Prior exposure to stress allows the maintenance of an ecosystem cycle following severe acidification

Ecosystem processes vary temporally due to environmental fluctuations, such as when variation in solar energy causes diurnal cycles in primary production. This normal variation in ecosystem functioning may be disrupted and even lost if taxa contributing to functioning go extinct due to environmental stress. However, when communities are exposed to the stress at sub-lethal levels over several generations, they may be able to develop community-level stress tolerance via ecological (e.g. species sorting) or evolutionary (e.g. selection for tolerant genotypes) mechanisms and thus avoid the loss of stability, as defined by the resistance of a process. Community tolerance to a novel stressor is expected to increase the resistance of key processes in stressed ecosystems. In freshwater communities we tested whether prolonged prior exposure to an environmental stressor, i.e. acidification, could increase ecosystem stability when the communities were exposed to a subsequent press perturbation of more severe acidification. As a measure of ecosystem stability, we quantified the diurnal variation in dissolved oxygen (DO), and the resistance of the DO cycle and phytoplankton biomass. High-frequency data from oxygen loggers deployed in 12 mesocosms showed that severe acidification with sulfuric acid to pH 3 could cause a temporary (i.e. two-week long) loss of diurnal variation in dissolved oxygen concentration. The loss of diurnal variation was accompanied by a strong reduction in phytoplankton biomass. However, the pre-exposure to acidification for several weeks resulted in the maintenance of the diurnal cycle and higher levels of phytoplankton biomass, though they did not return to as rapidly to pre-exposure functioning as non-exposed mesocosms. These results suggest that ecosystem stability is intrinsically linked to community-wide stress tolerance, and that a history of exposure to the stressor may increase resistance to it, though at the cost of some resilience

Prior selection prevents the loss of an ecosystem cycle during acidification

Ecosystem processes vary temporally due to variation in environmental variables, such as when diurnal variation in sunlight causes diurnal cycles in net primary production. This variability can be characterized by its frequency and amplitude, used to define “normal” functioning of an ecosystem. Relatively little research has addressed how normal modes of variability, such as diurnal cycles, are lost or recovered, following anthropogenic stress. We conducted an aquatic mesocosm experiment to test whether prior application of environmental stress, in the form of moderate acidification, affected the diurnal cycle of dissolved oxygen when exposed to severe acidification. High-frequency data from sensor loggers deployed in 12 mesocosms showed that severe acidification caused a temporary loss of diurnal variation in dissolved oxygen concentration. However, pre-exposure to an acidic environment resulted in the persistence of the diurnal cycle. We hypothesize that pre-exposure shifted the community to acid tolerant genotypes and/or species of algae and other photosynthetic organisms. Our findings suggest that the stability of ecosystem cycles is intrinsically liked to the stress tolerance of the species assemblage

Functional diversity can facilitate the collapse of an undesirable ecosystem state

Biodiversity may increase ecosystem resilience. However, we have limited understanding if this holds true for ecosystems that respond to gradual environmental change with abrupt shifts to an alternative state. We used a mathematical model of anoxic–oxic regime shifts and explored how trait diversity in three groups of bacteria influences resilience. We found that trait diversity did not always increase resilience: greater diversity in two of the groups increased but in one group decreased resilience of their preferred ecosystem state. We also found that simultaneous trait diversity in multiple groups often led to reduced or erased diversity effects. Overall, our results suggest that higher diversity can increase resilience but can also promote collapse when diversity occurs in a functional group that negatively influences the state it occurs in. We propose this mechanism as a potential management approach to facilitate the recovery of a desired ecosystem state

Feedbacks of plant identity and diversity on the diversity and community composition of rhizosphere microbiomes from a long-term biodiversity experiment

Soil microbes are known to be key drivers of several essential ecosystem processes such as nutrient cycling, plant productivity and the maintenance of plant species diversity. However, how plant species diversity and identity affect soil microbial diversity and community composition in the rhizosphere is largely unknown. We tested whether, over the course of 11 years, distinct soil bacterial communities developed under plant monocultures and mixtures, and if over this time frame plants with a monoculture or mixture history changed in the bacterial communities they associated with. For eight species, we grew offspring of plants that had been grown for 11 years in the same field monocultures or mixtures (plant history in monoculture vs. mixture) in pots inoculated with microbes extracted from the field monoculture and mixture soils attached to the roots of the host plants (soil legacy). After 5 months of growth in the glasshouse, we collected rhizosphere soil from each plant and used 16S rRNA gene sequencing to determine the community composition and diversity of the bacterial communities. Bacterial community structure in the plant rhizosphere was primarily determined by soil legacy and by plant species identity, but not by plant history. In seven of the eight plant species the number of individual operational taxonomic units with increased abundance was larger when inoculated with microbes from mixture soil. We conclude that plant species richness can affect below-ground community composition and diversity, feeding back to the assemblage of rhizosphere bacterial communities in newly establishing plants via the legacy in soil.</p

Limited added value of laboratory monitoring in thiopurine maintenance monotherapy in inflammatory bowel disease patients

