Magnetosonic waves, or equatorial noise, are whistler‐mode emissions distributed near the Earth's magnetic equator between proton cyclotron frequency and lower hybrid resonance frequency. Their ...origin and characteristics inside and outside the plasmasphere have been investigated due to their potential role in scattering energetic electrons and protons. However, their characteristics in plasmaspheric plumes remained undocumented. This study, for the first time, statistically investigated magnetosonic waves in the plasmaspheric plumes based on the entire mission period (2012–2019) of Van Allen Probes A and B. Results showed that the occurrence rate of magnetosonic waves in plumes was 25%, with an average amplitude and wave normal angles of 44 pT and 84°–88°, respectively. Increased geomagnetic activity enhanced its amplitude and ratio of plasma frequency to electron cyclotron frequency. Approximately 78% of selected magnetosonic wave events were simultaneously observed with plasmaspheric hiss that is most effective in scattering electrons in the plume.
Key Points
Magnetosonic waves were observed in the plasmaspheric plume with an average occurrence rate of ∼25%
Magnetosonic waves exhibited dependence on geomagnetic activity. High ratios of fpe/fce > 14 were typically observed in the plume
Approximately 78% of magnetosonic waves coexist with plasmaspheric hiss in the plume, and have two times higher amplitude, on average
Gut microbiota act beyond the gastrointestinal tract to regulate the physiology of the host. However, their contribution to the antioxidant capacity of the host remains largely understudied. In this ...study, we observe that gut bacteria increase the steady-state plasma levels of high-antioxidant molecules, reactive sulfur species (RSS), such as hydrogen sulfide and cysteine persulfide (CysSSH), in the host. Moreover, gut bacteria utilize cystine as a substrate to enzymatically produce CysSSH. Administration of cystine to mice increases their plasma levels of RSS and suppresses the concanavalin-A-induced oxidative stress and liver damage in a gut-microbiota-dependent manner. We find that gut bacteria belonging to the Lachnospiraceae and Ruminococcaceae families have a high capacity to produce RSS, requiring pyridoxal 5′-phosphate for their enzymatic reactions. Collectively, our data demonstrate that gut microbiota enhance the antioxidant capacity of the host through the generation of RSS.
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•Gut microbiota increase the levels of reactive sulfur species in the host•Gut bacteria utilize cystine as a substrate to produce cysteine persulfide•Reactive sulfur species levels are increased in mice given cystine via gut microbiota•Administration of cystine to mice suppresses concanavalin-A-induced oxidative stress
Host physiology is regulated by the gut microbiota. Uchiyama et al. demonstrate that gut bacteria increase an antioxidant reactive sulfur species in the host and they contribute to suppression of oxidative stress. Gut bacteria belonging to the Lachnospiraceae and Ruminococcaceae families have a high capacity to produce reactive sulfur species.
Methylmercury (MeHg), an environmental electrophile, binds covalently to the cysteine residues of proteins in organs, altering protein function and causing cytotoxicity. MeHg has also been shown to ...alter the composition of gut microbes. The gut microbiota is a complex community, the disturbance of which has been linked to the development of certain diseases. However, the relationship between MeHg and gut bacteria remains poorly understood. In this study, we showed that MeHg binds covalently to gut bacterial proteins via cysteine residues. We examined the effects of MeHg on the growth of selected Lactobacillus species, namely, L. reuteri, L. gasseri, L. casei, and L. acidophilus, that are frequently either positively or negatively correlated with human diseases. The results revealed that MeHg inhibits the growth of Lactobacillus to varying degrees depending on the species. Furthermore, the growth of L. reuteri, which was inhibited by MeHg exposure, was restored by Na2S2 treatment. By comparing mice with and without gut microbiota colonization, we found that gut bacteria contribute to the production of reactive sulfur species such as hydrogen sulfide and hydrogen persulfide in the gut. We also discovered that the removal of gut bacteria accelerated accumulation of mercury in the cerebellum, liver, and lungs of mice subsequent to MeHg exposure. These results accordingly indicate that MeHg is captured and inactivated by the hydrogen sulfide and hydrogen persulfide produced by intestinal microbes, thereby providing evidence for the role played by gut microbiota in reducing MeHg toxicity.
