scholarly journals Characterization of Early Life Stress-Affected Gut Microbiota

2021 ◽  
Vol 11 (7) ◽  
pp. 913
Author(s):  
Noriyoshi Usui ◽  
Hideo Matsuzaki ◽  
Shoichi Shimada
Keyword(s):  
Social Behavior ◽  
Gut Microbiota ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
The Body ◽  
Strong Impact ◽  
And Behavior ◽  
Bacterial Groups

Early life stress (ELS), such as neglect and maltreatment, exhibits a strong impact on the mental and brain development of children. However, it is not fully understood how ELS affects the body and behavior of children. Therefore, in this study, we performed social isolation on weaned pre-adolescent mice and investigated how ELS could affect gut microbiota and mouse behavior. Using the metagenomics approach, we detected an overall ELS-related change in the gut microbiota and identified Bacteroidales and Clostridiales as significantly altered bacterial groups. These metagenomic alterations impaired social behavior in ELS mice, which also correlated with the abundance of Bacteroidales and Clostridiales. Our results demonstrate that ELS alters the gut microbiota and reduces social behavior in adolescent mice.

scholarly journals Early-Life Stress Modulates Gut Microbiota and Peripheral and Central Inflammation in a Sex-Dependent Manner

2021 ◽  
Vol 22 (4) ◽  
pp. 1899 ◽  
Author(s):  
Hae Jeong Park ◽  
Sang A. Kim ◽  
Won Sub Kang ◽  
Jong Woo Kim
Keyword(s):  
Gut Microbiota ◽  
Relative Abundance ◽  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Early Life Stress ◽  
Female Rats ◽  
Rrna Gene ◽  
Dependent Manner ◽  
Male And Female Rats

Recent studies have reported that changes in gut microbiota composition could induce neuropsychiatric problems. In this study, we investigated alterations in gut microbiota induced by early-life stress (ELS) in rats subjected to maternal separation (MS; 6 h a day, postnatal days (PNDs) 1–21), along with changes in inflammatory cytokines and tryptophan-kynurenine (TRP-KYN) metabolism, and assessed the differences between sexes. High-throughput sequencing of the bacterial 16S rRNA gene showed that the relative abundance of the Bacteroides genus was increased and that of the Lachnospiraceae family was decreased in the feces of MS rats of both sexes (PND 56). By comparison, MS increased the relative abundance of the Streptococcus genus and decreased that of the Staphylococcus genus only in males, whereas the abundance of the Sporobacter genus was enhanced and that of the Mucispirillum genus was reduced by MS only in females. In addition, the levels of proinflammatory cytokines were increased in the colons (IFN-γ and IL-6) and sera (IL-1β) of the male MS rats, together with the elevation of the KYN/TRP ratio in the sera, but not in females. In the hippocampus, MS elevated the level of IL-1β and the KYN/TRP ratio in both male and female rats. These results indicate that MS induces peripheral and central inflammation and TRP-KYN metabolism in a sex-dependent manner, together with sex-specific changes in gut microbes.

scholarly journals Correction: N-3 Polyunsaturated Fatty Acids (PUFAs) Reverse the Impact of Early-Life Stress on the Gut Microbiota

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0142228 ◽  
Author(s):  
Matteo M. Pusceddu ◽  
Sahar El Aidy ◽  
Fiona Crispie ◽  
Orla O’Sullivan ◽  
Paul Cotter ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Gut Microbiota ◽  
Polyunsaturated Fatty Acids ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
The Impact

Early-life stress mediated modulation of adult neurogenesis and behavior

2012 ◽  
Vol 227 (2) ◽  
pp. 400-409 ◽  
Author(s):  
A. Korosi ◽  
E.F.G. Naninck ◽  
C.A. Oomen ◽  
M. Schouten ◽  
H. Krugers ◽  
...  
Keyword(s):  
Adult Neurogenesis ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
And Behavior

scholarly journals N-3 Polyunsaturated Fatty Acids (PUFAs) Reverse the Impact of Early-Life Stress on the Gut Microbiota

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0139721 ◽  
Author(s):  
Matteo M. Pusceddu ◽  
Sahar El Aidy ◽  
Fiona Crispie ◽  
Orla O’Sullivan ◽  
Paul Cotter ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Gut Microbiota ◽  
Polyunsaturated Fatty Acids ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
The Impact

scholarly journals Hippocampal astroglial hypertrophy in mice subjected to early life maternal deprivation

2021 ◽  
Author(s):  
Arnab Nandi ◽  
Garima Virmani ◽  
Swananda Marathe
Keyword(s):  
Immune Responses ◽  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Early Life Stress ◽  
Stratum Radiatum ◽  
Late Adulthood ◽  
Synaptic Physiology ◽  
And Behavior

