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Background The intestinal microbiota plays an important role in regulating gastrointestinal (GI) physiology in part through interactions with the enteric nervous system (ENS). Alterations in the gut microbiome frequently occur together with disturbances in enteric neural control in pathophysiological conditions. However, the mechanisms by which the microbiota regulates GI function and the structure of the ENS are incompletely understood. Using a mouse model of antibiotic (Abx)-induced bacterial depletion, we sought to determine the molecular mechanisms of microbial regulation of intestinal function and the integrity of the ENS. Spontaneous reconstitution of the Abx-depleted microbiota was used to assess the plasticity of structure and function of the GI tract and ENS. Microbiota-dependent molecular mechanisms of ENS neuronal survival and neurogenesis were also assessed. Results Adult male and female Abx-treated mice exhibited alterations in GI structure and function, including a longer small intestine, slower transit time, increased carbachol-stimulated ion secretion, and increased intestinal permeability. These alterations were accompanied by the loss of enteric neurons in the ileum and proximal colon in both submucosal and myenteric plexuses. A reduction in the number of enteric glia was only observed in the ileal myenteric plexus. Recovery of the microbiota restored intestinal function and stimulated enteric neurogenesis leading to increases in the number of enteric glia and neurons. Lipopolysaccharide (LPS) supplementation enhanced neuronal survival alongside bacterial depletion, but had no effect on neuronal recovery once the Abx-induced neuronal loss was established. In contrast, short-chain fatty acids (SCFA) were able to restore neuronal numbers after Abx-induced neuronal loss, demonstrating that SCFA stimulate enteric neurogenesis in vivo. Conclusions Our results demonstrate a role for the gut microbiota in regulating the structure and function of the GI tract in a sex-independent manner. Moreover, the microbiota is essential for the maintenance of ENS integrity, by regulating enteric neuronal survival and promoting neurogenesis. Molecular determinants of the microbiota, LPS and SCFA, regulate enteric neuronal survival, while SCFA also stimulates neurogenesis. Our data reveal new insights into the role of the gut microbiota that could lead to therapeutic developments for the treatment of enteric neuropathies. AxcJMXS31MXgoUKmPZDwRn Video abstract

The gut microbiome consists of a multi-kingdom microbial community. Whilst the role of bacteria as causal contributors governing host physiological development is well established, the role of fungi remains to be determined. Here, we use germ-free mice colonized with defined species of bacteria, fungi, or both to differentiate the causal role of fungi on microbiome assembly, immune development, susceptibility to colitis, and airway inflammation. Fungal colonization promotes major shifts in bacterial microbiome ecology, and has an independent effect on innate and adaptive immune development in young mice. While exclusive fungal colonization is insufficient to elicit overt dextran sulfate sodium-induced colitis, bacterial and fungal co-colonization increase colonic inflammation. Ovalbumin-induced airway inflammation reveals that bacterial, but not fungal colonization is necessary to decrease airway inflammation, yet fungi selectively promotes macrophage infiltration in the airway. Together, our findings demonstrate a causal role for fungi in microbial ecology and host immune functionality, and therefore prompt the inclusion of fungi in therapeutic approaches aimed at modulating early life microbiomes. The immunomodulatory role of commensal gut fungi and interactions with bacteria remain unclear. Here, using germ-free mice colonized with defined species of bacteria and fungi, the authors find that fungal colonization induces changes in bacterial microbiome ecology while having an independent effect on innate and adaptive immunity in mice.

Copper is a critical enzyme cofactor in the body but also a potent cellular toxin when intracellularly unbound. Thus, there is a delicate balance of intracellular copper, maintained by a series of complex interactions between the metal and specific copper transport and binding proteins. The gastrointestinal (GI) tract is the primary site of copper entry into the body and there has been considerable progress in understanding the intricacies of copper metabolism in this region. The GI tract is also host to diverse bacterial populations, and their role in copper metabolism is not well understood. In this study, we compared the isotopic fractionation of copper in the GI tract of mice with intestinal microbiota significantly depleted by antibiotic treatment to that in mice not receiving such treatment. We demonstrated variability in copper isotopic composition along the length of the gut. A significant difference, ~1.0‰, in copper isotope abundances was measured in the proximal colon of antibiotic-treated mice. The changes in copper isotopic composition in the colon are accompanied by changes in copper transporters. Both CTR1, a copper importer, and ATP7A, a copper transporter across membranes, were significantly down-regulated in the colon of antibiotic-treated mice. This study demonstrated that isotope abundance measurements of metals can be used as an indicator of changes in metabolic processes in vivo. These measurements revealed a host–microbial interaction in the GI tract involved in the regulation of copper transport.