Abstract
Background
Non-alcoholic liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome, and it can progress to non-alcoholic steatohepatitis (NASH). Alterations in the gut ...microbiome have been implicated in the development of NAFLD/NASH, although the underlying mechanisms remain unclear.
Results
We found that the consumption of the prebiotic inulin markedly ameliorated the phenotype of NAFLD/NASH, including hepatic steatosis and fibrosis, in mice. Inulin consumption resulted in global changes in the gut microbiome, including concomitant enrichment of the genera
Bacteroides
and
Blautia
, and increased concentrations of short-chain fatty acids, particularly acetate, in the gut lumen and portal blood. The consumption of acetate-releasing resistant starch protected against NAFLD development. Colonisation by
Bacteroides acidifaciens
and
Blautia producta
in germ-free mice resulted in synergetic effects on acetate production from inulin. Furthermore, the absence of free fatty acid receptor 2 (FFAR2), an acetate receptor, abolished the protective effect of inulin, as indicated by the more severe liver hypertrophy, hypercholesterolaemia and inflammation. These effects can be attributed to an exacerbation of insulin resistance in the liver, but not in muscle or adipose tissue.
Conclusion
These findings demonstrated that the commensal microbiome–acetate–FFAR2 molecular circuit improves insulin sensitivity in the liver and prevents the development of NAFLD/NASH.
The NOD-like receptors (NLRs) are a specialized group of intracellular receptors that represent a key component of the host innate immune system. Since the discovery of the first NLR almost 10 years ...ago, the study of this special class of microbial sensors has burgeoned; consequently, a better understanding of the mechanism by which these receptors recognize microbes and other danger signals and of how they activate inflammatory signaling pathways has emerged. Moreover, in addition to their primary role in host defense against invading pathogens, their ability to regulate nuclear factor-kappa B (NF-kappaB) signaling, interleukin-1-beta (IL-1beta) production, and cell death indicates that they are crucial to the pathogenesis of a variety of inflammatory human diseases.
The virulence mechanisms that allow pathogens to colonize the intestine remain unclear. Here, we show that germ-free animals are unable to eradicate Citrobacter rodentium, a model for human ...infections with attaching and effacing bacteria. Early in infection, virulence genes were expressed and required for pathogen growth in conventionally raised mice but not germ-free mice. Virulence gene expression was down-regulated during the late phase of infection, which led to relocation of the pathogen to the intestinal lumen where it was outcompeted by commensals. The ability of commensals to outcompete C. rodentium was determined, at least in part, by the capacity of the pathogen and commensals to grow on structurally similar carbohydrates. Thus, pathogen colonization is controlled by bacterial virulence and through competition with metabolically related commensals.
Although imbalances in gut microbiota composition, or “dysbiosis,” are associated with many diseases, the effects of gut dysbiosis on host systemic physiology are less well characterized. We report ...that gut dysbiosis induced by antibiotic (Abx) treatment promotes allergic airway inflammation by shifting macrophage polarization in the lung toward the alternatively activated M2 phenotype. Adoptive transfer of alveolar macrophages derived from Abx-treated mice was sufficient to increase allergic airway inflammation. Abx treatment resulted in the overgrowth of a commensal fungal Candida species in the gut and increased plasma concentrations of prostaglandin E2 (PGE2), which induced M2 macrophage polarization in the lung. Suppression of PGE2 synthesis by the cyclooxygenase inhibitors aspirin and celecoxib suppressed M2 macrophage polarization and decreased allergic airway inflammatory cell infiltration in Abx-treated mice. Thus, Abx treatment can cause overgrowth of particular fungal species in the gut and promote M2 macrophage activation at distant sites to influence systemic responses including allergic inflammation.
