Estudios locales sobre sustentabilidad del cultivo de vid en la provincia de San Juan, Argentina, han demostrado que el manejo tradicional del cultivo presenta un alto grado de insustentabilidad. ...Esto se debe a un inadecuado manejo de suelo, pérdida de biodiversidad y una dependencia del 100 % de insumos externos. Bajo este escenario, el objetivo del presente trabajo fue evaluar el manejo tradicional de suelo que realizan los productores locales, en comparación con manejos agroecológicos y su impacto sobre la composición química de suelo, rendimiento y calidad de la cv Malbec
Vitis vinífera L.
Los tratamientos fueron,
Control: manejo tradicional
(fertilizante sintético N 46, 100 kg ha
-1
),
Compost
(subproductos agroindustriales, CE 8980, pH 7.1, N 1.61, P 1.08, K 0.34, MO 27.8, 32000 kg ha
-1
),
Guano de gallina
(CE 9080, pH 7.3, N 2.00, P 1.5, K 0.29, MO 30.5, 32000 kg ha
-1
). Los tratamientos se llevaron a cabo durante tres temporadas 2019, 2020 y 2021. En el control se eliminaron las malezas con glifosato 36 %, (eliminación del 100% de la vegetación), mientras que en los tratamientos compost y guano, se mantuvo la vegetación espontánea con desbrozadora cada 20 días. Todos los tratamientos tuvieron efecto sobre la composición química del suelo, siendo el compost quien obtuvo los mayores valores, logrando incrementos del 40% N, 50% P, 19% K y 14% MO comparados con el control. Adicionalmente, el compost mantuvo el rendimiento y calidad de racimos. Sumado a los beneficios mencionados, el tratamiento a base de compost permite disminuir el uso de agroquímicos, la contaminación y la degradación del suelo e incrementar la biodiversidad mediante el mantenimiento de la vegetación espontánea.
Local studies on the sustainability of grapevine cultivation in the province of San Juan, Argentina, have shown that the traditional management of the crop is highly unsustainable. This is due to inadequate soil management, biodiversity loss and a 100% dependence on external inputs. Under this scenario, the objective of this study was to evaluate the traditional soil management carried out by local producers, in comparison with agroecological management and its impact on the chemical composition of the soil, yield and quality of the cv Malbec
Vitis vinifera
L. The treatments were, Control: traditional management (synthetic fertilizer N 46, 100 kg ha
-1
), Compost (agroindustrial byproducts, CE 8980, pH 7.1, N 1.61, P1.08, K 0.34, MO 27.8, 32000 kg ha
-1
), chicken manure (CE 9080, pH 7.3, N 2.00, P 1.5, K 0.29, MO 30.5, 32000 kg ha
-1
). The treatments were carried out during three seasons 2019, 2020 and 2021. Weed control was carried out with 36% glyphosate, (elimination of 100% of the vegetation) in the control, while in the compost and chicken manure treatments, spontaneous vegetation was maintained with a brush cutter every 20 days. All treatments had an effect on the chemical composition of the soil, with compost obtaining the highest values, achieving increases of 40% N, 50% P, 19% K and 14% MO compared to the control. Furthermore, the compost maintained the yield and bunches quality. In addition to the aforementioned benefits, the compost-based treatment makes it possible to reduce the use of agrochemicals, contamination and soil degradation, and increase biodiversity by maintaining spontaneous vegetation.
En orden a abordar los nuevos desafíos de la viticultura de precisión el uso de tecnologías digitales en sensado remoto resultan ser herramientas adecuadas para analizar y evaluar la variabilidad ...espacial dentro de un viñedo. En este trabajo se presenta el uso de imágenes multiespectrales y termográficas de alta resolución adquiridas con camaras especiales ubicadas en un vehículo aéreo no-tripulado (UAV) y el cálculo de diferentes índices del cultivo (derivado de las imagenes) para analizar y evaluar la variabilidad espacial dentro de un viñedo (Vitis vinifera L.). El viñedo de estudio se compone de tres sectores con diferentes sistemas de conducción (cordón libre, poda mínima y box pruning). Se adqurieron imágenes multiespectrales y termográficas de alta resolución en un día de verano y se calcularon diferentes índices espectrales de la vegetación (como NDVI y NDRE) y el índice de estrés hídrico (CWSI). Se estudió la distributión espacial de cada uno de los índices y la correlatión con mediciones de conductividad estomática (medida in-situ en plantas testigos) dentro de cada sistema de conducción para lo cual se observaron correlaciones de 53% con CWSI, 60% con NDRE y 44% con el NDVI; , además de realizo el análisis de correlación del peso de poda y los rendimientos productivos para lo cual se registraron bajos porcentajes de correlación con los índices calculados. En los mapas de índices se identifican diferencias entre los tres sistemas de conducción. Los resultados demostraron la utilidad de las imágenes de alta resolución adquiridas para conocer el estado del viñedo a nivel de plantas, permitiendo al productor realizar el manejo específico de cada sistema de conducción.