The action of an Agaricus blazei aqueous extract pretreatment on paracetamol injury in rats was examined not only in terms of the classical indicators (e.g., levels of hepatic enzymes in the plasma) but also in terms of functional and metabolic parameters (e.g., gluconeogenesis). Considering solely the classical indicators for tissue damage, the results can be regarded as an indication that the A. blazei extract is able to provide a reasonable degree of protection against the paracetamol injury in both the hepatic and brain tissues. The A. blazei pretreatment largely prevented the increased levels of hepatic enzymes in the plasma (ASP, ALT, LDH, and ALP) and practically normalized the TBARS levels in both liver and brain tissues. With respect to the functional and metabolic parameters of the liver, however, the extract provided little or no protection. This includes morphological signs of inflammation and the especially important functional parameter gluconeogenesis, which was impaired by paracetamol. Considering these results and the long list of extracts and substances that are said to have hepatoprotective effects, it would be useful to incorporate evaluations of functional parameters into the experimental protocols of studies aiming to attribute or refute effective hepatoprotective actions to natural products.

Gut microbiomes make major contributions to the physiological and immunological development of the host, but the relative importance of their bacterial and fungal components, and how they interact, remain largely unknown. We applied carefully controlled experiments in gnotobiotic mice colonized with defined communities of bacteria, fungi, or both to differentiate the direct role of fungi on microbiome assembly, host development, and susceptibility to colitis and airway inflammation. Our results revealed that fungal colonization alone was insufficient to promote the intestinal anatomic and physiological changes seen in mice colonized by bacteria, and had limited impact on the fecal metabolome. However, fungal colonization promoted major shifts in bacterial microbiome ecology, and had an independent effect on the innate and adaptive immune development in young mice. Fungi further exacerbated some aspects of the inflammatory effects of the bacterial community during OVA-induced airway inflammation by promoting macrophage infiltration in the airway. Our results demonstrate a dominant ecological and physiological role of bacteria in gut microbiomes, but highlight fungi as an ecological factor shaping the assembly of the bacterial community and a direct capacity to impact immune system and modulate disease susceptibility. These findings demonstrate that studies focused on bacteria alone provide an incomplete portrayal on microbiome ecology and functionality, and prompt for the inclusion of fungi in human microbiome studies.

The gut microbiota and immune system maintain intestinal homeostasis and regulate gut physiology in concert with the enteric nervous system (ENS). However, the underlying mechanisms remain incompletely understood. Using wildtype and T-cell deficient germ-free mice colonized with segmented filamentous bacteria (SFB) or specific pathogen-free (SPF) microbiota, we studied immune regulation of the ENS and intestinal motility. Colonization markedly increased Th17 cells and Treg expressing RORγ+T cells in both the ileum and colon of wildtype mice. T cells were necessary for the normalization of intestinal motility after colonization by SPF microbiota, and for SFB to restore neuronal density in the ENS of the ileum of germ-free mice. T cells were also required for neurogenic responses in myenteric neurons of the ileum, but not the colon, and for regulating the levels of nestin expression. The cytokines IL-1β and IL-17A mediate the enteric neurogenic response to an SPF microbiota but were not involved in the regulation of intestinal motility. Together, our findings provide new insights into the microbiota-neuroimmune dialogue that regulates intestinal physiology.

