Cytosolic alkalinization is a common and early messenger preceding the production of ROS and NO during stomatal closure by variable signals,including abscisic acid,methyl jasmonate and chitosan

Stomata are unique that they sense and respond to several internal and external stimuli, by modulating signaling components in guard cells. The levels of reactive oxygen species (ROS), nitric oxide (NO) and cytosolic calcium (Ca²⁺) increase significantly during stomatal closure by not only plant hormones [such as abscisic acid (ABA) or methyl jasmonate (MJ)] but also elicitors (such as chitosan). We observed that cytosolic alkalinization preceded the production of ROS as well as NO during ABA induced stomatal closure. We therefore propose that besides ROS and NO, the cytosolic pH is an important secondary messenger during stomatal closure by ABA or MJ. We also noticed that there is either a cross talk or feedback regulation by cytosolic Ca²⁺ and ROS (mostly H₂O₂). Further experiments on the interactions between cytosolic pH, ROS, NO and Ca²⁺ would yield interesting results.Key words: abscisic acid, methyl jasmonate, chitosan, cytosolic pH, reactive oxygen species, H₂O₂, nitric oxide, cytosolic calcium     

Complement driven innate immune response to malaria: fuelling severe malarial diseases

Severe malaria remains a major cause of global mortality. The innate immune response to infection is a key determinant of malaria severity and outcome. The complement system plays a key role in initiating and augmenting innate immune responses, including inflammation, endothelial activation, opsonization and coagulation, processes which have been implicated in malaria pathogenesis. In this review, we discuss the evidence supporting a role for excessive complement activation in the pathogenesis of severe malaria.     

Infection with the Lyme disease pathogen suppresses innate immunity in mice with diet‐induced obesity

Obesity is a major global public health concern. Immune responses implicated in obesity also control certain infections. We investigated the effects of high‐fat diet‐induced obesity (DIO) on infection with the Lyme disease bacterium Borrelia burgdorferi in mice. DIO was associated with systemic suppression of neutrophil‐ and macrophage‐based innate immune responses. These included bacterial uptake and cytokine production, and systemic, progressive impairment of bacterial clearance, and increased carditis severity. B. burgdorferi‐infected mice fed normal diet also gained weight at the same rate as uninfected mice fed high‐fat diet, toll‐like receptor 4 deficiency rescued bacterial clearance defects, which greater in female than male mice, and killing of an unrelated bacterium (Escherichia coli) by bone marrow‐derived macrophages from obese, B. burgdorferi‐infected mice was also affected. Importantly, innate immune suppression increased with infection duration and depended on cooperative and synergistic interactions between DIO and B. burgdorferi infection. Thus, obesity and B. burgdorferi infection cooperatively and progressively suppressed innate immunity in mice.     

Recent developments in amoebiasis:the Gal/GalNAc lectins of Entamoeba histolytica and Entamoeba dispar

Amoebiasis is responsible for 50000-100000 deaths annually. Invasive amoebic disease begins with the attachment of Entamoeba histolytica trophozoites to colonic mucin, a process mediated by the amoebic Gal/GalNAc lectin. The non-pathogenic counterpart, E. dispar, is morphologically identical but genetically distinct. Investigations comparing the Gal/GalNac lectin from these two organisms are under way.     

Ataxia telangiectasia mutated influences cytochrome c oxidase activity

Cells lacking ataxia telangiectasia mutated (ATM) have impaired mitochondrial function. Furthermore, mammalian cells lacking ATM have increased levels of reactive oxygen species (ROS) as well as mitochondrial DNA (mtDNA) deletions in the region encoding for cytochrome c oxidase (COX). We hypothesized that ATM specifically influences COX activity in skeletal muscle. COX activity was ∼40% lower in tibialis anterior from ATM-deficient mice than for wild-type mice (P < 0.01, n = 9/group). However, there were no ATM-related differences in activity of succinate dehydrogenase, isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, mitochondrial glycerol 3-phosphate dehydrogenase, or complex III. Incubation of wild-type extensor digitorum longus muscles for 1 h with the ATM inhibitor KU55933 caused a ∼50% reduction (P < 0.05, n = 5/group) in COX activity compared to muscles incubated with vehicle alone. Among the control muscles and muscles treated with the ATM inhibitor, COX activity was correlated (r = 0.61, P < 0.05) with activity of glucose 6-phosphate dehydrogenase, a key determinant of antioxidant defense through production of NADPH. Overall, the findings suggest that ATM has a protective role for COX activity.     

