Effects of Kumaizasa (Sasa senanensis) Leaf Extract on Innate Immune Regulation in HEK293 Cells and Macrophages

2021 ◽  
Vol 41 (8) ◽  
pp. 4093-4100
Author(s):  
KEISUKE SATO ◽  
RYOSUKE TATSUNAMI ◽  
AKIFUMI NAKATA ◽  
KEN-ICHI KOMATSU ◽  
SHINJI HARAKAWA ◽  
...  
Keyword(s):  
Immune Regulation ◽  
Leaf Extract ◽  
Innate Immune ◽  
Hek293 Cells ◽  
Sasa Senanensis

scholarly journals Geometrical reorganization of Dectin-1 and TLR2 on single phagosomes alters their synergistic immune signaling

2019 ◽  
Vol 116 (50) ◽  
pp. 25106-25114 ◽  
Author(s):  
Wenqian Li ◽  
Jun Yan ◽  
Yan Yu
Keyword(s):  
Immune Responses ◽  
Immune Regulation ◽  
Spatial Organization ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Membrane Composition ◽  
Intracellular Compartments ◽  
Synergistic Regulation ◽  
The Relationship

Receptors of innate immune cells function synergistically to detect pathogens and elicit appropriate immune responses. Many receptor pairs also appear “colocalized” on the membranes of phagosomes, the intracellular compartments for pathogen ingestion. However, the nature of the seemingly receptor colocalization and the role it plays in immune regulation are unclear, due to the inaccessibility of intracellular phagocytic receptors. Here, we report a geometric manipulation technique to directly probe the role of phagocytic receptor “colocalization” in innate immune regulation. Using particles with spatially patterned ligands as phagocytic targets, we can decouple the receptor pair, Dectin-1 and Toll-like receptor (TLR)2, to opposite sides on a single phagosome or bring them into nanoscale proximity without changing the overall membrane composition. We show that Dectin-1 enhances immune responses triggered predominantly by TLR2 when their centroid-to-centroid proximity is <500 nm, but this signaling synergy diminishes upon receptor segregation beyond this threshold distance. Our results demonstrate that nanoscale proximity, not necessarily colocalization, between Dectin-1 and TLR2 is required for their synergistic regulation of macrophage immune responses. This study elucidates the relationship between the spatial organization of phagocytic receptors and innate immune responses. It showcases a technique that allows spatial manipulation of receptors and their signal cross-talk on phagosomes inside living cells.

scholarly journals Decoding the noncoding: Prospective of lncRNA-mediated innate immune regulation

RNA Biology ◽  
2014 ◽  
Vol 11 (8) ◽  
pp. 979-985 ◽  
Author(s):  
Zhonghan Li ◽  
Tariq M Rana
Keyword(s):  
Immune Regulation ◽  
Innate Immune

scholarly journals Stages of Meningococcal Sepsis Simulated In Vitro, with Emphasis on Complement and Toll-Like Receptor Activation

2008 ◽  
Vol 76 (9) ◽  
pp. 4183-4189 ◽  
Author(s):  
Bernt Christian Hellerud ◽  
Jørgen Stenvik ◽  
Terje Espevik ◽  
John D. Lambris ◽  
Tom Eirik Mollnes ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Complement Activation ◽  
Bacterial Load ◽  
Receptor Activation ◽  
Innate Immune ◽  
Cytokine Secretion ◽  
Hek293 Cells ◽  
Toll Like Receptor ◽  
Bacterial Concentration