Innate lymphoid cells (ILCs) are tissue resident cells with organ-specific properties. Here, we show that the central nervous system (CNS) encompasses ILCs. In particular, CD3
NK1.1
cells present in ...the murine CNS comprise natural killer (NK) cells, ILC1s, intermediate ILC1s (intILC1s) and ex-ILC3s. We investigated the properties of CNS-ILC1s in comparison with CNS-NK cells during steady state and experimental autoimmune encephalomyelitis (EAE). ILC1s characteristically express CXCR3, CXCR6, DNAM-1, TRAIL, and CD200R and display heightened TNF-α production upon stimulation. In addition, ILC1s express perforin and are able to degranulate, although in a lesser extent than NK cells. Within the CNS compartments, ILC1s are enriched in the choroid plexus where very few NK cells are present, and also reside in the brain parenchyma and meninges. During EAE, ILC1s maintain stable IFN-γ and TNF-α levels while in NK cells the production of these cytokines increases as EAE progresses. Moreover, the amount of ILC1s and intILC1s increase in the parenchyma during EAE, but in contrast to NK cells, they show no signs of local proliferation. The upregulation in the inflamed brain of chemokines involved in ILC1 migration, such as CXCL9, CXCL10, and CXCL16 may lead to a recruitment of ILC1s from meninges or choroid plexus into the brain parenchyma. In sum, CNS-ILC1 phenotype, distribution and moderate inflammatory response during EAE suggest that they may act as gatekeepers involved in the control of neuroinflammation.
In demyelinating diseases including multiple sclerosis (MS), neural stem cells (NSCs) can replace damaged oligodendrocytes if the local microenvironment supports the required differentiation process. ...Although chitinase-like proteins (CLPs) form part of this microenvironment, their function in this differentiation process is unknown. Here, we demonstrate that murine Chitinase 3-like-3 (Chi3l3/Ym1), human Chi3L1 and Chit1 induce oligodendrogenesis. In mice, Chi3l3 is highly expressed in the subventricular zone, a stem cell niche of the adult brain, and in inflammatory brain lesions during experimental autoimmune encephalomyelitis (EAE). We find that silencing Chi3l3 increases severity of EAE. We present evidence that in NSCs Chi3l3 activates the epidermal growth factor receptor (EGFR), thereby inducing Pyk2-and Erk1/2- dependent expression of a pro-oligodendrogenic transcription factor signature. Our results implicate CLP-EGFR-Pyk2-MEK-ERK as a key intrinsic pathway controlling oligodendrogenesis.
Abstract
Background
In neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), neutrophils are found in CNS lesions. We previously ...demonstrated that NMOSD neutrophils show functional deficiencies. Thus, we hypothesized that neutrophil accumulation in the CNS may be facilitated by impairments affecting mechanisms of neutrophil death.
Objective
To evaluate cell death in blood neutrophils from aquaporin-4 (AQP4)-IgG-seropositive NMOSD and MOGAD patients as well as matched healthy controls (HC) using in vitro assays.
Methods
Twenty-eight AQP4 + NMOSD and 19 MOGAD patients in stable disease phase as well as 45 age- and sex-matched HC were prospectively recruited. To induce cell death, isolated neutrophils were cultured with/without phorbol 12-myristate 13-acetate (PMA). Spontaneous and PMA-induced NETosis and apoptosis were analyzed using 7-AAD and annexin-V by flow cytometry. Caspase-3 was assessed by western blot. Myeloperoxidase-DNA complexes (MPO-DNA), MPO and elastase were evaluated by ELISA, and cell-free DNA (cfDNA) by a fluorescence-based assay. Reactive oxygen species (ROS) were evaluated by a dihydrorhodamine 123-based cytometric assay. Serum GM-CSF, IL-6, IL-8, IL-15, TNF-ɑ and IL-10 were evaluated by multiplex assays, and neurofilament light chain (NfL) by single-molecule array assay.