Functionally diverse rhizobacteria of Saccharum munja (a native wild grass) colonizing abandoned morrum mine in Aravalli hills (Delhi)

Characterization of the rhizobacteria of native grasses naturally colonizing abandoned mine sites may help in identification of microbial inoculants for ecological-restoration programmes. Eighty one strains of Saccharum munja rhizobacteria isolated from an abandoned mine located on Aravalli mountain and 50 from bulk-region were identified using 16S rRNA sequence analyses. Based on chemical- and biological-assays they were categorized into ecologically diverse functional groups (siderophore-, IAA-, ACC-deaminase-, HCN-, polyphosphate-producers; phosphate-solubilizer; antagonistic). Eight genera, 25 species from rhizosphere and 2 genera, 5 species from bulk-region were dominated by Bacillus spp. (B. barbaricus, B. cereus, B. firmus, B. flexus, B. foraminis, B. licheniformis, B. megaterium, B. pumilus, B. subtilis, B. thuringiensis) and Paenibacillus spp. (P. alvei, P. apiarius, P. lautus, P. lentimorbus, P. polymyxa, P. popillae). Siderophore-producers were common in rhizosphere and bulk soil, whereas IAA-producers, N₂-fixers and FePO₄-solubilizers dominated rhizosphere samples. During the reproductive phase (winter) of S. munja, siderophore-, ACC-deaminase- and polyP-producers were predominant; however dominance of HCN-producers in summer might be associated with termite-infestation. In vivo ability of selected rhizobacteria (B. megaterium BOSm201, B. subtilis BGSm253, B. pumilus BGSm157, P. alvei BGSm255, P. putida BOSm217, P. aeruginosa BGSm 306) to enhance seed-germination and seedling-growth of S. munja in mine-spoil suggest their significance in natural colonization and potential for ecological-restoration of Bhatti mine.     

PPARγ Agonists Improve Survival and Neurocognitive Outcomes in Experimental Cerebral Malaria and Induce Neuroprotective Pathways in Human Malaria

Cerebral malaria (CM) is associated with a high mortality rate, and long-term neurocognitive impairment in approximately one third of survivors. Adjunctive therapies that modify the pathophysiological processes involved in CM may improve outcome over anti-malarial therapy alone. PPARγ agonists have been reported to have immunomodulatory effects in a variety of disease models. Here we report that adjunctive therapy with PPARγ agonists improved survival and long-term neurocognitive outcomes in the Plasmodium berghei ANKA experimental model of CM. Compared to anti-malarial therapy alone, PPARγ adjunctive therapy administered to mice at the onset of CM signs, was associated with reduced endothelial activation, and enhanced expression of the anti-oxidant enzymes SOD-1 and catalase and the neurotrophic factors brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in the brains of infected mice. Two months following infection, mice that were treated with anti-malarials alone demonstrated cognitive dysfunction, while mice that received PPARγ adjunctive therapy were completely protected from neurocognitive impairment and from PbA-infection induced brain atrophy. In humans with P. falciparum malaria, PPARγ therapy was associated with reduced endothelial activation and with induction of neuroprotective pathways, such as BDNF. These findings provide insight into mechanisms conferring improved survival and preventing neurocognitive injury in CM, and support the evaluation of PPARγ agonists in human CM.     

Neurocognitive outcomes in Malawian children exposed to malaria during pregnancy: An observational birth cohort study

