Influence of soil moisture level on metabolism of non-structural carbohydrates in Quercus robur leaves

The long-term increases in average temperature and intensification of droughts which characterise the current state of the Earth’s climate system have a negative impact on forest ecosystems and can lead to a decrease in their area and deterioration of the living conditions of their components. In the conditions of the Ukrainian Steppe an important environmental, antierosion, water-protective and soil-protective role belongs to the ravine forests. The most valuable component of the ravine forests is presented by natural populations of common oak (Quercus robur L.), which are able to tolerate the arid climate typical of the steppe region. But with global warming, the endurance of this species is changing. It is believed that a significant role in plant adaptation to drought and high temperatures may belong to non-structural carbohydrates. Therefore, it is important to study changes in the concentration of these substances in the leaves of this leading species under the action of adverse hydrothermal conditions. The article analyzes the content and dynamics of soluble sugars (glucose, fructose, sucrose) and starch in the leaves of Quercus robur L. under different forest growth conditions of the ravine forest (hygromesophilic (CL2–3), mesoxerophilic (CL1) and xerophilic (CL0)). The research was conducted in the forest in the Viyskove area (steppe zone of Ukraine) in the thalweg and at different levels of slope of southern exposure. Content of glucose, fructose, sugar and starch in Quercus robur leaves was determined. It was found that when exposed to high temperatures and increasing water stress during the vegetation period in xerophilic (CL0–1) and mesoxerophilic (CL1) forest growth conditions, the concentration of both glucose and sucrose in the leaves of Q. robur increases and it becomes much higher than in conditions of more optimal water supply. At the same time, the disaccharide content increases more significantly than that of monosaccharide. The greatest amount of these sugars is observed in the driest months (July, August), when conditions for providing plants with water are the most stressful. When water stress grows the increase in concentration of glucose and sucrose is correlated with reduction of starch content. It has been found that the concentration of fructose in Q. robur leaves in droughty conditions of growing was comparable to more favourable conditions of moisture. In September, there is a decline in the content of all forms of non-structural carbohydrates in the leaves of plants of all variants compared to the previous month, especially in conditions of adverse water supply. Therefore, forest growth conditions do not affect the nature of the dynamics of soluble sugars and starch in the leaves of Q. robur, although they change their quantitative indicators. Based on the protective function of sugars under the action of stressors on plants, we can assume that in conditions of significant lack of moisture in the soil their accumulation in the leaves in areas with mesoxerophilic and xerophilic hygrotopes plays an important role in increasing Q. robur drought resistance.

Cross-reactive memory T cells associate with protection against SARS-CoV-2 infection in COVID-19 contacts

Cross-reactive immune responses to SARS-CoV-2 have been observed in pre-pandemic cohorts and proposed to contribute to host protection. Here we assess 52 COVID-19 household contacts to capture immune responses at the earliest timepoints after SARS-CoV-2 exposure. Using a dual cytokine FLISpot assay on peripheral blood mononuclear cells, we enumerate the frequency of T cells specific for spike, nucleocapsid, membrane, envelope and ORF1 SARS-CoV-2 epitopes that cross-react with human endemic coronaviruses. We observe higher frequencies of cross-reactive (p = 0.0139), and nucleocapsid-specific (p = 0.0355) IL-2-secreting memory T cells in contacts who remained PCR-negative despite exposure (n = 26), when compared with those who convert to PCR-positive (n = 26); no significant difference in the frequency of responses to spike is observed, hinting at a limited protective function of spike-cross-reactive T cells. Our results are thus consistent with pre-existing non-spike cross-reactive memory T cells protecting SARS-CoV-2-naïve contacts from infection, thereby supporting the inclusion of non-spike antigens in second-generation vaccines.

The transcription factor ZIP-1 promotes resistance to intracellular infection in Caenorhabditis elegans

Defense against intracellular infection has been extensively studied in vertebrate hosts, but less is known about invertebrate hosts; specifically, the transcription factors that induce defense against intracellular intestinal infection in the model nematode Caenorhabditis elegans remain understudied. Two different types of intracellular pathogens that naturally infect the C. elegans intestine are the Orsay virus, which is an RNA virus, and microsporidia, which comprise a phylum of fungal pathogens. Despite their molecular differences, these pathogens induce a common host transcriptional response called the intracellular pathogen response (IPR). Here we show that zip-1 is an IPR regulator that functions downstream of all known IPR-activating and regulatory pathways. zip-1 encodes a putative bZIP transcription factor, and we show that zip-1 controls induction of a subset of genes upon IPR activation. ZIP-1 protein is expressed in the nuclei of intestinal cells, and is at least partially required in the intestine to upregulate IPR gene expression. Importantly, zip-1 promotes resistance to infection by the Orsay virus and by microsporidia in intestinal cells. Altogether, our results indicate that zip-1 represents a central hub for triggers of the IPR, and that this transcription factor has a protective function against intracellular pathogen infection in C. elegans.

