summary: Researchers have found a significant link between the gut microbiota of male mice and the health and survival of their offspring. This study shows that gut microbiota imbalance caused by antibiotics can lead to lower birth weight and higher mortality in the next generation.
The findings highlight the “gut-germline axis,” in which changes in the gut environment influence testicular metabolite and hormonal signaling, which in turn affects reproduction and offspring health. Importantly, these effects are reversible, suggesting that restoring the balance of the gut microbiota can prevent these negative outcomes.
Important facts:
- Influence of intestinal flora: Antibiotic-induced disruption of the gut microbiota in male mice has a significant impact on the birth weight and survival of their offspring, highlighting that microbial health can have intergenerational effects.
- Reversible effect: The negative effects on offspring caused by changes in the paternal gut microbiota are reversible and return to normal once the gut microbiota is restored after antibiotic treatment is discontinued.
- Impact on human health: Although this study was conducted in mice, similar effects may occur in humans, especially given common practices such as antibiotic use that can affect the gut microbiome. Important questions arise.
sauce: EMBL
The intestinal flora is the microbial community that occupies the gastrointestinal tract. It is responsible for the production of enzymes, metabolites, and other molecules that are important for host metabolism and response to the environment.
A balanced gut microbiome is therefore important for mammalian health in many ways, including helping to regulate the immune and endocrine systems. This affects the physiology of tissues throughout the body.
However, little was known about the influence of the gut microbiota on host reproduction or whether changes in the paternal microbiota influence offspring fitness.
The Hackett Group at EMBL Rome, in collaboration with the Bork Group and the Zimmermann Group at EMBL Heidelberg, worked to answer this question, and the results are now published in the journal. Nature.
Scientists have shown that disrupting the gut microbiota of male mice increases the likelihood that their offspring will be born with low body weight and die prematurely.
What is passed down to the next generation
To study the influence of the gut microbiome on male reproduction and their offspring, researchers investigated the effects of gut microbiota in male mice by treating them with common antibiotics that do not enter the bloodstream. The composition of This causes an imbalance in the microbial ecosystem in the intestines, a condition called dysbiosis.
The scientists then analyzed changes in the composition of key testicular metabolites. They found that in male mice, dysbiosis affects testicular physiology as well as metabolite composition and hormonal signaling.
This effect was mediated, at least in part, by changes in the levels of leptin, an important hormone, in the blood and testes of men who had induced dysbiosis. These observations suggest the existence of a “gut-germline axis” in mammals as a critical connection between the gut, its microbiota, and the germline.
To understand the link between this “gut germline” axis and the traits passed on to offspring, researchers mated untreated or dysbiotic males with untreated females. Mice offspring born to fathers with dysbiosis had significantly lower birth weight and increased postnatal mortality.
Treatment with different combinations of antibiotics and laxatives that disrupt the intestinal flora (which also disrupts the microbiome) had similar effects on the offspring.
Importantly, this effect is reversible. When antibiotics are discontinued, the father’s microbiome recovers. When mice with restored microbiota were bred with untreated females, their offspring were born with normal birth weight and normal development.
“We observed that once the microbiota was restored to normal, the intergenerational effects disappeared. This suggests that changes in the gut microbiota that can cause intergenerational effects may be more likely to occur in paternal This means that it can be prevented in some children,” said Pia Bork, director of EMBL Heidelberg, who participated in the study.
“The next step is to understand in detail how different environmental factors, such as medicines, including antibiotics, can affect the paternal germline and thus the development of the embryo.” This publication added Ail Demboba, lead author of the book and a former postdoctoral fellow in the Hackett group and now group leader at the Max Planck Institute for Immunology and Epigenetics in Freiburg, Germany.
“This study began with the aim of understanding the influence of the environment on paternity by considering the gut microbiota as a nexus of host-environment interactions. A sufficient cause model has been created to assess the health risks of
Impact on fathers’ risk of pregnancy diseases
In their study, Hackett and colleagues also found that placental abnormalities, such as poor vascularization and reduced growth, occur more frequently in pregnancies of men with internal abnormalities.
Placental defects are characteristic of a common pregnancy complication in humans called preeclampsia, which causes impaired growth in offspring and is a risk factor for developing a variety of common diseases later in life.
“Our study demonstrates that a communication channel exists between the mammalian gut microbiota and the reproductive system.
“Furthermore, environmental factors that interfere with these signals in prospective fathers increase the risk of negative outcomes for offspring health through changes in placental development,” said Jamie, research project coordinator and EMBL Rome group leader. Hackett said.
“This means that in mice, the father’s environment just before conception can influence traits in the offspring, independent of genetic inheritance.”
“At the same time, we found that this effect is only one generation. Further research is needed to investigate how pervasive these effects are and whether they are relevant to humans.” It must be made clear that there are essential differences that must be taken into account when translating results from mouse models to humans.
Mr Hackett continued: “However, given the prevalence of dietary and antibiotic practices in Western culture that are known to disrupt the gut microbiome, it is important to note that patrilineal intergenerational influences and their impact on pregnancy outcomes and It is important to consider more carefully how this is impacting population disease risk.”
About this microbiome and neurodevelopment research news
author: Lisa Vollmar
sauce: EMBL
contact: Lisa Vollmer – EMBL
image: Image credited to Neuroscience News
Original research: Open access.
“Disruption of the father’s microbiome affects offspring’s fitnessWritten by Pia Bork et al. Nature
abstract
Disruption of the father’s microbiome affects offspring’s fitness
The gut microbiota functions at the interface of host-environment interactions and influences human homeostasis and metabolic networks.
Therefore, environmental factors that disrupt the balance of the gut microbial ecosystem can shape physiological and disease-related responses across somatic tissues.
However, systemic effects of the gut microbiome on the germline and, as a result, F.1 The offspring it produces is unknown.
Here we show that the mouse gut microbiota acts as an important interface between the paternal preconception environment and intergenerational health status.
Disturbances in the future father’s gut microbiome increase the likelihood that his offspring will have low birth weight, severe growth restriction, and early death.
Transmission of disease risk occurs through the germ line and is caused by pervasive gut microbiota disruption, such as non-absorbable antibiotics and osmotic laxatives, but can be reversed by restoring the paternal microbiota before pregnancy. To do.
This effect is associated with dynamic responses to gut microbiota dysbiosis induced in the male reproductive system, including impaired leptin signaling, altered testicular metabolite profiles, and remapping of small RNA payloads within sperm. I am.
The results showed that fathers with dysbiosis caused an increased risk of intrauterine placental insufficiency, indicating that the origin of intergenerational effects in mammals lies in the placenta.
Our study defines a regulatory “gut-germline axis” in males that is sensitive to environmental exposures and programs offspring fitness by influencing placental function. Masu.
