacterial species or strictly anaerobic bacteria respectively. Only metronidazole significantly increased the rates of translocation of normal intestinal bacteria into mesenteric lymph nodes. Cohort groups of mice were then orally inoculated with drug resistant Escherichia coli C25, which actively colonized the cecum of all drug treated mice and translocated to the mesenteric lymph nodes of approximately half the streptomycin and metronidazole treated mice and nearly all the bacitracin/streptomycin treated mice. These results indicate that anaerobic bacteria play a pivotal role in limiting the translocation of normal intestinal bacteria, but that other bacterial groups also have a role in preventing the intestinal colonization and translocation of potential pathogens.
Animals↗
Effect of T cell modulation on the translocation of bacteria from the gut and mesenteric lymph node.
Although the ability of the gut-associated lymphoid tissue (GALT) to respond to orally ingested foreign antigens has been studied extensively, its function in preventing or limiting escape of resident gut bacteria has not been assessed. The following studies were performed to examine what role cell-mediated immunity (CMI) plays in this process. The ability of suppression of CMI to induce escape of gut bacteria (translocation) to the mesenteric lymph node (MLN) in immunocompetent mice whose gut flora was unaltered was examined. Administration of cyclosporine or anti-L3T4 antibody failed to induce translocation of indigenous gut bacteria after 7 or 14 days of treatment. Antithymocyte globulin (ATG) also failed to induce translocation after 7 days of treatment, despite depletion of all Thy 1, Lyt 1, L3T4, and Lyt 2 positive cells from the spleen, MLN, and intestine as demonstrated by immunofluorescent microscopy. Finally, cultures of the MLN, spleen, liver, and peritoneum of T cell-deficient BALB/c nude mice and their heterozygous T cell-replete littermates were also sterile, demonstrating that congenital suppression of T CMI also does not lead to translocation of indigenous gut bacteria. The role of CMI in limiting systemic spread of bacteria that were already translocating to the MLN was also examined. Translocation of Escherichia coli C25 to the MLN was induced by gastrointestinal (GI) monoassociation, which leads to translocation of E. coli C25 to the MLN in 80-100% of mice. Treatment with ATG during monoassociation failed to induce spread of E. coli C25 to the spleen, liver, or peritoneum, despite the same degree of T cell depletion achieved with ATG in the previous experiment. Monoassociation of conventional T cell-deficient BALB/c nude and heterozygous mice and germ-free T cell-deficient BALB/c nude and heterozygous mice also did not lead to spread of E. coli C25 beyond the MLN. However, in ATG-treated, conventional nude, and germ-free nude mice, the average number of translocating E. coli C25 per MLN was consistently higher. In separate experiments the ability of stimulation of T cell function to inhibit translocation of E. coli C25 was examined. Recombinant interleukin-2, 25,000 units, was administered intraperitoneally every 8 hours during exposure to E. coli C25. This reduced the incidence of translocation of E. coli C25 from 85% to 51% (p = 0.02). Suppression of CMI, either systemically or within the GALT, has a minimal influence on the mechanisms by which the normal gut flora are translocated to the MLN.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Effects of clindamycin and metronidazole on the intestinal colonization and translocation of enterococci in mice.