Complement Inhibition Alleviates Cholestatic Liver Injury Through Mediating Macrophage Infiltration and Function in Mice

Background and AimsCholestatic liver injury (CLI), which is associated with inflammatory reactions and oxidative stress, is a serious risk factor for postoperative complications. Complement system is involved in a wide range of liver disorders, including cholestasis. The present study assessed the role of complement in CLI and the therapeutic effect of the site-targeted complement inhibitor CR2-Crry in CLI.MethodsWild-type and complement gene deficient mice underwent common bile duct ligation (BDL) to induce CLI or a sham operation, followed by treatment with CR2-Crry or GdCl3. The roles of complement in CLI and the potential therapeutic effects of CR2-Crry were investigated by biochemical analysis, flow cytometry, immunohistochemistry, ELISA, and quantitative RT-PCR.ResultsC3 deficiency and CR2-Crry significantly reduced liver injuries in mice with CLI, and also markedly decreasing the numbers of neutrophils and macrophages in the liver. C3 deficiency and CR2-Crry also significantly reduced neutrophil expression of Mac-1 and liver expression of VCAM-1. More importantly, C3 deficiency and CR2-Crry significantly inhibited M1 macrophage polarization in these mice. Intravenous injection of GdCl3 inhibited macrophage infiltration and activation in the liver. However, the liver injury increased significantly. BDL significantly increased the level of lipopolysaccharide (LPS) in portal blood, but not in peripheral blood. GdCl3 significantly increased LPS in peripheral blood, suggesting that macrophages clear portal blood LPS. Oral administration of ampicillin to in GdCl3 treated mice reduced LPS levels in portal blood and alleviated liver damage. In contrast, intraperitoneal injection LPS increased portal blood LPS and reversed the protective effect of ampicillin. Interestingly, C3 deficiency did not affect the clearance of LPS.ConclusionsComplement is involved in CLI, perhaps mediating the infiltration and activation of neutrophils and macrophage M1 polarization in the liver. C3 deficiency and CR2-Crry significantly alleviated CLI. Inhibition of complement could preserve the protective function of macrophages in clearing LPS, suggesting that complement inhibition could be useful in treating CLI.

Parameterization of Mangrove Root Structure of Rhizophora stylosa in Coastal Hydrodynamic Model

Mangroves are able to attenuate tsunamis, storm surges, and waves. Their protective function against wave disasters is gaining increasing attention as a typical example of the green infrastructure/Eco-DRR (Ecosystem-based Disaster Risk Reduction) in coastal regions. Hydrodynamic models commonly employed additional friction or a drag forcing term to represent mangrove-induced energy dissipation for simplicity. The well-known Morison-type formula (Morison et al. 1950) has been considered appropriate to model vegetation-induced resistance in which the information of the geometric properties of mangroves, including the root system, is needed. However, idealized vegetation configurations mainly were applied in the existing numerical models, and only a few field observations provided the empirical parameterization of the complex mangrove root structures. In this study, we conducted field surveys on the Iriomote Island of Okinawa, Japan, and Tarawa, Kiribati. We measured the representative parameters for the geometric properties of mangroves, Rhizophora stylosa, and their root system. By analyzing the data, significant correlations for hydrodynamic modeling were found among the key parameters such as the trunk diameter at breast height (DBH), the tree height H, the height of prop roots, and the projected areas of the root system. We also discussed the correlation of these representative factors with the tree age. These empirical relationships are summarized for numerical modeling at the end.

A Systematic Review and Meta-Analysis on Multiple Cytokine Gene Polymorphisms in the Pathogenesis of Periodontitis

AimPeriodontitis is an inflammatory disease that destroys both soft and hard periodontal tissues. However, a complex periodontal cytokine network remains unclear. This systematic review explored multiple cytokine gene polymorphisms in the pathogenesis of periodontitis.Material and MethodsA systematic search was performed using the databases from previous publications, which indicated the association between cytokine polymorphisms and periodontitis pathogenesis. Meta-analysis was conducted using fixed or randomized models to calculate the significance of multiple cytokine polymorphisms. A total of 147 articles were analyzed with polymorphisms in 12 interleukins [Th1 (IL-2, IFN-γ, and TNF-α), Th2 (IL-4 and IL-13), Th17 (IL-1α, IL-1β, IL-6, and IL-17), and Treg cytokines (IL-10 and TGF-β)]. Doi plot was used to probe the occurrence of publication bias.ResultsThe polymorphisms of IL-2 and TNF-α of Th1 cytokine family may be associated with the pathogenesis or the prevention of periodontitis risk, while the polymorphism of IFN-γ is not related to periodontitis risk. The polymorphisms for IL-4 and IL-13 of Th2 cytokine family are not found to be associated with the pathogenesis of periodontitis. For the polymorphisms of the members of Th17 cytokine family, different IL-1α polymorphisms may have inverse actions in the pathogenesis of periodontitis. IL-1β is a noteworthy cytokine biomarker in periodontitis development and progression. IL-6 may have a protective function in the inflammatory responses of periodontitis, and IL-17 has a weak relationship the inflammatory responses. The polymorphisms for the members of Treg cell cytokines may have a protective function against periodontitis risk. LFK indexes show the major asymmetry due to publication bias.ConclusionIL-1β is a notable cytokine biomarker in periodontitis risk. Treg cytokines favor an anti-inflammatory and protective environment. Further data are needed to confirm the present conclusion due to publication bias.