Results
In response to PMA, neutrophils from AQP4 + NMOSD but not from MOGAD patients showed an increased survival, and subsequent reduced cell death (29.6% annexin V
+
7-AAD
+
) when compared to HC (44.7%,
p
= 0.0006). However, AQP4 + NMOSD also showed a mild increase in annexin V
+
7-AAD
−
early apoptotic neutrophils (24.5%) compared to HC (20.8%,
p
= 0.048). PMA-induced reduction of caspase-3 activation was more pronounced in HC (
p
= 0.020) than in AQP4 + NMOSD neutrophils (
p
= 0.052). No differences were observed in neutrophil-derived MPO-DNA or serum levels of MPO, elastase, IL-6, IL-8 and TNF-ɑ. IL-15 levels were increased in both groups of patients. In AQP4 + NMOSD, an increase in cfDNA, GM-CSF and IL-10 was found in serum. A positive correlation among cfDNA and NfL was found in AQP4 + NMOSD.
Conclusions
AQP4 + NMOSD neutrophils showed an increased survival capacity in response to PMA when compared to matched HC neutrophils. Although the data indicate that the apoptotic but not the NETotic response is altered in these neutrophils, additional evaluations are required to validate this observation.
Fractalkine receptor (CX3CR1)‐deficient mice develop very severe experimental autoimmune encephalomyelitis (EAE), associated with impaired NK cell recruitment into the CNS. Yet, the precise ...implications of NK cells in autoimmune neuroinflammation remain elusive. Here, we investigated the pattern of NK cell mobilization and the contribution of CX3CR1 to NK cell dynamics in the EAE. We show that in both wild‐type and CX3CR1‐deficient EAE mice, NK cells are mobilized from the periphery and accumulate in the inflamed CNS. However, in CX3CR1‐deficient mice, the infiltrated NK cells displayed an immature phenotype contrasting with the mature infiltrates in WT mice. This shift in the immature/mature CNS ratio contributes to EAE exacerbation in CX3CR1‐deficient mice, since transfer of mature WT NK cells prior to immunization exerted a protective effect and normalized the CNS NK cell ratio. Moreover, mature CD11b+ NK cells show higher degranulation in the presence of autoreactive 2D2 transgenic CD4+ T cells and kill these autoreactive cells more efficiently than the immature CD11b− fraction. Together, these data suggest a protective role of mature NK cells in EAE, possibly through direct modulation of T cells inside the CNS, and demonstrate that mature and immature NK cells are recruited into the CNS by distinct chemotactic signals.
Fractalkine receptor‐mediated recruitment of mature CD11b+ NK cells into the CNS contributes to control neuroinflammation in the EAE. Modulation of autoreactive CD4+ T‐cell response by mature NK cells inside the CNS may represent a mechanism of EAE regulation.
Background:
In contrast to multiple sclerosis (MS), lesions in neuromyelitis optica (NMO) frequently contain neutrophils. However, the phenotypic profile of neutrophils in these two distinct ...pathologies remains unknown.
Objective:
Our aim is to better understand the potential contribution of neutrophils to NMO and MS pathology.
Methods:
We performed the first functional analysis of blood neutrophils in NMO and MS, including evaluation of neutrophil immune response (fMLP receptor, TLR2), chemotaxis and migration (CXCR1, CD62L, CD43), regulation of complement (CD46, CD55, CD59), respiratory burst, phagocytosis and degranulation.
Results:
Compared with healthy controls (HC), neutrophils in NMO and MS show an activated phenotype characterized by an increased surface expression of TLR2 and fMLP receptor. However, contrary to MS neutrophils, NMO neutrophils show reduced adhesion and migratory capacity as well as decreased reduced production of reactive oxygen species (respiratory burst) and degranulation.
