Hiding in the background: community-level patterns in invertebrate herbivory across the tundra biome

© 2019, Springer-Verlag GmbH Germany, part of Springer Nature. Invertebrate herbivores depend on external temperature for growth and metabolism. Continued warming in tundra ecosystems is proposed to result in increased invertebrate herbivory. However, empirical data about how current levels of invertebrate herbivory vary across the Arctic is limited and generally restricted to a single host plant or a small group of species, so predicting future change remains challenging. We investigated large-scale patterns of invertebrate herbivory across the tundra biome at the community level and explored how these patterns are related to long-term climatic conditions and year-of-sampling weather, habitat characteristics, and aboveground biomass production. Utilizing a standardized protocol, we collected samples from 92 plots nested within 20 tundra sites during summer 2015. We estimated the community-weighted biomass lost based on the total leaf area consumed by invertebrates for the most common plant species within each plot. Overall, invertebrate herbivory was prevalent at low intensities across the tundra, with estimates averaging 0.94% and ranging between 0.02 and 5.69% of plant biomass. Our results suggest that mid-summer temperature influences the intensity of invertebrate herbivory at the community level, consistent with the hypothesis that climate warming should increase plant losses to invertebrates in the tundra. However, most of the observed variation in herbivory was associated with other site level characteristics, indicating that other local ecological factors also play an important role. More details about the local drivers of invertebrate herbivory are necessary to predict the consequences for rapidly changing tundra ecosystems

歯石はヒトおよびマウス貪食細胞においてNLRP3インフラマソームを活性化してインターロイキン1β産生を刺激する

Dental calculus is a mineralized deposit associated with periodontitis. The bacterial components contained in dental calculus can be recognized by host immune sensors, such as Toll-like receptors (TLRs), and induce transcription of proinflammatory cytokines, such as IL-1β. Studies have shown that cellular uptake of crystalline particles may trigger NLRP3 inflammasome activation, leading to the cleavage of the IL-1β precursor to its mature form. Phagocytosis of dental calculus in the periodontal pocket may therefore lead to the secretion of IL-1β, promoting inflammatory responses in periodontal tissues. However, the capacity of dental calculus to induce IL-1β secretion in human phagocytes has not been explored. To study this, we stimulated human polymorphonuclear leukocytes (PMNs) and peripheral blood mononuclear cells (PBMCs) with dental calculus collected from periodontitis patients, and measured IL-1β secretion by ELISA. We found that calculus induced IL-1β secretion in both human PMNs and PBMCs. Calculus also induced IL-1β in macrophages from wild-type mice, but not in macrophages from NLRP3- and ASC-deficient mice, indicating the involvement of NLRP3 and ASC. IL-1β induction was inhibited by polymyxin B, suggesting that LPS is one of the components of calculus that induces pro-IL-1β transcription. To analyze the effect of the inorganic structure, we baked calculus at 250°C for 1 h. This baked calculus failed to induce pro-IL-1β transcription. However, it did induce IL-1β secretion in lipid A-primed cells, indicating that the crystalline structure of calculus induces inflammasome activation. Furthermore, hydroxyapatite crystals, a component of dental calculus, induced IL-1β in mouse macrophages, and baked calculus induced IL-1β in lipid A-primed human PMNs and PBMCs. These results indicate that dental calculus stimulates IL-1β secretion via NLRP3 inflammasome in human and mouse phagocytes, and that the crystalline structure has a partial role in the activation of NLRP3 inflammasome.長崎大学学位論文 学位記番号:博(医歯薬)甲第907号 学位授与年月日:平成29年3月21日Author: Jorge Luis Montenegro Raudales, Atsutoshi Yoshimura, Ziauddin SM, Takashi Kaneko, Yukio Ozaki, Takashi Ukai, Toshihiro Miyazaki, Eicke Latz, Yoshitaka HaraCitation: PLOS ONE, 11(9), e0162865; 2016Nagasaki University (長崎大学)課程博