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•Antibiotic treatment induced gut fungal overgrowth•Gut fungal overgrowth promoted allergic airway inflammation•Gut fungal overgrowth elevated plasma PGE2 that promoted M2 macrophage polarization•M2 macrophage was involved in allergic airway inflammation
Antibiotic treatment induces dysbiosis. The effects of dysbiosis on host physiology are just emerging. Kim et al. find that antibiotic treatment of mice facilitates overgrowth of a gut commensal Candida species, which increases plasma concentration of prostaglandin E2. Fungi-induced prostaglandin E2 in turn promotes M2 macrophage activation and thus exacerbates allergic airway inflammation.
The high susceptibility of neonates to infections has been assumed to be due to immaturity of the immune system, but the mechanism remains unclear. By colonizing adult germ-free mice with the cecal ...contents of neonatal and adult mice, we show that the neonatal microbiota is unable to prevent colonization by two bacterial pathogens that cause mortality in neonates. The lack of colonization resistance occurred when Clostridiales were absent in the neonatal microbiota. Administration of Clostridiales, but not Bacteroidales, protected neonatal mice from pathogen infection and abrogated intestinal pathology upon pathogen challenge. Depletion of Clostridiales also abolished colonization resistance in adult mice. The neonatal bacteria enhanced the ability of protective Clostridiales to colonize the gut.
Cholera toxin (CT) is a potent adjuvant for inducing mucosal immune responses. However, the mechanism by which CT induces adjuvant activity remains unclear. Here we show that the microbiota is ...critical for inducing antigen-specific IgG production after intranasal immunization. After mucosal vaccination with CT, both antibiotic-treated and germ-free (GF) mice had reduced amounts of antigen-specific IgG, smaller recall-stimulated cytokine responses, impaired follicular helper T (TFH) cell responses and reduced numbers of plasma cells. Recognition of symbiotic bacteria via the nucleotide-binding oligomerization domain containing 2 (Nod2) sensor in cells that express the integrin CD11c (encoded by Itgax) was required for the adjuvanticity of CT. Reconstitution of GF mice with a Nod2 agonist or monocolonization with Staphylococcus sciuri, which has high Nod2-stimulatory activity, was sufficient to promote robust CT adjuvant activity, whereas bacteria with low Nod2-stimulatory activity did not. Mechanistically, CT enhanced Nod2-mediated cytokine production in dendritic cells via intracellular cyclic AMP. These results show a role for the microbiota and the intracellular receptor Nod2 in promoting the mucosal adjuvant activity of CT.
A transmitter coil (TX-coil) as well as a receiver coil (RX-coil) has been designed at 6.78 MHz for magnetic resonant wireless power transfer systems not only to have high efficiency at medium ...distances, which is comparable to the coil dimensions, but also to provide stable efficiency over the position variation of the RX-coil. For mobile devices, the coils should be compact and have low profile and asymmetric, meaning that TX- and RX-coils have different dimensions. In this paper, TX-coil is designed by adding a small coil in series to achieve high quality factor (Q-factor) as well as relatively uniform magnetic field distribution. On the other hand, the scaling factor is introduced for wire width to design RX-coil with higher Q-factor. As a result, the proposed asymmetric coils reveal improved efficiency and degree of freedom in terms of position variation. This has been verified by measuring the system performance, including a power amplifier, full-wave rectifier, regulator, and load. The proposed TX-coil has size of <inline-formula> <tex-math notation="LaTeX">200 \times 200 \times 1 </tex-math></inline-formula> mm 3 , while the size of the RX-coil is <inline-formula> <tex-math notation="LaTeX">100\times 100\times0.4 </tex-math></inline-formula> mm 3 . The power transfer efficiency is 96% and 39% at the transmission distances of 50 and 300 mm, respectively.
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