A microbiological survey of Montserrat Island hydrothermal biotopes

In March 1996, a survey of hydrothermal sites on the island of Montserrat was carried out. Six sites (Galway's Soufrière, Gages Upper and Lower Soufrières, Hot Water Pond, Hot River, and Tar River Soufrière) were mapped and sampled for chemical, ATP, and microbial analyses. The hydrothermal Soufrière sites on the slopes of the active Chances Peak volcano exhibited temperatures up to almost 100°C and were generally either mildly acidic at pH 5–7 or strongly acidic at pH 1.5–3, but with some hot streams and pools of low redox potential at pH 7–8. Hot Water Pond sites, comprising a series of heated pools near the western shoreline of the island, were neutral and saline, consistent with subsurface heating of entrained seawater. Biological activity shown by ATP analyses was greatest in near-neutral pH samples and generally decreased as acidity increased. A variety of heterotrophic and chemolithotrophic thermophilic organisms were isolated or observed in enrichment cultures. Most of the bacteria that were obtained in pure culture were familiar acidophiles and neutrophiles, but novel, iron-oxidizing species of Sulfobacillus were revealed. These species included the first mesophilic iron-oxidizing Sulfobacillus strains to be isolated and a strain with a higher maximum growth temperature (65°C) than the previously described moderately thermophilic Sulfobacillus species. Received: March 19, 2000 / Accepted: August 2, 2000     

Retinoic acid reduces p11 protein levels in bronchial epithelial cells by a posttranslational mechanism

p11 is a member of the S100 family of proteins, is the cellular ligand of annexin II, and interacts with the carboxyl region of 85-kDa cytosolic phospholipase A(2) (cPLA(2)), inhibiting cPLA(2) activity and arachidonic acid (AA) release. We studied the effect of retinoic acid (RA) on PLA(2) activity in human bronchial epithelial cells and whether p11 contributes to these effects. The addition of 10(-6) M RA resulted in reduced p11 protein levels at 4 days, with the greatest effect observed on days 6 and 7. This effect was dose related (10(-6) to 10(-9) M). RA treatment (10(-6) M) had no effect on cPLA(2) protein levels. p11 mRNA levels were unchanged at 6 and 8 days of treatment (correlating with maximum p11 protein reduction). Treatment with RA reduced p11 levels in control cells and in cells transfected with a p11 expression vector, suggesting a posttranslational mechanism. Lactacystin (10(-6) M), an inhibitor of the human 26S proteasome, blocked the decrease in p11 observed with RA treatment. Compared with control cells (n = 3), RA-treated cells (n = 3) had significantly increased AA release after treatment with the calcium ionophore A-23187 (P = 0.006). Therefore, RA reduces p11 protein expression and increases PLA(2) activity and AA release.     

Polyamine-mediated reduction in human airway epithelial migration in response to wounding is PGE2 dependent through decreases in COX-2 and cPLA2 protein levels.

Both ornithine decarboxylase inhibition to deplete polyamines and cyclooxygenase inhibition diminish the migration response to injury of human airway epithelial cells in tissue culture monolayers by approximately 75%. Restoration of normal migration responses is achieved in the polyamine depleted system either by exogenous reconstitution of polyamines or the addition of prostaglandin E(2) (PGE(2)). However, only PGE(2) was able to restore migration in the cyclooxygenase-inhibited systems. Western blot for cyclooxygenase-2 and cytosolic phospholipase A(2) protein levels and ELISAs for PGE(2) secretion demonstrate dramatic increases over 24-48 h after monolayer wounding. These increases are completely abolished by polyamine depletion or cyclooxygenase inhibition. We conclude that polyamine inhibition decreases cellular migration in response to injury in airway epithelial cells at least in part through inhibiting normal PGE(2) production in response to injury. This may be brought about by decreases in cytosolic phospholipase A(2) and cyclooxygenase-2 protein levels.     

FPLD2 LMNA mutation R482W dysregulates iPSC-derived adipocyte function and lipid metabolism

Lipodystrophies are disorders that directly affect lipid metabolism and storage. Familial partial lipodystrophy type 2 (FPLD2) is caused by an autosomal dominant mutation in the LMNA gene. FPLD2 is characterized by abnormal adipose tissue distribution. This leads to metabolic deficiencies, such as insulin-resistant diabetes mellitus and hypertriglyceridemia. Here we have derived iPSC lines from two individuals diagnosed with FPLD2, and differentiated these cells into adipocytes. Adipogenesis and certain adipocyte functions are impaired in FPLD2-adipocytes. Consistent with the lipodystrophic phenotype, FPLD2-adipocytes appear to accumulate markers of autophagy and catabolize triglycerides at higher levels than control adipocytes. These data are suggestive of a mechanism causing the lack of adipose tissue in FPLD2 patients.     

Temporal shifts of fungal communities in the rhizosphere and on tubers in potato fields

Soil fungal communities perform important ecological roles determining, at least in part, agricultural productivity. This study aimed at examining the fungal community dynamics in the potato rhizosphere across different development stages in two consecutive growing seasons (winter and summer). Microbial fingerprinting of rhizosphere soil samples collected at pre-planting, tuber initiation, flowering and at senescence was performed using ARISA in conjunction with Next Generation Sequencing (Illumina MiSeq). The epiphytic fungal communities on tubers at harvest were also investigated. Alpha-diversity was stable over time within and across the two seasons. In contrast, rhizospheric fungal community structure and composition were different between the two seasons and in the different plant growth stages within a given season, indicating the significance of the rhizosphere in shaping microbial communities. The phylum Ascomycota was dominant in the potato fungal rhizosphere, with Operational Taxonomic Units (OTUs) belonging to the genus Peyronellaea being the most abundant in all samples. Important fungal pathogens of potato, together with potential biological control agents and saprophytic species, were identified as indicator OTUs at different plant growth stages. These findings indicate that potato rhizosphere fungal communities are functionally diverse, which may contribute to soil health.     

Gutsy Moves: The Amygdala as a Critical Node in Microbiota to Brain Signaling

The amygdala is a key brain area regulating responses to stress and emotional stimuli, so improving our understanding of how it is regulated could offer novel strategies for treating disturbances in emotion regulation. As we review here, a growing body of evidence indicates that the gut microbiota may contribute to a range of amygdala‐dependent brain functions from pain sensitivity to social behavior, emotion regulation, and therefore, psychiatric health. In addition, it appears that the microbiota is necessary for normal development of the amygdala at both the structural and functional levels. While further investigations are needed to elucidate the exact mechanisms of microbiota‐to‐amygdala communication, ultimately, this work raises the intriguing possibility that the gut microbiota may become a viable treatment target in disorders associated with amygdala dysregulation, including visceral pain, post‐traumatic stress disorder, and beyond. Also see the video abstract here: https://youtu.be/O5gvxVJjX18     

The CD39-adenosinergic axis in the pathogenesis of renal ischemia–reperfusion injury

Hypoxic injury occurs when the blood supply to an organ is interrupted; subsequent reperfusion halts ongoing ischemic damage but paradoxically leads to further inflammation. Together this is termed ischemia–reperfusion injury (IRI). IRI is inherent to organ transplantation and impacts both the short- and long-term outcomes of the transplanted organ. Activation of the purinergic signalling pathway is intrinsic to the pathogenesis of, and endogenous response to IRI. Therapies targeting the purinergic pathway in IRI are an attractive avenue for the improvement of transplant outcomes and the basis of ongoing research. This review aims to examine the role of adenosine receptor signalling and the ecto-nucleotidases, CD39 and CD73, in IRI, with a particular focus on renal IRI.