MEF2A Is the Trigger of Resveratrol Exerting Protection on Vascular Endothelial Cell

Both resveratrol and myocyte enhancer factor 2A (MEF2A) may protect vascular endothelial cell (VEC) through activating the expression of SIRT1. However, the relationship between resveratrol and MEF2A is unclear. We aimed to investigate the deeper mechanism of resveratrol in protecting vascular endothelial cells and whether MEF2A plays a key role in the protective function of resveratrol. Human umbilical vein endothelial cell (HUVEC) was used for in vitro study, and small interfere RNA was used for silencing MEF2A. Silencing MEF2A in the vascular endothelium (VE) of ApoE−/− mice was performed by tail injection with adeno associated virus expressing si-mef2a-shRNA. The results showed that treatment of HUVEC with resveratrol significantly up-regulated MEF2A, and prevented H2O2-induced but not siRNA-induced down-regulation of MEF2A. Under various experimental conditions, the expression of SIRT1 changed with the level of MEF2A. Resveratrol could rescue from cell apoptosis, reduction of cell proliferation and viability induced by H2O2, but could not prevent against that caused by silencing MEF2A with siRNA. Silencing MEF2A in VE of apoE−/− mice decreased the expression of SIRT1, increased the plasma LDL-c, and abrogated the function of resveratrol on reducing triglyceride. Impaired integrity of VE and aggravated atherosclerotic lesion were observed in MEF2A silenced mice through immunofluorescence and oil red O staining, respectively. In conclusion, resveratrol enhances MEF2A expression, and the upregulation of MEF2A is required for the endothelial protective benefits of resveratrol in vitro via activating SIRT1. Our work has also explored the in vivo relevance of this signaling pathway in experimental models of atherosclerosis and lipid dysregulation, setting the stage for more comprehensive phenotyping in vivo and further defining the molecular mechanisms.

Flavopiridol Protects Against Fungal Keratitis by Alleviating Inflammation Through the Promotion of Autophagy

Background: Fungal keratitis is a serious infectious keratopathy related to fungal virulence and excessive inflammatory responses. Autophagy exhibits a potent ability to resolve inflammation during fungal infection. This study aimed to investigate the protective function of flavopiridol in fungal keratitis and explore its effects on autophagy.Methods: A mouse model of fungal keratitis was established and then treated with 5 μM flavopiridol. RAW 264.7 cells were treated with 200 nM flavopiridol before fungal stimulation. The severity of corneal diseases was evaluated by slit-lamp microscopy. The expression levels of cytokines were detected by RT-PCR and ELISA. The protein levels of LC3, Beclin-1 and Atg7 were determined by western blot and immunofluorescence. A Cell Counting Kit-8 assay was used to test cell viability. Autolysosomes were detected by transmission electron microscopy (TEM). An inhibitor of autophagy, 3-methyladenine (3-MA), was used to pretreat RAW 264.7 cells. Phagocytosis of RAW 264.7 cells was evaluated by counting colony forming units. A. fumigatus was incubated with flavopiridol, and the hyphae were stained with calcofluor white. Absorbance assay, crystal violet staining and adherence assay were used to detect the antifungal activity of flavopiridol.Results: Flavopiridol treatment notably reduced corneal opacity and the clinical scores of infected corneas. Compared with DMSO treatment, flavopiridol treatment greatly downregulated IL-1β, IL-6 and TNF-a expression in infected corneas. In RAW 264.7 cells, flavopiridol treatment inhibited IL-1β, IL-6 and TNF-a expression but promoted IL-10 expression. TEM images showed that more autolysosomes were presented in infected corneas and RAW 264.7 cells after flavopiridol treatment than after DMSO treatment. Flavopiridol treatment notably upregulated the protein expression of LC3, Beclin-1 and Atg7 in infected corneas as well as in RAW 264.7 cells. 3-MA pretreatment counteracted the cytokine regulation induced by flavopiridol. Moreover, flavopiridol promoted the phagocytosis of RAW 264.7 cells. Flavopiridol also exhibited antifungal activity by restricting fungal growth and limiting fungal biofilm formation and conidial adhesion. Conclusions: Flavopiridol significantly alleviated the inflammation of fungal keratitis by activating autophagy. In addition, flavopiridol promoted the phagocytosis of RAW 264.7 cells and exhibited antifungal function, indicating the potential therapeutic role of flavopiridol in fungal keratitis.