Genetic Susceptibility to Mucosal Damage Leads to Bacterial Translocation in a Murine Burn Model

Ma, Li; Ma, Jingwen; Deitch, Edwin A.; Specian, Robert D.; Berg, Rodney D.

doi:10.1097/00005373-198909000-00010

Cited by 39 publications

(9 citation statements)

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“…Bacterial translocation after thermal injury appears to be the result of ischemic changes within the intestine associated with decreased splanchnic blood blow (13) and activation of tissue xanthine oxidase (7). However, some evidence suggests that the continued translocation associated with subsequent infection after thermal injury may occur independently of intestinal ischemia (4a; W. G. Jones, A. E. Barber, J. P. Minei, T. J. Fahey, R. Inamdar, G. T. Shires III, and G. T. Shires, Abstr.…”

Section: Discussionmentioning

confidence: 99%

“…Aliquots (200 RI each) from each broth culture were addi-tionally plated on both tryptic soy agar with 5% sheep blood and MacConkey agar plates, allowing enumeration of the number of gram-negative CFU recovered per gram of tissue cultured. This method of reporting quantitative culture results as CFU per gram of tissue has previously been employed in similar studies of bacterial translocation by us and others (1,5,(7)(8)(9). All cultures were incubated at 37°C and examined at 24 and 48 h for bacterial growth.…”

Section: Methodsmentioning

confidence: 99%

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Pathophysiologic glucocorticoid elevations promote bacterial translocation after thermal injury

et al. 1990

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Thermal injury results in transient elevations of plasma glucocorticoids and promotes translocation of bacteria from the gut to the mesenteric lymph nodes (MLN) in rats. Translocated organisms are quickly cleared following uncomplicated thermal injury. However, subsequent burn wound infection, in temporal association with sustained pathophysiologic elevations of plasma corticosterone, results in the continued presence of enteric bacteria in the MLN. To study the role of sustained pathophysiologic steroid elevations in the mediation of this prolonged bacterial translocation, Wistar rats were randomly placed in groups receiving one of the following:(i) a 30% total body surface area scald injury with placement of a subcutaneous corticosterone pellet, (ii) a 30% total body surface area scald and a sham pellet implanatation, (iii) a sham burn and a corticosterone pellet implantation, or (iv) a sham burn and a sham pellet implantation. The animals were sacrificed on days 1 and 4 after injury, and cultures of the MLN, as well as the liver and spleen, were taken. Implantation of corticosterone pellets resulted in sustained elevations of plasma corticosterone compared with controls not receiving corticosterone pellets, similar to results seen in association with injury and infection. These * Corresponding author. t Present address:

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Pathophysiologic glucocorticoid elevations promote bacterial translocation after thermal injury

et al. 1990

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“…16,17 Not only does the gut-associated lymphoid tissue compose the body's largest lymphoid "organ," but the intestinal immune system is continually exposed to potential proinflammatory stimuli. 27 Since thermal injury is associated with intestinal ischemia, loss of gut barrier function, and subsequent bacterial translocation, [28][29][30] it appears logical that the level of gutassociated lymphoid tissue activation should also be increased and that the gut may then be involved in the pathogenesis of pulmonary injury following thermal injury. Consequently, we tested the hypothesis that after a nonlethal but severe burn, gut-derived factors are present in the mesenteric lymph and contribute to burninduced lung injury.…”

Section: Commentmentioning

confidence: 99%

Gut-Derived Mesenteric Lymph

Magnotti¹

1999

Arch Surg

131

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Background: Previously, we showed that mesenteric lymph generated following hemorrhagic shock increases endothelial cell permeability and contributes to lung injury. It has also been shown that lymph produced at the site of burn injury plays a role in altering pulmonary vascular hemodynamics. In addition, previous experimental work has suggested that organs and tissues distant from the injury site may contribute to pulmonary dysfunction. One explanation would be that gutderived inflammatory factors (in addition to those produced locally at the site of injury) are reaching the pulmonary circulation, where they exert their effects via the gut lymphatics. Hypotheses: The 2 hypotheses herein were that (1) gutderived factors carried in the mesenteric lymph of rats generated following thermal injury will contribute to lung injury and (2) intestinal bacterial overgrowth will potentiate the degree of burn-induced lung injury. These hypotheses were tested by examining the effect of mesenteric lymph flow interruption prior to thermal injury on burn-induced lung injury in rats with a normal intestinal bacterial flora and in rats with intestinal Escherichia coli overgrowth. These rats were termed E colimonoassociated rats. Methods: Normal intestinal bacterial flora and monoassociated male Sprague-Dawley rats were subjected to sham burn, 40% total body surface area burn, or lymphatic division plus burn. After 3 hours, 10 mg of Evans PAPER

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“…This decreased barrier function is associated with increased bacterial translocation (14)(15)(16). Furthermore, bacterial infection either alone or with burn decreases T cell function in Peyer's patches within 24 h of initial insult, as determined by cellular proliferation, interleukin-2 production, and calcium signaling (17).…”

Section: Discussionmentioning

confidence: 99%

Decreased Lymphocyte Apoptosis by Anti-Tumor Necrosis Factor Antibody in Peyerʼs Patches After Severe Burn

Woodside

Spies

et al. 2003

Shock

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Severe burn results in immunosuppression, with increased lymphocyte apoptosis in both the central and peripheral immune system. As atrophy of the small intestine has been described in mouse models and intestinal lymphocytes have been implicated in the burn inflammatory response, we examined the effects of burn and tumor necrosis factor (TNF)-alpha on lymphocytes in intestinal Peyer's patches. Anesthetized C57BL6 mice received a 30% full-thickness scald burn on the upper back. Sham-burned animals served as controls. Anti-TNF or control immunoglobulin (Ig) G antibody (200 microg) was given immediately after the burn. The animals were initially resuscitated with 2 mL of normal saline, and were then sacrificed 12 h postburn. Terminal deoxyuridine nick-end labeling (TUNEL) and proliferative cell nuclear antigen (PCNA) staining was performed. Apoptosis was quantified as apoptotic lymphocytes/high-powered field (hpf). Results, expressed as mean +/- SEM, were compared using analysis of variance (ANOVA) and the Student-Newman-Keuls test. All mice survived the burn. An initial time-course experiment demonstrated maximal Peyer's patch apoptosis 12 h after the burn. Sham mice had 25 +/- 7 TUNEL-stained cells/hpf in Peyer's patches, whereas burned mice had 93 +/- 18 cells/hpf (P < 0.05). In contrast, burned mice receiving anti-TNF antibody had 28 +/- 8 TUNEL-stained cells/hpf (P < 0.05 vs. burn), whereas sham mice receiving anti-TNF antibody had 20 +/- 4 cells/hpf. There were no significant differences in PCNA staining between the groups. Scald burn results in lymphocyte apoptosis in Peyer's patches. This apoptosis can be abrogated by the addition of anti-TNF antibody. Apoptotic changes may lead to the failure of the intestinal immunological barrier and increased risk of sepsis.

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Genetic Susceptibility to Mucosal Damage Leads to Bacterial Translocation in a Murine Burn Model

Cited by 39 publications

References 0 publications

Pathophysiologic glucocorticoid elevations promote bacterial translocation after thermal injury

Pathophysiologic glucocorticoid elevations promote bacterial translocation after thermal injury

Gut-Derived Mesenteric Lymph

Decreased Lymphocyte Apoptosis by Anti-Tumor Necrosis Factor Antibody in Peyerʼs Patches After Severe Burn

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