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The effect of gut microbiome on expression of genes involved in regulation of stress response in chronic stress

The scientists from the Institutes of Physiology and Microbiology CAS have shown, that absence of gut microbiota leads to altered behavior in social conflict and changes of expression of genes involved in regulation of stress response in chronically stressed mice.

Mammals are naturally colonized by microorganisms, commonly referred as the microbiome. Substantial fraction of the microbiome represent bacteria. Some bacteria are capable of synthetizing chemical substances, such as hormones or neurotransmitters, and thus influence the host both on local and whole-organism level. Disruption of the microbiome is associated with several immune and neuropsychiatric disorders and stress may disrupt the balance between the host and the microbiome. When facing potential danger, stress response acts towards maintaining the homeostasis by activating variety of mechanisms such as sympatho-adrenal system or the hypothalamo-pituitary-adrenal (HPA) axis. Acute stress is generally not harmful, however when prolonged or poorly managed, it can lead to serious side effects.

For studying the effects of microbiome on the host the germ-free mice are used as animal model. It is known that microbiome alters the behavior and can alter humoral response to acute stress. In collaboration with our colleagues from the Institute of Microbiology CAS we have focused on the effects of chronic psychosocial stress in germ-free mice. Our results have shown that the absence of microbiome affects the murine behavior in social conflicts (Fig. 1) and modulates the expression of genes involved in regulation of stress response in adrenal gland (Fig. 2), local paracrine signalization in colon and expression of cytokines in mesentery lymph nodes and colon. This study contributes to understanding the crosstalk between microbiota and the host brain, especially during chronic stress.


Fig. 1. Time spent in individual defensive behavioral patterns (upright posture, freezing and escape/flight) and in total defensive behavior (B) of specific pathogen-free (SPF) and germ-free (GF) mice. Data are expressed as the means ± SEM; *P < 0.05.


Fig. 2. Responses of genes encoding adrenal steroidogenesis, catecholamine biogenesis and glucocorticoid metabolism following social defeat in specific pathogen-free (SPF) and germ-free (GF) mice. MC2R, melanocortin 2 receptor; StAR, steroidogenic acute regulatory protein; Cyp11a1, cholesterol side-chain cleavage enzyme; TH, tyrosine hydroxylase; PNMT, phenylethanolamine N-methyltransferase; 11HSD1 and 11HSD2, 11b-hydroxysteroid dehydrogenase type 1 and type 2. The data are expressed as the means ± SEM; *P < 0.05, **P < 0.01, ***P < 0.001.


Vodička, Martin - Ergang, Peter - Hrnčíř, Tomáš - Mikulecká, Anna - Kvapilová, Pavlína - Vagnerová, Karla - Šestáková, Blanka - Fajstová, Alena - Hermanová, Petra - Hudcovic, Tomáš - Kozáková, Hana - Pácha, Jiří: Microbiota affects the expression of genes involved in HPA axis regulation and local metabolism of glucocorticoids in chronic psychosocial stress. Brain Behavior and Immunity. Roč. 73, Oct 2018 (2018), s. 615-624. ISSN 0889-1591, IF: 6.306, 2017.