Early-life stress (ELS), including chronic deprivation of maternal care, exerts persistent life-long effects on animal physiology and behavior, and is associated with several neurodevelopmental disorders. Long-lasting changes in neuronal plasticity and electrophysiology are documented extensively in the animal models of ELS. However, the role of astroglia in the lasting effects of ELS remains elusive. Astrocytes are intricately involved in the regulation of synaptic physiology and behavior. Moreover, astrocytes play a major role in the innate and adaptive immune responses in the central nervous system (CNS). The role of immune responses and neuroinflammation in the altered brain development and persistent adverse effects of ELS are beginning to be explored. Innate immune response in the CNS is characterized by a phenomenon called astrogliosis, a process in which astrocytes undergo hypertrophy, along with changes in gene expression and function. While the immune activation and neuroinflammatory changes concomitant with ELS, or in juveniles and young adults have been reported, it is unclear whether mice subjected to ELS exhibit astrogliosis-like alterations well into late-adulthood. Here, we subjected mice to maternal separation from postnatal day 2 to day 22 and performed comprehensive morphometric analysis of hippocampal astrocytes during late-adulthood. We found that the astrocytes in the stratum radiatum region of the CA1 hippocampal subfield from maternally separated mice exhibit significant hypertrophy as late as 8 months of age, revealing the crucial changes in astrocytes that manifest long after the cessation of ELS. This study highlights the persistence of neuroinflammatory changes in mice exposed to ELS.

Early life stress in mice alters gut microbiota independent of maternal microbiota inheritance

2021 ◽  
Vol 320 (5) ◽  
pp. R663-R674
Author(s):  
Keri M. Kemp ◽  
Jackson Colson ◽  
Robin G. Lorenz ◽  
Craig L. Maynard ◽  
Jennifer S. Pollock
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Disease ◽  
Gut Microbiota ◽  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Microbial Community Composition ◽  
Early Life Stress ◽  
Alpha Diversity ◽  
Disease Development

Exposure to early life stress (ELS) is associated with a greater risk of chronic disease development including depression and cardiovascular disease. Altered gut microbiota has been linked to both depression and cardiovascular disease in mice and humans. Rodent models of early life neglect are used to characterize the mechanistic links between early life stress (ELS) and the risk of disease later in life. However, little is understood about ELS exposure and the gut microbiota in the young mice and the influence of the maternal inheritance of the gut microbiota. We used a mouse model of ELS, maternal separation with early weaning (MSEW), and normally reared mice to determine whether the neonate microbiota is altered, and if so, are the differences attributable to changes in dam microbiota that are then transmitted to their offspring. Individual amplicon sequence variants (ASVs) displayed differential abundance in the microbiota of MSEW compared with normally reared pups at postnatal day ( PD) 28. Additionally, ELS exposure reduced the alpha diversity and altered microbial community composition at PD28. The composition, levels of alpha diversity, and abundance of individual ASVs in the microbiota of dams were similar from MSEW or normally reared cohorts. Thus, the observed shifts in the abundance of individual bacterial ASVs in the neonates and young pups are likely driven by endogenous effects of MSEW in the offspring host and are not due to inherited differences from the dam. This knowledge suggests that exposure to ELS has a direct effect on microbial factors on the risk of chronic disease development.

scholarly journals Characterization of astrocytes throughout life in wildtype and APP/PS1 mice after early-life stress exposure

2020 ◽  
Author(s):  
Maralinde R. Abbink ◽  
Janssen M. Kotah ◽  
Lianne Hoeijmakers ◽  
Aline Mak ◽  
Genevieve Yvon-Durocher ◽  
...  
Keyword(s):  
Life Stress ◽  
Early Life ◽  
Amyloid Β ◽  
Early Life Stress ◽  
Later Life ◽  
Amyloid Pathology ◽  
Emerging Risk ◽  
Microglial Response ◽  
The Relationship

Abstract Background Early-life stress (ES) is an emerging risk factor for later-life development of Alzheimer’s disease (AD). We have previously shown that ES modulates amyloid-beta pathology and the microglial response to it in the APPswe/PS1dE9 mouse model. Because astrocytes are key players in the pathogenesis of AD, we studied here if and how ES affects astrocytes in wildtype (WT) and APP/PS1 mice, and how these relate to the previously reported amyloid pathology and microglial profile. Methods We induced ES by limiting nesting and bedding material from postnatal days (P) 2-9. We studied in WT mice (at P9, P30 and 6 months) and in APP/PS1 mice (at 4 and 10 months) i) GFAP coverage, cell density and complexity in hippocampus (HPC) and entorhinal cortex (EC); ii) hippocampal gene expression of astrocyte markers; and iii) the relationship between astrocyte, microglia and amyloid markers. Results In WT mice, ES increased GFAP coverage in HPC subregions at P9, and decreased it at 10 months. APP/PS1 mice at 10 months exhibited both individual cell as well as clustered GFAP signals. APP/PS1 mice when compared to WT exhibited reduced total GFAP coverage in HPC, which is increased in the EC, while coverage of the clustered GFAP signal in the HPC was increased and accompanied by increased expression of several astrocytic genes. While measured astrocytic parameters in APP/PS1 mice appear not be further modulated by ES, analyzing these in the context of ES-induced alterations to amyloid pathology and microglial shows alterations at both 4 and 10 months of age. Conclusions Our data suggest that ES leads to alterations to the astrocytic response to amyloid-β pathology.

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