Beneficial bacteria inhibit cachexia

Muscle wasting, known as cachexia, is a debilitating condition associated with chronic inflammation such as during cancer. Beneficial microbes have been shown to optimize systemic inflammatory tone during good health; however, interactions between microbes and host immunity in the context of cachexi...

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Bibliographic Details
Published in:Oncotarget 2016-03, Vol.7 (11), p.11803-11816
Main Authors: Varian, Bernard J, Gourishetti, Sravya, Poutahidis, Theofilos, Lakritz, Jessica R, Levkovich, Tatiana, Kwok, Caitlin, Teliousis, Konstantinos, Ibrahim, Yassin M, Mirabal, Sheyla, Erdman, Susan E
Format: Article
Language:English
Subjects:
Animals
Cachexia - microbiology
Cachexia - prevention & control
Cell Proliferation
Cells, Cultured
Forkhead Transcription Factors - genetics
Forkhead Transcription Factors - metabolism
Lactobacillus reuteri - physiology
Longevity
Mice
Mice, Inbred C57BL
Priority Research Paper
Probiotics - pharmacology
Sarcopenia - microbiology
Sarcopenia - prevention & control
Thymus Gland - cytology
Thymus Gland - microbiology
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Summary:Muscle wasting, known as cachexia, is a debilitating condition associated with chronic inflammation such as during cancer. Beneficial microbes have been shown to optimize systemic inflammatory tone during good health; however, interactions between microbes and host immunity in the context of cachexia are incompletely understood. Here we use mouse models to test roles for bacteria in muscle wasting syndromes. We find that feeding of a human commensal microbe, Lactobacillus reuteri, to mice is sufficient to lower systemic indices of inflammation and inhibit cachexia. Further, the microbial muscle-building phenomenon extends to normal aging as wild type animals exhibited increased growth hormone levels and up-regulation of transcription factor Forkhead Box N1 [FoxN1] associated with thymus gland retention and longevity. Interestingly, mice with a defective FoxN1 gene (athymic nude) fail to inhibit sarcopenia after L. reuteri therapy, indicating a FoxN1-mediated mechanism. In conclusion, symbiotic bacteria may serve to stimulate FoxN1 and thymic functions that regulate inflammation, offering possible alternatives for cachexia prevention and novel insights into roles for microbiota in mammalian ontogeny and phylogeny.
ISSN:1949-2553
1949-2553
DOI:10.18632/oncotarget.7730