Pattern of plant communities' influence to grasshopper abundance distribution in heterogeneous landscapes at the upper reaches of Heihe River, Qilian Mountains, China.

Understanding the impact of the heterogeneity of the ecological environment on biodiversity is a key issue in ecology. Topographical heterogeneity was potentially important in grassland systems to create or change habitats for grasshopper settlement and foraging. Yet, there was little knowledge of how grasshopper communities respond to plant communities along the altitude gradient. We investigated the role of plant communities on grasshopper diversity with geostatistical methods to test the effects of heterogeneity in the natural grassland on the upper reaches of the Heihe River, Qilian Mountains. To aim the goal of the study, nonreturn experiments were used to collect the grasshoppers' diversity and populations, and the plant's community was sampled at the same location. The results showed that the semivariograms of grasshopper abundance and plant communities were both nonlinear models, while the grasshopper abundance typically produces heterogeneity with a larger range and nuggets than plant communities (except the plant coverage range in the model, range <1.5 m). The two communities presented the spatial distribution pattern of aggregated distribution, and the spatial trend is more intense in the northeast-southwest direction than in the northwest-southeast. The grasshopper species developed a good selection on microenvironment to habitat and the distribution consistent with plants, forming the horizontal distribution with a flaky and plaque distribution pattern. The relationship between grasshoppers and plants was highly dependent on the altitude, and grasshopper abundance has a positive correlation with plant richness (F = 0.68) and plant coverage (F = 0.32) and has a negative correlation with plant height (F = 0.13). In summary, the spatial distribution and correlation characteristics of plant communities and grasshoppers formed a plaque heterogeneity structure under the altitude gradients.

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.