Conclusion:
Although NMO and MS neutrophils display an activated phenotype in comparison with HC, NMO neutrophils show a compromised functionality when compared with MS patients. These results suggest a distinct functional profile of neutrophils in MS and NMO.
Cerebral infections are restrained by a complex interplay of tissue-resident and recruited peripheral immune cells. Whether innate lymphoid cells (ILCs) are involved in the orchestration of the ...neuroinflammatory dynamics is not fully understood. Here, we demonstrate that ILCs accumulate in the cerebral parenchyma, the choroid plexus, and the meninges in the onset of cerebral Toxoplasma gondii infection. Antibody-mediated depletion of conventional natural killer (cNK) cells and ILC1s in the early stage of infection results in diminished cytokine and chemokine expression and increased cerebral parasite burden. Using cNK- and ILC1-deficient murine models, we demonstrate that exclusively the lack of ILC1s affects cerebral immune responses. In summary, our results provide evidence that ILC1s are an early source of IFN-γ and TNF in response to cerebral T. gondii infection, thereby inducing host defense factors and initiating the development of a neuroinflammatory response.
Display omitted
•ILCs are present in distinct CNS compartments•cNK cells and ILC1s accumulate during the onset of cerebral toxoplasmosis•ILC1 loss results in reduced IFN-γ levels and increased parasite burden in the brain
Steffen et al. report that ILC1s are an early source of IFN-γ in the CNS during the onset of cerebral T. gondii infection. Loss of ILC1s delays the production of IFN-γ-associated host defense factors and subsequent pathogen control.
We previously demonstrated that epigallocatechin-3-gallate (EGCG) synergizes with the immunomodulatory agent glatiramer acetate (GA) in eliciting anti-inflammatory and neuroprotective effects in the ...relapsing-remitting EAE model. Thus, we hypothesized that mice with chronic EAE may also benefit from this combination therapy. We first assessed how a treatment with a single dose of GA together with daily application of EGCG may modulate EAE. Although single therapies with a suboptimal dose of GA or EGCG led to disease amelioration and reduced CNS inflammation, the combination therapy had no effects. While EGCG appeared to preserve axons and myelin, the single GA dose did not improve axonal damage or demyelination. Interestingly, the neuroprotective effect of EGCG was abolished when GA was applied in combination. To elucidate how a single dose of GA may interfere with EGCG, we focused on the anti-inflammatory, iron chelating and anti-oxidant properties of EGCG. Surprisingly, we observed that while EGCG induced a downregulation of the gene expression of heme oxygenase-1 (HO-1) in affected CNS areas, the combined therapy of GA+EGCG seems to promote an increased HO-1 expression. These data suggest that upregulation of HO-1 may contribute to diminish the neuroprotective benefits of EGCG alone in this EAE model. Altogether, our data indicate that neuroprotection by EGCG in chronic EAE may involve regulation of oxidative processes, including downmodulation of HO-1. Further investigation of the re-dox balance in chronic neuroinflammation and in particular functional studies on HO-1 are warranted to understand its role in disease progression.
Arachidonic acid 5-lipoxygenase (ALOX5) is the key enzyme in the biosynthesis of pro-inflammatory leukotrienes. We recently created knock-in mice (Alox5-KI) which express an arachidonic acid ...15-lipoxygenating Alox5 mutant instead of the 5-lipoxygenating wildtype enzyme. These mice were leukotriene deficient but exhibited an elevated linoleic acid oxygenase activity. Here we characterized the polyenoic fatty acid metabolism of these mice in more detail and tested the animals in three different experimental inflammation models. In experimental autoimmune encephalomyelitis (EAE), Alox5-KI mice displayed an earlier disease onset and a significantly higher cumulative incidence rate than wildtype controls but the clinical score kinetics were not significantly different. In dextran sodium sulfate-induced colitis (DSS) and in the chronic constriction nerve injury model (CCI), Alox5-KI mice performed like wildtype controls with similar genetic background. These results were somewhat surprising since in previous loss-of-function studies targeting leukotriene biosynthesis (Alox5−/− mice, inhibitor studies), more severe inflammatory symptoms were observed in the EAE model but the degree of inflammation in DSS colitis was attenuated. Taken together, our data indicate that these mutant Alox5-KI mice respond differently in two models of experimental inflammation than Alox5−/− animals tested previously in similar experimental setups.
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