Reduced soil multifunctionality and microbial network complexity in degraded and revegetated alpine meadows.

Understanding how microbial processes develop and change in alpine meadow soils is key to global initiatives toward environmental sustainability and local land management. Yet, how microbial interactions mediate soil multifunctionality in disturbed and managed alpine meadows remains understudied. Here, we investigated multiple community metrics, particularly microbial network properties and assembly processes, of soil bacterial and fungal communities and their links to certain soil functions along a degradation-restoration sequence of alpine meadows in the Qinghai-Tibetan Plateau. Meadow degradation caused significant declines in soil hydraulic conductivity (e.g., higher bulk density, reduced soil porosity and water content) and nitrogen availability, leading to lowered soil multifunctionality. Meadow degradation only caused weak changes in microbial abundance, alpha diversity, and community composition, but remarkably reduced bacterial network complexity, to a less extent for fungal network properties. Short-term artificial restoration with productive grass monocultures did not restore soil multifunctionality, in turn even destabilized bacterial network and favored pathogenic over mutualistic fungi. Soil fungi community are more stable than bacteria in disturbed alpine meadows, and they evolved with distinct assembly strategies (stochastic-dominant versus deterministic-driven processes, respectively). Further, microbial network complexity, positively and better predicts soil multifunctionality than alpha diversity. Our work shows how microbial interaction complexity may enhance soil multifunctionality in degraded alpine meadow ecosystems, noting that meadow restoration with low plant species diversity may failed in restoring multiple ecosystem functions. These findings would help predict the outcomes of global environmental changes and inform management strategies in regional grassland conservation and restoration.

Benzoic and salicylic acid are the signaling molecules of Chlorella cells for improving cell growth.

Cell-to-cell communication regulates microalgae production via signaling molecules (SMs), but few microalgal SM species are known. Here, we document two new microalgae SMs, benzoic acid (BA) and salicylic acid (SA). Initially, crude SMs were extracted from a microalgae culture in which microalgae grew on heterotrophic-enriched phosphorus nutrition. The extracted SMs enhanced Chlorella growth by ∼72%, promoted nutrient uptake, and up-regulated the mitogen-activated protein-kinase signaling cascade. Fourier transform infrared and nuclear magnetic resonance analyses identified the putative SMs was aromatic carboxylic acids. BA and SA were identified using high-resolution mass spectrometry. BA and SA addition increased cell growth by ∼75% and ∼25%; and improved ATP production by ∼35% and ∼20%. Transcriptomic analysis showed that BA and SA were biosynthesized via CoA-dependent, non-oxidative pathway. The SMs upregulated TCA-cycle enzymes, which promoted carbon assimilation and activated DNA-replicating enzyme, so that accelerated cell division. This study identified two new SMs for microalgae cell communication and provides means to identify other SMs.

IRAK Inhibitor Protects the Intestinal Tract of Necrotizing Enterocolitis by Inhibiting the Toll-Like Receptor (TLR) Inflammatory Signaling Pathway in Rats.

BACKGROUND The aim of this study was to assess the effects of interleukin-1 (IL-1) receptor associated kinase (IRAK) inhibitors on intestinal injury induced by necrotizing enterocolitis (NEC) in neonatal rats and its regulation on the intestinal Toll-like receptor (TLR) inflammatory signaling pathway. MATERIAL AND METHODS The neonatal rat models of NEC were established though hypoxia-cold stimulation. All rats were divided into 3 groups: an NEC model group (NEC group), an IRAK inhibitor group (IRAKI group), and a normal control group (NC group). At 72 h after the models were established, intestinal tissues were collected for histopathological examination, enzyme-linked immunosorbent assay (ELISA), Western blotting, and immunohistochemistry. RESULTS After IRAK inhibitor intervention, the symptoms of NEC in neonatal rats were alleviated, and the degree of weight loss was reduced. In the IRAK group, the intestinal pathology of neonatal rats was improved, pathological score was decreased, and the incidence rate of NEC was significantly reduced. The levels of tumor necrosis factor-alpha (TNF-α), IL-1ß, and IL-6 in the IRAK group were significantly decreased compared with those in the NEC group. There were no significant differences in IRAK1 and IRAK4 protein expression levels between the IRAK group and the NEC group. The phosphorylated IRAK1 and IRAK4 in the IRAK group were significantly decreased. Nuclear factor-kappa B (NF-κB) level of intestinal tissues in the IRAK group was reduced compared with that in the NEC group. CONCLUSIONS IRAK inhibitors can inhibit the inflammatory response of the NEC model, reduce the release of pro-inflammatory cytokines, and alleviate the damage to intestinal tissues by inhibiting conduction of the TLR signaling pathway.