Background. Early-life disruptions to the gut microbiome and stress-axis significantly influence the development of immune, neuroendocrine, and other physiological systems. However, the precise microbial species and pathways mediating these effects remain poorly characterized. Using a murine model, we investigated the individual and combined effects of early-life antibiotic exposure and chronic stress on gut microbiota composition, short-chain fatty acid (SCFA) production, hypothalamic-pituitary-adrenal (HPA) axis activity, and systemic, mucosal, and neuroimmune responses. Results. Broad-spectrum antibiotic treatments severely reduced microbial diversity and SCFA concentrations, with changes persisting into adulthood. Chronic early-life stress exerted more modest but notable effects, reducing key SCFA-producing taxa and impacting microbiome metabolic output. Combined disruptions led to altered microglial active phenotype and cytokine profiles, impaired immune cell populations, and suppressed HPA axis activity. Multi-omic correlational analyses revealed strong associations between SCFAs, specific gut microbes, and immune responses, implicating SCFAs as critical mediators of gut-brain communication. Notably, antibiotic exposure exacerbated susceptibility to allergic airway inflammation, highlighting the systemic consequences of early-life microbiome disturbances. Conclusions. These findings demonstrate that early microbial perturbations impair neuroimmune maturation, HPA axis regulation, and host resilience to inflammatory diseases. Our study underscores the importance of preserving the early-life microbiome to support long-term immune and neurodevelopmental health, offering insights into potential therapeutic interventions for mitigating the impact of early-life microbiota disruptions.

A carbon paste electrode (CPE) was modified with graphite oxide (GrO) and [beta]-cyclodextrin (CD) to obtain a sensor for simultaneous voltammetric determination of levodopa (LD), piroxicam (PRX), ofloxacin (OFX) and methocarbamol (MCB). The morphology, structure and electrochemical properties of the functionalized GrO were characterized by scanning electron microscopy, energy-dispersive X-ray spectroscopy, contact angle measurements and cyclic voltammetry. Under the optimal experimental conditions, the sensor is capable of detecting LD, PRX, OFX and MCB by square wave voltammetry (SWV) at working potentials of +0.40, +0.60, +1.03 and + 1.27 V (versus Ag/AgCl), respectively. Response is linear from 1.0 to 20 [mu]M for LD, from 1.0 to 15 [mu]M for PRX, from 1.0 to 20 [mu]M for OFX, and from 1.0 to 50 [mu]M for MCB. The respective limits of detection are 65, 105, 89 and 400 nM. The method was successfully applied to the simultaneous determination of LD, PRX, OFX and MCB in (spiked) real river water and synthetic urine samples, and the results were in agreement with those obtained using a spectrophotometric method, with recoveries close to 100%.

Body dissatisfaction (BD) is a conception constructed from influences since childhood, with the practice of exercise being an alternative to obtain the ideal body. Muscle dysmorphia (MD) is characterized as an exaggerated visualization of body imperfections and can lead to the search for substances such as anabolic steroids (AAS). Therefore, the aim of the present study was to compare body image (BI), MD and attitudes towards doping according to gender, educational level and age group of exercise practitioners at gyms. A total of 264 individuals (92 men and 172 women), with a mean age of 27.43 years (SD = 7.03), participated in the study. The instruments used were the Body Shape Questionnaire (BSQ), the Questionnaire of Attitudes towards Doping in Fitness (QAD-fit) and the Adonis Complex questionnaire (ACQ). Data analysis was conducted using the Kolmogorov-Smirnov, independent Student’s t-tests and MANOVA (p<0.05). The results showed a higher BD among women, and more behaviors towards doping in the males (p<0.05). A positive relationship was found between attitudes towards doping in individuals who had completed high school. Also, higher scores for attitudes and beliefs towards doping in the age group of 31-40 years was found. It is concluded that sociodemographic factors such as gender, age group and educational level maybe involved in BD, MD and in behaviors towards doping in people who practice exercise at gyms.

This study evaluated the influence of environmental temperature on thermoregulation, hormonal, and hematological characteristics in Caracu cattle. Blood samples, hair length, coat and muzzle colors, rectal (RT), and surface temperatures were collected from 48 males and 43 females before (morning) and after sun exposure for eight hours (afternoon). Infrared thermography (IRT) was used to identify superficial temperature that exhibits a high correlation with RT. Hematological parameters, hormone concentrations, RT, and the superficial temperature obtained by IRT that exhibited the highest correlation with RT were evaluated by variance analysis. Regarding IRT, the lower left side of the body (LS) showed the highest correlation with the RT. Interaction between period and sex was observed for LS, cortisol, and eosinophils. Cortisone, progesterone, and RT were influenced by period and sex. Neutrophils and segmented neutrophils were influenced by the period, which showed the highest concentrations after sun exposure. Platelets, leukocytes, lymphocytes, and monocytes were influenced by sex. Heat stress changes several physiological characteristics where males and females exhibited differences in their responses to heat stress. Furthermore, most characteristics evaluated remained within the regular values observed for taurine Creole breeds, showing that Caracu is adapted to tropical climates.