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Paradoxes in leaky microbial trade.

ABSTRACT: Microbes produce metabolic resources that are important for cell growth yet leak into the environment. Other microbes can use these resources, adjust their own metabolic production accordingly, and alter the resources available for others. We analyze a model in which metabolite concentrations, production regulation, and population frequencies coevolve in the simple case of two cell types producing two metabolites. We identify three paradoxes where changes that should intuitively benefit a cell type actually harm it. For example, a cell type can become more efficient at producing a metabolite and its relative frequency can decrease-or alternatively the total population growth rate can decrease. Another paradox occurs when a cell type manipulates its counterpart's production so as to maximize its own instantaneous growth rate, only to achieve a lower final growth rate than had it not manipulated. These paradoxes highlight the complex and counterintuitive dynamics that emerge in simple microbial economies.

SUBMITTER: Kallus Y

PROVIDER: S-EPMC5678203 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature

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Paradoxes in leaky microbial trade.

Kallus Yoav Y Miller John H JH Libby Eric E

Nature communications 20171108 1

Microbes produce metabolic resources that are important for cell growth yet leak into the environment. Other microbes can use these resources, adjust their own metabolic production accordingly, and alter the resources available for others. We analyze a model in which metabolite concentrations, production regulation, and population frequencies coevolve in the simple case of two cell types producing two metabolites. We identify three paradoxes where changes that should intuitively benefit a cell t ...[more]

PMID: 29118345

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Project description:The mechanisms that underlie various inflammation paradoxes, metabolically healthy obesity, and increased inflammations after inflammatory cytokine blockades and deficiencies remain poorly determined. We performed an extensive -omics database mining, determined the expressions of 1367 innate immune regulators in 18 microarrays after deficiencies of 15 proinflammatory cytokines/regulators and eight microarray datasets of patients receiving Mab therapies, and made a set of significant findings: 1) proinflammatory cytokines/regulators suppress the expressions of innate immune regulators; 2) upregulations of innate immune regulators in the deficiencies of IFNγ/IFNγR1, IL-17A, STAT3 and miR155 are more than that after deficiencies of TNFα, IL-1β, IL-6, IL-18, STAT1, NF-kB, and miR221; 3) IFNγ, IFNγR and IL-17RA inhibit 10, 59 and 39 proinflammatory cytokine/regulator pathways, respectively; in contrast, TNFα, IL-6 and IL-18 each inhibits only four to five pathways; 4) The IFNγ-promoted and -suppressed innate immune regulators have four shared pathways; the IFNγR1-promoted and -suppressed innate immune regulators have 11 shared pathways; and the miR155-promoted and -suppressed innate immune regulators have 13 shared pathways, suggesting negative-feedback mechanisms in their conserved regulatory pathways for innate immune regulators; 5) Deficiencies of proinflammatory cytokine/regulator-suppressed, promoted programs share signaling pathways and increase the likelihood of developing 11 diseases including cardiovascular disease; 6) There are the shared innate immune regulators and pathways between deficiency of TNFα in mice and anti-TNF therapy in clinical patients; 7) Mechanistically, up-regulated reactive oxygen species regulators such as myeloperoxidase caused by suppression of proinflammatory cytokines/regulators can drive the upregulation of suppressed innate immune regulators. Our findings have provided novel insights on various inflammation paradoxes and proinflammatory cytokines regulation of innate immune regulators; and may re-shape new therapeutic strategies for cardiovascular disease and other inflammatory diseases.

Dataset Information

Paradoxes in leaky microbial trade.

Publications

Paradoxes in leaky microbial trade.

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