BackgroundAnnually 125 million pregnancies are at risk of malaria infection. However, the impact of exposure to malaria in pregnancy on neurodevelopment in children is not well understood. We hypothesized that malaria in pregnancy and associated maternal immune activation result in neurodevelopmental delay in exposed offspring.Methods and findingsBetween April 2014 and April 2015, we followed 421 Malawian mother–baby dyads (median [IQR] maternal age: 21 [19, 28] years) who were previously enrolled (median [IQR] gestational age at enrollment: 19.7 [17.9, 22.1] weeks) in a randomized controlled malaria prevention trial with 5 or 6 scheduled assessments of antenatal malaria infection by PCR. Children were evaluated at 12, 18, and/or 24 months of age with cognitive tests previously validated in Malawi: the Malawi Developmental Assessment Tool (MDAT) and the MacArthur–Bates Communicative Development Inventories (MCAB-CDI). We assessed the impact of antenatal malaria (n [%] positive: 240 [57.3]), placental malaria (n [%] positive: 112 [29.6]), and maternal immune activation on neurocognitive development in children. Linear mixed-effects analysis showed that children exposed to antenatal malaria between 33 and 37 weeks gestation had delayed language development across the 2-year follow-up, as measured by MCAB-CDI (adjusted beta estimate [95% CI], −7.53 [−13.04, −2.02], p = 0.008). Maternal immune activation, characterized by increased maternal sTNFRII concentration, between 33 and 37 weeks was associated with lower MCAB-CDI language score (adjusted beta estimate [95% CI], −8.57 [−13.09, −4.06], p < 0.001). Main limitations of this study include a relatively short length of follow-up and a potential for residual confounding that is characteristic of observational studies.ConclusionsThis mother–baby cohort presents evidence of a relationship between malaria in pregnancy and neurodevelopmental delay in offspring. Malaria in pregnancy may be a modifiable risk factor for neurodevelopmental injury independent of birth weight or prematurity. Successful interventions to prevent malaria during pregnancy may reduce the risk of neurocognitive delay in children.

Andrea Weckman and co-workers study associations between children’s neurodevelopmental outcomes and malaria in pregnancy.     

PATTERNS OF RELATIVE GROWTH IN NEREOCYSTIS LUETKEANA (PHAEOPHYTA)1

Plants of Nereocystis luetkeana (Mert.) Post. et Rupr. of different sizes were held on a raft at the surface of the sea off the Friday Harbor Laboratories, San Juan Island, Washington for 5 day periods for observation of detailed relative growth of different parts. Each stipe was marked at intervals with injected Indian ink and each blade was punched with a series of holes. Measurements of diameter, length, width and thickness were made before and after the 5 day periods. Blades showed a very similar pattern of relative growth rate (R) over an 18-fold range of sizes. The maximum local R in length was about 0.2 day⁻¹ and occurred at 6.5% of the distance from the bulb to the tip, declining to 0.01 at half way. Half the linear growth occurred in the proximal one tenth of the blade and 95% within the proximal half. The relative growth rate of the whole blade declined only slightly with increased size and lay between 0.0.3 and 0.06 day⁻¹ (approx. 3–6% day⁻¹). The linear growth rate therefore increased with blade size, the maximum observed being 14 cm day⁻¹. The maximum relative growth rate in blade width was slower, and sited more distally than that in length. Unless fertile tissue was involved all blade tissue, except that closely adjoining the bulb, became thinner during growth. R in volume reached 0.3 day⁻¹. Presumably because the plants were held near the sea surface stipes grew slowly, with a maximum linear rate of 9 mm day⁻¹. The maximum R in length decreased with stipe length. Bulb R in volume also decreased as size increased, from a maximum of 0.3 day⁻¹.     

Responses of crustose corallines to epiphyte and canopy cover

Although a dense cover of epiphytes is generally considered to be harmful for some coralline algae (Corallinaceae, Rhodophyta), crustose corallines in the littoral zone seem to be preserved from bleaching when covered by canopy plants and epiphytes during summer. This study aimed to test the responses of coralline crusts to epiphytes and canopy algae and their interaction with grazing limpets. Growth rates and color changes were followed in two crust species in areas with or without canopy algae in the Isle of Man, British Isles. Limpets were excluded, to allow epiphytes to grow upon crusts. Responses were measured both on pieces of crusts upon acrylic plates and on crusts growing naturally on the shore. Fucus canopy and epiphytic Enteromorpha significantly influenced the crusts' growth, depending on season. Epiphytes reduced the light levels beneath by up to 78%, more than the canopy algae (62%). Crusts exposed outside the canopy bleached in summer, but gradually restored their color once they were covered by epiphytes. The fast-growing Phymatolithon lenormandii (Aresch.) Adey recovered its coloration more quickly than the slow-growing P. purpureum (P. et H. Crouan) Woelkerling et Irvine. However, neither crust species could restore its color when epiphytes were reduced by grazing limpets, Patella vulgata L. Bleaching did not kill the crusts, but seemed to interfere with crusts' growth. Restoration of pigmentation was quantified for the first time on bleached coralline crusts. Epiphyte and canopy algae were experimentally shown to be beneficial, probably by providing shade and also protecting crusts from desiccation.