The intestinal colonization and translocation of enterococci was studied in mice treated intramuscularly with metronidazole or clindamycin, with or without oral streptomycin. Treatment with metronidazole resulted in selective elimination of strictly anaerobic cecal bacteria, with a 100-fold increase in the numbers of aerobic and facultative gram-negative bacilli and a 10,000-fold increase in the numbers of aerobic and facultative gram-positive species. Clindamycin had a similar effect on the cecal flora except that the numbers of aerobic and facultative gram-positive bacteria decreased at least 10-fold. The predominating gram-positive species in the cecal flora or metronidazole-treated mice was an enterococcus, but this organism could not be recovered from the ceca of clindamycin-treated mice. Translocating bacteria (primarily gram-negative enteric bacteria) were recovered from the mesenteric lymph nodes of the majority of mice given metronidazole or clindamycin. Gram-positive bacteria were not recovered from the mesenteric lymph nodes of 20 clindamycin-treated mice, whereas 26% of 19 metronidazole-treated mice had translocating enterococci. With addition of streptomycin to the metronidazole and clindamycin regimens, mice treated with metronidazole-streptomycin became colonized predominantly with an enterococcus, and this was the only translocating species recovered from 13% of 23 mice; however, enterococci could not be detected in the ceca of clindamycin-streptomycin-treated mice, and Bacillus spp. were recovered from the mesenteric lymph nodes of 8% of 24 mice, reflecting the composition of the cecal flora. The apparent elimination of enterococci from the ceca of clindamycin and clindamycin-streptomycin-treated mice was inconsistent with the observation that the average (n=6) peak levels of clindamycin in blood and ceca were 25 and 21 microgram/ml, respectively, whereas the in vitro MIC was 128 microgram/ml. However, this apparent in vivo activity of clindamycin against enterococci was not evident in mice given 10(9) oral enterococci; the concentrations of cecal enterococci in both clindamycin-streptomycin- and metronidazole-streptomycin-treated mice were 10(10) to 10(11) enterococci per g, with translocating enterococci recovered from approximately half of these antibiotic-treated mice. Thus antibiotic therapy with metronidazole, clindamycin, metronidazole-streptomycin, and clindamycin-streptomycin resulted in a wide variation in the cecal population levels and translocation frequencies of enterococci. This variation appeared to be related to the discrepancy between the in vivo and in vitro activities of clindamycin against enterococci.
Animals↗
Evidence for the phagocytic transport of intestinal particles in dogs and rats.
Fluorescent latex beads of two different colors were implanted into separate intestinal segments in individual dogs and rats. Mesenteric lymph node phagocytes subsequently contained multiple beads of one or the other color but rarely both colors, indicating that intestinal phagocytes transported the latex beads to the draining lymph node. Fluorescent labeled Escherichia coli was implanted into rat ligated intestinal segments, and rare mesenteric lymph node phagocytes subsequently contained fluorescent bacteria, suggesting that intestinal bacteria might be transported in the same manner as inert latex beads.
Animals↗
Measured and predicted total body water in premenarcheal athletes and nonathletes.
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Adolescent↗
Validity of hydrodensitometry for determination of body composition in spinal injured subjects.
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Adipose Tissue↗
Role of the macrophage in the translocation of intestinal bacteria.
To clarify the role of the macrophage in the translocation of intestinal bacteria, groups (n = 10) of Swiss Webster mice (Immunocompetent) and C3H/HeJ mice (macrophage defective) were given bacitracin/streptomycin in their drinking water to eliminate the majority of the intestinal microflora. These mice were then "monoassociated" with a streptomycin-resistant strain of Escherichia coli. Forty-eight hours later, E coli was present in all animals at a concentration of 10(11)/g of cecum. In four separate experiments, E coli was recovered from 100% of the mesenteric lymph nodes (MLNs) of the immunocompetent Swiss Webster mice and from 10%, 40%, 30%, and 50% of the MLNs of macrophage-defective C3H/HeJ mice. Swiss Webster mice were then similarly monoassociated by antibiotic decontamination followed by administration of antibiotic-resistant, fluorescein-labeled E coli in their drinking water; cohort groups of mice were given fluorescein-labeled latex beads (1 micron in diameter) in their drinking water. Two, four, and 11 days later, the MLNs were removed and single cell suspensions were analyzed in the fluorescence-activated cell sorter. The fluorescein label was detected exclusively in the macrophage (esterase-positive) population. These results support the hypothesis that intestinal macrophages may play a key role in the transport of intestinal particles (including bacteria) into extraintestinal sites.
Animals↗
Succinic acid production by Bacteroides fragilis. A potential bacterial virulence factor.
We previously demonstrated that Bacteroides species elaborate a factor that impairs polymorphonuclear leukocyte (PMN) migration. This factor, active at a pH of 5.5 but not at 7.4, had similar inhibitory characteristics as the Bacteroides metabolite succinic acid. We examined the kinetics of production of this inhibitory factor and correlated its presence with succinic acid concentrations in the culture filtrate. In the four to six hours after Bacteroides fragilis 9032 reached the stationary phase of growth, there was a large increase in succinic acid production with an accompanying reduction in culture pH. This correlated well with the generation of a leukocyte-inhibitory factor. Pure succinic acid in sterile culture medium at concentrations similar to those detected in the 18-hour culture filtrate (20 mmol/L) produced comparable reduction in PMN migration. Following gel filtration chromatography of B fragilis culture filtrate, the fractions containing succinic acid labeled with carbon 14 inhibited PMN migration.
Bacteroides↗