scholarly journals Toll-Like Receptor 4 Signalling and Its Impact on Platelet Function, Thrombosis, and Haemostasis

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Thomas M. Vallance ◽  
Marie-Theres Zeuner ◽  
Harry F. Williams ◽  
Darius Widera ◽  
Sakthivel Vaiyapuri
Keyword(s):  
Platelet Function ◽  
Current Knowledge ◽  
Innate Immune ◽  
Inflammatory Factors ◽  
Toll Like Receptor ◽  
Platelet Activity ◽  
Toll Like Receptor 4 ◽  
Open Questions ◽  
Activation Of Transcription ◽  
Wide Range

Platelets are anucleated blood cells that participate in a wide range of physiological and pathological functions. Their major role is mediating haemostasis and thrombosis. In addition to these classic functions, platelets have emerged as important players in the innate immune system. In particular, they interact with leukocytes, secrete pro- and anti-inflammatory factors, and express a wide range of inflammatory receptors including Toll-like receptors (TLRs), for example, Toll-like receptor 4 (TLR4). TLR4, which is the most extensively studied TLR in nucleated cells, recognises lipopolysaccharides (LPS) that are compounds of the outer surface of Gram-negative bacteria. Unlike other TLRs, TLR4 is able to signal through both the MyD88-dependent and MyD88-independent signalling pathways. Notably, despite both pathways culminating in the activation of transcription factors, TLR4 has a prominent functional impact on platelet activity, haemostasis, and thrombosis. In this review, we summarise the current knowledge on TLR4 signalling in platelets, critically discuss its impact on platelet function, and highlight the open questions in this area.

scholarly journals Variability among Macaca fascicularis in the innate immune response to Toll‐like receptor 4 (TLR4) agonists

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Charles Wayne Frevert ◽  
Renee Hukkanen ◽  
Steve Mongovin ◽  
Kay Larsen ◽  
Mike Agy ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Macaca Fascicularis ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

scholarly journals Key Player in Cardiac Hypertrophy, Emphasizing the Role of Toll-Like Receptor 4

2020 ◽  
Vol 7 ◽  
Author(s):  
Zheng Xiao ◽  
Bin Kong ◽  
Hongjie Yang ◽  
Chang Dai ◽  
Jin Fang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Cardiac Hypertrophy ◽  
Intracellular Signaling ◽  
Molecular Mechanisms ◽  
New Technologies ◽  
Immune Cell ◽  
Current Knowledge ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Tlr4 Signaling

Toll-like receptor 4 (TLR4), a key pattern recognition receptor, initiates the innate immune response and leads to chronic and acute inflammation. In the past decades, accumulating evidence has implicated TLR4-mediated inflammatory response in regulation of myocardium hypertrophic remodeling, indicating that regulation of the TLR4 signaling pathway may be an effective strategy for managing cardiac hypertrophy's pathophysiology. Given TLR4's significance, it is imperative to review the molecular mechanisms and roles underlying TLR4 signaling in cardiac hypertrophy. Here, we comprehensively review the current knowledge of TLR4-mediated inflammatory response and its interaction ligands and co-receptors, as well as activation of various intracellular signaling. We also describe the associated roles in promoting immune cell infiltration and inflammatory mediator secretion, that ultimately cause cardiac hypertrophy. Finally, we provide examples of some of the most promising drugs and new technologies that have the potential to attenuate TLR4-mediated inflammatory response and prevent or reverse the ominous cardiac hypertrophy outcomes.

Toll-like receptor-4 expressed on gastric pit cells may initiate innate immune response of gastric mucosa against Helicobactor pylori infection

2001 ◽  
Vol 120 (5) ◽  
pp. A59
Author(s):  
Kazuhito Rokutan ◽  
Shigetada Teshima ◽  
Tsukasa Kawahara ◽  
Tomoko Kawai ◽  
Takeshi Nikawa ◽  
...  
Keyword(s):  
Immune Response ◽  
Gastric Mucosa ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Helicobactor Pylori ◽  
Pit Cells

scholarly journals Toll-Like Receptor 4 Mediates Innate Immune Responses to Haemophilus influenzae Infection in Mouse Lung