ABSTRACT The clinical presentation of meningococcal disease is closely related to the number of meningococci in the circulation. This study aimed to examine the activation of the innate immune system after being exposed to increasing and clinically relevant concentrations of meningococci. We incubated representative Neisseria meningitidis serogroup B (ST-32) and serogroup C (ST-11) strains and a lipopolysaccharide (LPS)-deficient mutant (the 44/76 lpxA mutant) in human serum and whole blood and measured complement activation and cytokine secretion and the effect of blocking these systems. HEK293 cells transfected with Toll-like receptors (TLRs) were examined for activation of NF-κB. The threshold for cytokine secretion and activation of NF-κB was 103 to 104 meningococci/ml. LPS was the sole inflammation-inducing molecule at concentrations up to 105 to 106 meningococci/ml. The activation was dependent on TLR4-MD2-CD14. Complement contributed to the inflammatory response at ≥105 to 106 meningococci/ml, and complement activation increased exponentially at ≥107 bacteria/ml. Non-LPS components initiated TLR2-mediated activation at ≥107 bacteria/ml. As the bacterial concentration exceeded 107/ml, TLR4 and TLR2 were increasingly activated, independent of CD14. In this model mimicking human disease, the inflammatory response to N. meningitidis was closely associated with the bacterial concentration. Therapeutically, CD14 inhibition alone was most efficient at a low bacterial concentration, whereas addition of a complement inhibitor may be beneficial when the bacterial load increases.

scholarly journals Innate Immune Regulation ofSerratia marcescens–Induced Corneal Inflammation and Infection

2012 ◽  
Vol 53 (11) ◽  
pp. 7382 ◽  
Author(s):  
Rong Zhou ◽  
Rui Zhang ◽  
Yan Sun ◽  
Sean Platt ◽  
Loretta Szczotka-Flynn ◽  
...  
Keyword(s):  
Immune Regulation ◽  
Innate Immune ◽  
Corneal Inflammation

scholarly journals Innate Immune Regulation by Toll-Like Receptors in the Brain

2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Carina Mallard
Keyword(s):  
Immune Regulation ◽  
Innate Immune System ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Toll Like Receptors ◽  
Receptor Ligands ◽  
Health And Disease ◽  
Cerebral Inflammation ◽  
The Brain

The innate immune system plays an important role in cerebral health and disease. In recent years the role of innate immune regulation by toll-like receptors in the brain has been highlighted. In this paper the expression of toll-like receptors and endogenous toll-like receptor ligands in the brain and their role in cerebral ischemia will be discussed. Further, the ability of systemic toll-like receptor ligands to induce cerebral inflammation will be reviewed. Finally, the capacity of toll-like receptors to both increase (sensitization) and decrease (preconditioning/tolerance) the vulnerability of the brain to damage will be disclosed. Studies investigating the role of toll-like receptors in the developing brain will be emphasized.

scholarly journals The Macrophage Galactose-Type Lectin-1 (MGL1) RecognizesTaenia crassicepsAntigens, Triggers Intracellular Signaling, and Is Critical for Resistance to This Infection

2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
Daniel Montero-Barrera ◽  
Héctor Valderrama-Carvajal ◽  
César A. Terrazas ◽  
Saúl Rojas-Hernández ◽  
Yadira Ledesma-Soto ◽  
...  
Keyword(s):  
Immune Regulation ◽  
Intracellular Signaling ◽  
Innate Immune ◽  
Helminth Parasites ◽  
Wild Type ◽  
Rt Pcr ◽  
Binding Ability ◽  
Arginase 1 ◽  
Mannose Receptors ◽  
Signaling Activity

C-type lectins are multifunctional sugar-binding molecules expressed on dendritic cells (DCs) and macrophages that internalize antigens for processing and presentation. Macrophage galactose-type lectin 1 (MGL1) recognizes glycoconjugates expressing Lewis X structures which contain galactose residues, and it is selectively expressed on immature DCs and macrophages. Helminth parasites contain large amounts of glycosylated components, which play a role in the immune regulation induced by such infections. Macrophages from MGL1−/−mice showed less binding ability toward parasite antigens than their wild-type (WT) counterparts. Exposure of WT macrophages toT. crassicepsantigens triggered tyrosine phosphorylation signaling activity, which was diminished in MGL1−/−macrophages. FollowingT. crassicepsinfection, MGL1−/−mice failed to produce significant levels of inflammatory cytokines early in the infection compared to WT mice. In contrast, MGL1−/−mice developed a Th2-dominant immune response that was associated with significantly higher parasite loads, whereas WT mice were resistant. Flow cytometry and RT-PCR analyses showed overexpression of the mannose receptors, IL-4Rα, PDL2, arginase-1, Ym1, and RELM-αon MGL1−/−macrophages. These studies indicate that MGL1 is involved inT. crassicepsrecognition and subsequent innate immune activation and resistance.

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