Effect of gastrointestinal flora on body temperature of rats and mice

Kluger, Matthew J.; Conn, Carole A.; Franklin, Brian J.; Freter, Rolf; Abrams, Gerald D.

doi:10.1152/ajpregu.1990.258.2.r552

Cited by 32 publications

(31 citation statements)

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“…This difference in temperature was not related to the temperature in the animal rooms (all housed at 21°C room temperature) but was found to be related to the GI microbiota in BF mice, which was in accordance with a previous study. 15 In that study, Kluger and colleagues demonstrated that GI flora in BF-raised mice had a stimulatory effect on body temperature (unrelated to physical activity) compared with germfree mice. 15 In addition to the untreated SPF mice, we examined BF mice that were first treated with broad spectrum antibiotics, a widely established technique to significantly deplete the gut flora (supplemental Figure 2).…”

Section: Discussionmentioning

confidence: 98%

“…15 In that study, Kluger and colleagues demonstrated that GI flora in BF-raised mice had a stimulatory effect on body temperature (unrelated to physical activity) compared with germfree mice. 15 In addition to the untreated SPF mice, we examined BF mice that were first treated with broad spectrum antibiotics, a widely established technique to significantly deplete the gut flora (supplemental Figure 2). [28][29][30][31] We observed that after depletion of the GI flora in BF mice (supplemental Figure 2), their rectal temperatures remained static after housing for 1 week (Figure 1).…”

Section: Discussionmentioning

confidence: 98%

“…It has been described that GI flora can upregulate body temperature in mice 15 ; therefore, we assessed temperatures in the indicated mouse groups. Compared with the SPF-housed mice, after 1 week of housing, the temperatures of BF mice significantly increased ( Figure 1).…”

Section: Bf Mice Display Elevated Body Temperatures Indicative Of a Dmentioning

confidence: 99%

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Gastrointestinal microbiota contributes to the development of murine transfusion-related acute lung injury

et al. 2018

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Key Points• Gastrointestinal flora contributes to development of antibody-mediated murine TRALI.• Depletion of gastrointestinal flora prevents TRALI by inhibiting MIP-2 secretion and pulmonary neutrophil accumulation.Transfusion-related acute lung injury (TRALI) is a syndrome of respiratory distress upon blood transfusion and is the leading cause of transfusion-related fatalities. Whether the gut microbiota plays any role in the development of TRALI is currently unknown. We observed that untreated barrier-free (BF) mice suffered from severe antibody-mediated acute lung injury, whereas the more sterile housed specific pathogen-free (SPF) mice and gut flora-depleted BF mice were both protected from lung injury. The prevention of TRALI in the SPF mice and gut flora-depleted BF mice was associated with decreased plasma macrophage inflammatory protein-2 levels as well as decreased pulmonary neutrophil accumulation. DNA sequencing of amplicons of the 16S ribosomal RNA gene revealed a varying gastrointestinal bacterial composition between BF and SPF mice. BF fecal matter transferred into SPF mice significantly restored TRALI susceptibility in SPF mice. These data reveal a link between the gut flora composition and the development of antibody-mediated TRALI in mice. Assessment of gut microbial composition may help in TRALI risk assessment before transfusion.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 98%

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Gastrointestinal microbiota contributes to the development of murine transfusion-related acute lung injury

et al. 2018

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“…Both basal metabolic rate (Levenson et al 1969) and thermoregulatory setpoint (Kluger et al 1990) are lower in the germ-free animals, but can be restored through reconstitution of the normal enteric flora.…”

Section: The Indigenous Gut Floramentioning

confidence: 99%

The gut as a potential trigger of exercise-induced inflammatory responses

Marshall¹

1998

Can. J. Physiol. Pharmacol.

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Multiple lines of evidence support the hypothesis that ischemia-induced impairment of normal gut barrier function, with loss of the normal tonic counterinflammatory influence of the gut immune system, contributes to the expression of uncontrolled inflammation in critically ill victims of trauma and overwhelming infection. The clinical syndrome known as the systemic inflammatory response syndrome (SIRS), which embodies uncontrolled inflammation in trauma and sepsis, is reproduced in its entirety by vigourous exercise, raising the possibility that the gut may also play a role in exercise-induced inflammation. Both strenuous exercise and systemic sepsis result in impairment of the normal gut barrier to luminal microorganisms, and result in elevated circulating levels of bacterial endotoxin. Under normal circumstances, the immune tissues of the gut-liver axis inhibit the expression of a host response to foodstuffs in the gut lumen, or to the indigenous microbial flora of the gut wall. This influence is an active, energy-requiring process. Both strenuous exercise and critical illness are associated with gut ischemia, providing a common biologic basis for the initiation of a dysregulated inflammatory response. Although direct evidence supporting or refuting the hypothesis that the gut can serve as a trigger for systemic inflammation following strenuous exercise is sparse, the similarities in the clinical manifestations of SIRS and exercise, and the promising results of prophylactic or therapeutic gut-directed strategies in critical illness, suggest that similar approaches may provide benefit for individuals engaged in extreme physical exercise.

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“…Starch gives rise to more butyric acid, whereas non-starch polysaccharides result in a greater production of acetic and propionic acids (Pryde et al, 2002). In 1990 to 1991, Kluger and colleagues showed that germ-free rats produced by oral administration of bacitracin/ streptomycin had a significantly lower CBT than controls (Conn et al, 1991;Kluger et al, 1990). Their lower CBT was reversed by inoculation with spore-forming Gram-positive flora, prepared by 10 min heating cecal homogenate anaerobically collected from stock mice (Conn et al, 1991).…”

Section: Ucp1 Independent Thermogenesis a Cost-inefficient Means To mentioning

confidence: 99%

Immunity-Based Evolutionary Interpretation of Diet-Induced Thermogenesis

2016

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Diet-induced thermogenesis (DIT) has often been argued to be a physiological defense against obesity, but no empirical proof of its effectiveness in limiting human body weight gain is available. We here propose an immune explanation of DIT-i.e., that it results from the coevolution of host and gut microbiota (especially Firmicutes) that ferment ingested food and proliferate, causing periodic, vagally mediated increases in thermogenesis aimed at curtailing their expansion. Because of this evolutionary adaptive significance related to the immune system, DIT is not effective as an "adaptation" to maintain a certain body mass. Were DIT an effective adaptation to prevent obesity, the current obesity epidemic might not have occurred.

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Effect of gastrointestinal flora on body temperature of rats and mice

Cited by 32 publications

References 0 publications

Gastrointestinal microbiota contributes to the development of murine transfusion-related acute lung injury

Gastrointestinal microbiota contributes to the development of murine transfusion-related acute lung injury

The gut as a potential trigger of exercise-induced inflammatory responses

Immunity-Based Evolutionary Interpretation of Diet-Induced Thermogenesis

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