2002 ◽  
Vol 168 (2) ◽  
pp. 810-815 ◽  
Author(s):  
Xiaorong Wang ◽  
Christian Moser ◽  
Jean-Pierre Louboutin ◽  
Elena S. Lysenko ◽  
Daniel J. Weiner ◽  
...  
Keyword(s):  
Immune Responses ◽  
Haemophilus Influenzae ◽  
Innate Immune ◽  
Mouse Lung ◽  
Innate Immune Responses ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

scholarly journals Hypertension and Erectile Dysfunction: Breaking Down the Challenges

2020 ◽  
Author(s):  
Amanda Almeida de Oliveira ◽  
Kenia Pedrosa Nunes
Keyword(s):  
Erectile Dysfunction ◽  
Innate Immune System ◽  
Innate Immune ◽  
Low Grade ◽  
Oxygen Species ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Corpora Cavernosa ◽  
Inflammatory State ◽  
Antioxidant Mechanisms

Abstract A diagnostic of hypertension increases the risk of erectile dysfunction (ED); likewise, ED can be an early sign of hypertension. In both cases, there is evidence that endothelial dysfunction is a common link between the 2 conditions. During hypertension, the sustained and widespread release of procontractile factors (e.g., angiotensin II, endothelin 1, and aldosterone) impairs the balance between vasoconstrictors and vasodilators and, in turn, detrimentally impacts vascular and erectile structures. This prohypertensive state associates with an enhancement in the generation of reactive oxygen species, which is not compensated by internal antioxidant mechanisms. Recently, the innate immune system, mainly via Toll-like receptor 4, has also been shown to actively contribute to the pathophysiology of hypertension and ED not only by inducing oxidative stress but also by sustaining a low-grade inflammatory state. Furthermore, some drugs used to treat hypertension can cause ED and, consequently, reduce compliance with the prescribed pharmacotherapy. To break down these challenges, in this review, we focus on discussing the well-established as well as the emerging mechanisms linking hypertension and ED with an emphasis on the signaling network of the vasculature and corpora cavernosa, the vascular-like structure of the penis.

scholarly journals Energetics of Endotoxin Recognition in the Toll-Like Receptor 4 Innate Immune Response

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Teresa Paramo ◽  
Susana M. Tomasio ◽  
Kate L. Irvine ◽  
Clare E. Bryant ◽  
Peter J. Bond
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

194 A Non-Gluten Component of Wheat is a Strong Stimulator of Innate Immune Responses In Vitro and In Vivo and Acts via Toll Like Receptor 4

2010 ◽  
Vol 138 (5) ◽  
pp. S-36
Author(s):  
Yvonne Junker ◽  
Donatella Barisani ◽  
Daniel A. Leffler ◽  
Towia Libermann ◽  
Simon T. Dillon ◽  
...  
Keyword(s):  
Immune Responses ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4

Creating a customized intracellular niche: subversion of host cell signaling byLegionellatype IV secretion system effectors

2015 ◽  
Vol 61 (9) ◽  
pp. 617-635 ◽  
Author(s):  
Ernest C. So ◽  
Corinna Mattheis ◽  
Edward W. Tate ◽  
Gad Frankel ◽  
Gunnar N. Schroeder
Keyword(s):  
Host Cell ◽  
Legionella Pneumophila ◽  
Current Knowledge ◽  
Secretion System ◽  
Effector Proteins ◽  
Cellular Processes ◽  
Type Iv ◽  
Open Questions ◽  
Exact Function ◽  
Wide Range

The Gram-negative facultative intracellular pathogen Legionella pneumophila infects a wide range of different protozoa in the environment and also human alveolar macrophages upon inhalation of contaminated aerosols. Inside its hosts, it creates a defined and unique compartment, termed the Legionella-containing vacuole (LCV), for survival and replication. To establish the LCV, L. pneumophila uses its Dot/Icm type IV secretion system (T4SS) to translocate more than 300 effector proteins into the host cell. Although it has become apparent in the past years that these effectors subvert a multitude of cellular processes and allow Legionella to take control of host cell vesicle trafficking, transcription, and translation, the exact function of the vast majority of effectors still remains unknown. This is partly due to high functional redundancy among the effectors, which renders conventional genetic approaches to elucidate their role ineffective. Here, we review the current knowledge about Legionella T4SS effectors, highlight open questions, and discuss new methods that promise to facilitate the characterization of T4SS effector functions in the future.

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