TRIM21 negatively regulates Corynebacterium pseudotuberculosis-induced inflammation and is critical for the survival of C. pseudotuberculosis infected C57BL6 mice.

Corynebacterium pseudotuberculosis, a facultative intracellular bacterium, is an important zoonotic pathogen responsible for chronic inflammatory diseases. TRIM21, an E3 ubiquitin-protein ligase, plays pivotal roles in inflammation regulation. However, its role during C. pseudotuberculosis infection is unclear. Here, we found that TRIM21 expression was significantly increased in C. pseudotuberculosis-infected macrophages. Following infection by C. pseudotuberculosis, we observed a significantly higher number of bacteria and a higher degree of LDH release from Trim21-/- macrophages compared to wild-type (WT) macrophages, suggesting that TRIM21 limits C. pseudotuberculosis replication in macrophages and protects the infected cells from death. Further in vivo experiments showed a significantly higher mortality, higher bacterial load, much more severe abscess formation, and lesions in the organs of C. pseudotuberculosis-infected Trim21-/- mice compared to those of the infected WT mice, suggesting that TRIM21 plays critical roles in protecting against C. pseudotuberculosis infection. Moreover, the secretory levels of IL-1α, IL-1ß, IL-6, and TNF-α were significantly higher in C. pseudotuberculosis-infected Trim21-/- macrophages compared to infected WT macrophages; the levels of these cytokines were also higher in the sera, organs, and ascites of C. pseudotuberculosis-infected Trim21-/- mice compared to infected WT mice. These findings suggest that TRIM21 negatively regulates the secretion of pro-inflammatory cytokines in macrophages, sera, organs, and ascites of mice following C. pseudotuberculosis infection. Collectively, the present study demonstrates that TRIM21 plays a vital role in preventing C. pseudotuberculosis infection, which may be related to the negative regulation of pro-inflammatory cytokines production by TRIM21 during this pathogen infection.

Responses of forest ecosystems to increasing N deposition in China: A critical review.

China has been experiencing a rapid increase in nitrogen (N) deposition due to intensified anthropogenic N emissions since the late 1970s. By synthesizing experimental and observational data taken from literature, we reviewed the responses of China's forests to increasing N deposition over time, with a focus on soil biogeochemical properties and acidification, plant nutrient stoichiometry, understory biodiversity, forest growth, and carbon (C) sequestration. Nitrogen deposition generally increased soil N availability and soil N leaching and decreased soil pH in China's forests. Consequently, microbial biomass C and microbial biomass N were both decreased, especially in subtropical forests. Nitrogen deposition increased the leaf N concentration and phosphorus resorption efficiency, which might induce nutrient imbalances in the forest ecosystems. Although experimental N addition might not affect plant species richness in the overstorey, it did significantly alter species composition of understory plants. Increased N stimulated tree growth in temperate forests, but this effect was weak in subtropical and tropical forests. Soil respiration in temperate forests was non-linearly responsive to N additions, with an increase at dosages of <60 kg N ha-1 yr-1 and a decrease at dosages of >60 kg N ha-1 yr-1. However, it was consistently decreased by increased N inputs in subtropical and tropical forests. In light of future trends in the composition (e.g., reduced N vs. oxidized N) and the loads of N deposition in China, further research on the effects of N deposition on forest ecosystems will have critical implications for the management strategies of China's forests.