Background: To timely detect myelotoxicity and hepatotoxicity, laboratory monitoring at 3-month intervals is advised throughout thiopurine maintenance treatment for IBD. However, reported incidence rates of myelotoxicity and hepatotoxicity in maintenance treatment are low. Aim: To assess incidence rates and clinical consequences of myelotoxicity and hepatotoxicity in thiopurine maintenance therapy after at least 1 year of thiopurine treatment. Methods: Retrospective analysis of therapy adjustment for laboratory toxicity in adult IBD patients after 12 consecutive months of azathioprine (AZA) or mercaptopurine monotherapy (ie baseline) between 2000 and 2016. Incidence rates of laboratory toxicity (ie myelotoxicity [leucocyte count <4.0 × 10e9/L, and/or platelet count <150 × 10e9/L] and/or hepatotoxicity (gamma-glutamyltransferase [GGT], alkaline phosphatase [AP], ALT and/or AST above ULN, excluding isolated increased AST/AP]) and associated diagnostic procedures and complications were assessed. Results: In total, 12.391 laboratory assessments were performed on 1132 patients (56% female, AZA 74%) during 3.3 years of median follow-up. Median monitoring frequency was 3.1 assessments/treatment year. Only 83/12.391 (0.7%) assessments resulted in therapy adjustment, dose reduction in 46 patients, cessation in 28 and allopurinol initiation in nine; risk of therapy adjustment was 1.9% per treatment year. Incidence rates of myelotoxicity were 7.1% (5.1% mild/1.8% moderate/0.1% severe) and hepatotoxicity 5.1% (3.8% mild/1.1% moderate/0.2% severe) per treatment year. Treatment-related complications with concurrent laboratory toxicity occurred in 12 patients (1.1%) and would not have been prevented by monitoring. Conclusion: Severe laboratory toxicity is uncommon after 1 year of thiopurine monotherapy at 4-month monitoring intervals. Therapy adjustments are rare after detection of laboratory toxicity. After 1 year of thiopurine monotherapy, laboratory monitoring may be lowered to less than a 4-month interval

Antagonistic interactions between filamentous heterotrophs and the cyanobacterium Nostoc muscorum

Background: Little is known about interactions between filamentous heterotrophs and filamentous cyanobacteria. Here, interactions between the filamentous heterotrophic bacteria Fibrella aestuarina (strain BUZ 2) and Fibrisoma limi (BUZ 3) with an axenic strain of the autotrophic filamentous cyanobacterium Nostoc muscorum (SAG 25.82) were studied in mixed cultures under nutrient rich (carbon source present in medium) and poor (carbon source absent in medium) conditions. Findings: F. aestuarina BUZ 2 significantly reduced the cyanobacterial population whereas F. limi BUZ 3 did not. Physical contact between heterotrophs and autotroph was observed and the cyanobacterial cells showed some level of damage and lysis. Therefore, either contact lysis or entrapment with production of extracellular compounds in close vicinity of host cells could be considered as potential modes of action. The supernatants from pure heterotrophic cultures did not have an effect on Nostoc cultures. However, supernatant from mixed cultures of BUZ 2 and Nostoc had a negative effect on cyanobacterial growth, indicating that the lytic compounds were only produced in the presence of Nostoc. The growth and survival of tested heterotrophs was enhanced by the presence of Nostoc or its metabolites, suggesting that the heterotrophs could utilize the autotrophs and its products as a nutrient source. However, the autotroph could withstand and out-compete the heterotrophs under nutrient poor conditions. Conclusions: Our results suggest that the nutrients in cultivation media, which boost or reduce the number of heterotrophs, were the important factor influencing the outcome of the interplay between filamentous heterotrophs and autotrophs. For better understanding of these interactions, additional research is needed. In particular, it is necessary to elucidate the mode of action for lysis by heterotrophs, and the possible defense mechanisms of the autotrophs

Prevalence and clinical associations of myositis antibodies in a large cohort of interstitial lung diseases

Background Serologic testing for autoantibodies is recommended in interstitial lung diseases (ILDs), as connective tissue diseases (CTDs) are an important secondary cause. Myositis antibodies are associated with CTD-ILD, but clinical associations with other ILDs are unclear. In this study, associations of myositis antibodies in various ILDs were evaluated. Methods 1463 ILD patients and 116 healthy subjects were screened for myositis antibodies with a line-blot assay on serum available at time of diagnosis. Additionally, bronchoalveolar lavage fluid (BALf) was analysed. Results A total of 394 patients demonstrated reactivity to at least one antibody, including anti-Ro52 (36.0%), anti-Mi-2β (17.3%) and anti-Jo-1 (10.9%). Anti-Jo-1 (OR 6.4; p<0.100) and anti- Ro52 (OR 6.0; p<0.001) were associated with CTD-ILD. Interestingly, anti-Mi-2β was associated with idiopathic pulmonary fibrosis (IPF; OR 5.3; p = 0.001) and hypersensitivity pneumonitis (HP; OR 5.9; p<0.001). Furthermore, anti-Mi-2β was strongly associated with a histological usual interstitial pneumonia (UIP) pattern (OR 6.5; p < 0.001). Moreover, anti- Mi-2β reactivity was identified in BALf and correlated with serum anti-Mi-2β (r = 0.64; p = 0.002). No differences were found in survival rates between ILD patients with and without serum Mi-2β reactivity (hazard ratio 0.835; 95% CI 0.442-1.575; p = 0.577). Conclusion In conclusion, novel associations of antibody Mi-2β with fibrotic ILD were found. Furthermore, serum anti-Mi-2β was associated with a histological UIP pattern and presence of anti- Mi-2β in BALf. Possibly, anti-Mi-2β could be implemented as a future diagnostic biomarker for fibrotic ILD