scholarly journals TmToll-7 Plays a Crucial Role in Innate Immune Responses Against Gram-Negative Bacteria by Regulating 5 AMP Genes in Tenebrio molitor

2019 ◽  
Vol 10 ◽  
Author(s):  
Soyi Park ◽  
Yong Hun Jo ◽  
Ki Beom Park ◽  
Hye Jin Ko ◽  
Chang Eun Kim ◽  
...  
Keyword(s):  
Immune Responses ◽  
Crucial Role ◽  
Tenebrio Molitor ◽  
Innate Immune ◽  
Gram Negative Bacteria ◽  
Innate Immune Responses ◽  
Gram Negative

scholarly journals The role of type 1 interferons in Gram-negative bacteria-induced coagulation

Blood ◽  
2020 ◽  
Author(s):  
Xinyu Yang ◽  
Xiaoye Cheng ◽  
Yiting Tang ◽  
Xianhui Qiu ◽  
Zhongtai Wang ◽  
...  
Keyword(s):  
Immune Responses ◽  
Bacterial Infection ◽  
Innate Immune ◽  
Coagulation Cascade ◽  
Outer Cell ◽  
Gram Negative Bacteria ◽  
Innate Immune Responses ◽  
Gram Negative ◽  
Type 1 Interferons

Bacterial infection not only stimulates innate immune responses but also activates the coagulation cascades. Over-activation of the coagulation system in bacterial sepsis leads to disseminated intravascular coagulation (DIC), a life-threatening condition. However, the mechanisms by which bacterial infection activates the coagulation cascade are not fully understood. Here we show that type 1 interferons (IFNs), widely expressed family of cytokines that orchestrate innate antiviral and antibacterial immunity, mediate bacterial infection-induced DIC through amplifying the release of high mobility box group box 1 (HMGB1) into the blood stream. Inhibition of the expression of type 1 IFNs, disruption of their receptor IFN-α/βR or downstream effector (e.g., HMGB1) uniformly decreased Gram-negative bacteria-induced DIC. Mechanistically, extracellular HMGB1 markedly increased the pro-coagulant activity of tissue factor (TF) by promoting the externalization of phosphatidylserine (PS) to the outer cell surface, where PS assembles a complex of cofactor-proteases of the coagulation cascades. These findings not only provide novel insights into the link between innate immune responses and coagulation, but also open a new avenue for developing novel therapeutic strategies to prevent DIC in sepsis.

Differences in innate immune responses upon stimulation with gram-positive and gram-negative bacteria

2006 ◽  
Vol 41 (5) ◽  
pp. 447-454 ◽  
Author(s):  
Konrad Tietze ◽  
Alexander Dalpke ◽  
Sigfried Morath ◽  
Reinier Mutters ◽  
Klaus Heeg ◽  
...  
Keyword(s):  
Immune Responses ◽  
Innate Immune ◽  
Gram Negative Bacteria ◽  
Innate Immune Responses ◽  
Gram Positive ◽  
Gram Negative

scholarly journals Ironing Out the Details: How Iron Orchestrates Macrophage Polarization

2021 ◽  
Vol 12 ◽  
Author(s):  
Yaoyao Xia ◽  
Yikun Li ◽  
Xiaoyan Wu ◽  
Qingzhuo Zhang ◽  
Siyuan Chen ◽  
...  
Keyword(s):  
Adjuvant Therapy ◽  
Immune Responses ◽  
Epigenetic Regulation ◽  
Crucial Role ◽  
Liver Diseases ◽  
Iron Supplementation ◽  
Macrophage Polarization ◽  
Innate Immune ◽  
Innate Immune Responses

Iron fine-tunes innate immune responses, including macrophage inflammation. In this review, we summarize the current understanding about the iron in dictating macrophage polarization. Mechanistically, iron orchestrates macrophage polarization through several aspects, including cellular signaling, cellular metabolism, and epigenetic regulation. Therefore, iron modulates the development and progression of multiple macrophage-associated diseases, such as cancer, atherosclerosis, and liver diseases. Collectively, this review highlights the crucial role of iron for macrophage polarization, and indicates the potential application of iron supplementation as an adjuvant therapy in different inflammatory disorders relative to the balance of macrophage polarization.

scholarly journals Dimerization and auto-processing induce caspase-11 protease activation within the non-canonical inflammasome

2018 ◽  
Vol 1 (6) ◽  
pp. e201800237 ◽  
Author(s):  
Connie Ross ◽  
Amy H Chan ◽  
Jessica Von Pein ◽  
Dave Boucher ◽  
Kate Schroder
Keyword(s):  
Cell Death ◽  
Immune Responses ◽  
Endotoxic Shock ◽  
Innate Immune ◽  
Order Structure ◽  
Gram Negative Bacteria ◽  
Innate Immune Responses ◽  
Protease Activation ◽  
Necessary And Sufficient ◽  
Active Caspase

Caspase-11 is a cytosolic sensor and protease that drives innate immune responses to the bacterial cell wall component, LPS. Caspase-11 provides defence against cytosolic Gram-negative bacteria; however, excessive caspase-11 responses contribute to murine endotoxic shock. Upon sensing LPS, caspase-11 assembles a higher order structure called the non-canonical inflammasome that enables the activation of caspase-11 protease function, leading to gasdermin D cleavage and cell death. The mechanism by which caspase-11 acquires protease function is, however, poorly defined. Here, we show that caspase-11 dimerization is necessary and sufficient for eliciting basal caspase-11 protease function, such as the ability to auto-cleave. We further show that during non-canonical inflammasome signalling, caspase-11 self-cleaves at site (D285) within the linker connecting the large and small enzymatic subunits. Self-cleavage at the D285 site is required to generate the fully active caspase-11 protease (proposed here to be p32/p10) that mediates gasdermin D cleavage, macrophage death, and NLRP3-dependent IL-1β production. This study provides a detailed molecular mechanism by which LPS induces caspase-11–driven inflammation and cell death to provide host defence against cytosolic bacterial infection.

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