Thermal injury promotes bacterial translocation from the gastrointestinal tract in mice with impaired T-cell-mediated immunity
E. A. Deitch, J. Winterton and R. Berg
We have shown previously that after thermal trauma viable bacteria will
cross the intact gastrointestinal mucosa (bacterial translocation) to
invade the mesenteric lymph nodes and other organs if the normal indigenous
microflora is disrupted, allowing bacterial overgrowth. To determine
whether T-cell-mediated immunity (T-CMI) was important in preventing
translocation after thermal injury in animals with an intact normal flora,
conventional (+/+), athymic (nu/nu), and heterozygous (nu/+) mice receiving
a 30% third-degree burn were killed at various intervals after burn and
their organs cultured. Bacterial translocation did not occur in control or
burned specific pathogen-free mice with intact T-CMI but did occur in
athymic mice with deficient T-CMI. Both the incidence of positive organs
and the numbers of translocated bacteria per gram of organ were increased
after thermal injury. Bacterial overgrowth was not responsible for these
findings, since the levels of cecal enteric bacteria were not different
between the burned and nonburned groups. Since translocation occurred to a
greater extent in athymic burned mice than control athymic mice, it appears
that a thermal injury promotes translocation by impairing other host
defense systems in addition to the T-CMI.
Reducing susceptibility to bacteremia after experimental burn injury: a role for selective decontamination of the digestive tract
Horton et al.
J. Appl. Physiol. 2007;102:2207-2216.
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Efficacy of Bacteriophage Therapy against Gut-Derived Sepsis Caused by Pseudomonas aeruginosa in Mice
Watanabe et al.
Antimicrob. Agents Chemother. 2007;51:446-452.
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A role of PP1/PP2A in mesenteric lymph node T cell suppression in a two-hit rodent model of alcohol intoxication and injury
Li et al.
J. Leukoc. Biol. 2006;79:453-462.
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Corticosterone suppresses mesenteric lymph node T cells by inhibiting p38/ERK pathway and promotes bacterial translocation after alcohol and burn injury
Li et al.
Am. J. Physiol. Regul. Integr. Comp. Physiol. 2005;289:R37-R44.
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Selective decontamination of the digestive tract attenuated the myocardial inflammation and dysfunction that occur with burn injury
Horton et al.
Am. J. Physiol. Heart Circ. Physiol. 2004;287:H2241-H2251.
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IFN-{gamma} Production from Liver Mononuclear Cells of Mice in Burn Injury As Well As in Postburn Bacterial Infection Models and the Therapeutic Effect of IL-18
Ami et al.
J. Immunol. 2002;169:4437-4442.
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Role of p38 mitogen-activated protein kinase in cardiac myocyte secretion of the inflammatory cytokine TNF-{alpha}
Ballard-Croft et al.
Am. J. Physiol. Heart Circ. Physiol. 2001;280:H1970-H1981.
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Effect of Antiflagellar Human Monoclonal Antibody on Gut-Derived Pseudomonas aeruginosa Sepsis in Mice
Matsumoto et al.
CVI 1999;6:537-541.
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Effect of Interleukin-10 on Gut-Derived Sepsis Caused by Pseudomonas aeruginosa in Mice
Matsumoto et al.
Antimicrob. Agents Chemother. 1998;42:2853-2857.
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Arginine in burn injury improves cardiac performance and prevents bacterial translocation
Horton et al.
J. Appl. Physiol. 1998;84:695-702.
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Burn Wound Sepsis
Hansbrough
J Intensive Care Med 1987;2:313-327.
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