Pyroptosis, a type of programmed cell death that along with inflammation, is mainly regulated by two main pathways, cysteinyl aspartate specific proteinase (caspase)-1-induced canonical inflammatory pathway and caspase-11-induced non-canonical inflammatory pathway. The non-canonical inflammatory pathway-induced pyroptosis is a unique immune response in response to gram-negative (G−) bacteria. It is induced by lipopolysaccharide (LPS) on the surface of G− bacteria. This activates caspase-11 which, in turn, activates a series of downstream proteins eventually forming protein pores on the cell membrane and inducing cell sacrificial processes. Caspase-11 belongs to the caspase family and is an homologous protein of caspase-1. It has the ability to specifically hydrolyze proteins, but it is still unclear how it regulates cell death caused by non-canonical inflammatory pathways. The present study describes a pathway that enables LPS to directly enter the cell and activate caspase-11, and the key role caspase-11 plays in the activation of pyroptosis and inflammation.

Background: Maintaining osmotic equilibrium plays an important role in the survival of cold-water fishes. Heat stress has been proven to reduce the activity of Na⁺/K⁺-ATPase in the gill tissue, leading to destruction of the osmotic equilibrium. However, the mechanism of megatemperature affecting gill osmoregulation has not been fully elucidated. Results: In this study, Siberian sturgeon (Acipenser baerii) was used to analyze histopathological change, plasma ion level, and transcriptome of gill tissue subjected to 20℃, 24℃and 28℃. The results showed that ROS level and damage were increased in gill tissue with the increasing of heat stress temperature. Plasma Cl⁻ level at 28℃ was distinctly lower than that at 20℃ and 24℃, while no significant difference was found in Na⁺ and K⁺ ion levels among different groups. Transcriptome analysis displayed that osmoregulation-, DNA-repair- and apoptosis-related terms or pathways were enriched in GO and KEGG analysis. Moreover, 194 osmoregulation-related genes were identified. Amongst, the expression of genes limiting ion outflow, occluding (OCLN), and ion absorption, solute carrier family 4, member 2 (AE2) solute carrier family 9, member 3 (NHE3) chloride channel 2 (CLC-2) were increased, while Na⁺/K⁺-ATPase alpha (NKA-a) expression was decreased after heat stress. Conclusions: This study reveals for the first time that the effect of heat stress on damage and osmotic regulation in gill tissue of cold-water fishes. Heat stress increases the permeability of fish’s gill tissue, and induces the gill tissue to keep ion balance through active ion absorption and passive ion outflow. Our study will contribute to research of global-warming-caused effects on cold-water fishes.

Chronic heat stress caused by global warming can have serious implications for fish survival. The kidney plays a central role in many homeostatic functions, including water and electrolyte regulation. However, there is limited knowledge about the effect of heat stress on fish kidneys. In this study, water temperatures were increased from 20 °C to 24 °C and 28 °C in 8 days at a warming rate of 1 °C/d, and then maintained for 12 days. We investigated the effects of mild heat stress (24 °C) and high heat stress (28 °C) on Siberian Sturgeon (Acipenser baerii) kidneys using histological observation, flow cytometry detection, and RT-qPCR. Our histological observations revealed that heat stress caused significant infiltration of inflammatory cells in the kidney, especially at 28 °C. The flow cytometry assay demonstrated a significant increase in the number of apoptotic cells after heat stress at 28 °C compared to a control group at 20 °C (p = 0.033). The level of plasma creatinine was significantly increased in the 28 °C group compared to the control group (p = 0.001). In addition, the mRNA expression levels of heat shock protein GRP75 increased (p = 0.009). The results indicate that heat stress at 28 °C caused damage to the kidneys of A. baerii and triggered the protective response of heat shock proteins. In conclusion, this study contributes to the understanding of the coping strategies of the kidney of A. baerii for chronic heat stress.

Crustaceans have a more persistent starvation tolerance than mammals, birds, reptiles, and even fish. This study is aimed at assessing the survival strategy and regulatory mechanism of crustaceans in response to starvation through an animal model using Eriocheir sinensis. In the 42-day starvation experiment, the hepatopancreas was found to become the target organ, which was characterized by atrophy of the thin wall in the hepatic tubules and expansion of the lumen. During short-term starvation, E. sinensis activates lipid and glycogen metabolism in the hepatopancreas with lipid metabolism dominating. In lipid metabolism, there was a significant decline in triglyceride, whereas cholesterol did not change significantly. Meanwhile, the fatty acid metabolism pathway was inhibited, but autophagy increased in the hepatopancreas, which may be the selective pathway for the decomposition of intracellular substances. However, under long-term starvation, the stored energy in the hepatopancreas was depleted, and E. sinensis selects to consume hepatopancreatic cells and maintain energy metabolism through apoptosis, which was triggered by both the death receptor pathway and the mitochondrial pathway. In addition, cell proliferation was blocked to reduce unnecessary energy consumption.