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Parasite Versus Host: Pathology and Disease
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
Hemozoin’s toxic effect may be in part due to the fact that following its release from lysed erythrocytes, it is ingested by macrophages and other phagocytes. Because hemozoin cannot be efficiently degraded within the phagocyte’s endomembrane system, further phagocytosis is impeded. At least part of hemozoin’s effect, however, may be more indirect and be better understood as immunopathology: pathology caused by an overzealous or otherwise damaging immune response. Hemozoin is known to form complexes with other parasite-derived molecules, including Plasmodium DNA. These complexes may then bind specific Toll-like receptors on the surface of phagocytes. The subsequent signal transduction results in an inflammatory response via an up-regulation of the cytokines IL-12 and TNFα.
Septic shock
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Bryan E. Freeman, Michael R. Foley
One popular area of sepsis research is the examination and elucidation of mechanisms behind the action of toll-like receptors (TLRs). Essentially, TLRs function to activate immune responses once the body’s natural barriers (skin, vascular system, etc.) have been breached. Current research has shown that binding of TLRs causes activation of intracellular transcription activators including interferon regulator factors, phosphoinositide 3-kinase (PI3K), and cytosolic nuclear factor-kappa β (NF-β). NF-β then enters the nucleus and ultimately causes the activation of genes for acute phase proteins, inducible nitric oxide synthase, coagulation factors, and pro-inflammatory cytokines, among others (8).
Immune system and Innate Immunity
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Immature dendritic cells are highly phagocytic and express low levels of major histocompatibility complex (MHC) that capture and process pathogens into antigenic fragments. When dendritic cells are exposed to pathogens, toll-like receptors are activated and stimulate maturation of the dendritic cells. When mature, dendritic cells express abundant MHC and become antigen-presenting cells (APCs).
Gastric protective effect of Alpinia officinarum flavonoids: mediating TLR4/NF-κB and TRPV1 signalling pathways and gastric mucosal healing
Published in Pharmaceutical Biology, 2023
Kaiwen Lin, Tang Deng, Huijuan Qu, Hongya Ou, Qifeng Huang, Bingmiao Gao, Xiaoliang Li, Na Wei
Toll-like receptor signalling pathways are widely distributed in immune cells and play an important role in recognizing specific pathogen molecular patterns and initiating inflammatory immune responses to pathogens (Fitzgerald and Kagan 2020). TLR2 and TLR4 are mostly under expressed or silenced in TLR family, but when inflammation occurs, they can pass through MYD88. The action of junction molecules such as IRAK4 TRAF6 promotes the activation of the transcription factor NF-κB and induces cytokine secretion and inflammatory responses (Hu et al. 2021; Pereira et al. 2022). This study found that acetic acid activated the expression of some genes and proteins in the Toll-like receptor signalling pathway. On the contrary, F.AOH treatment significantly inhibited the activation of some Toll-like receptor signalling pathways and regulated the expression of related genes and proteins. Based on this, we concluded that F.AOH treatment could block TLR4/MYD88/NF-κB signalling pathway, thereby affecting its adhesion chemotaxis, proliferation, activation and activation. Apoptosis and secretion of inflammatory cytokines promote gastric protection (Figure 7(E–H)).
New insight into gut microbiota-derived metabolites to enhance liver regeneration via network pharmacology study
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Ki-Kwang Oh, Ickwon Choi, Haripriya Gupta, Ganesan Raja, Satya Priya Sharma, Sung-Min Won, Jin-Ju Jeong, Su-Been Lee, Min-Gi Cha, Goo-Hyun Kwon, Min-Kyo Jeong, Byeong-Hyun Min, Ji-Ye Hyun, Jung-A Eom, Hee-Jin Park, Sang-Jun Yoon, Mi-Ran Choi, Dong Joon Kim, Ki-Tae Suk
The associations of the top 10 pathways with LR were concisely described as follows, and these findings are based on rich factors. Activation of the AGE-RAGE signalling pathway can enhance intestinal permeability. Thus, lipopolysaccharides (LPS) can cross the intestinal epithelial barrier [57]. This finding implies that the AGE-RAGE signalling pathway induces systemic inflammation and exacerbates liver injury. The Fc epsilon RI signalling pathway is activated by immunoglobulin E (IgE), which has negative effects on LR [57,58]. The Toll-like receptor signalling pathway has two functions. On one hand, the pathway results in favourable effects that improve LR. On the other hand, the pathway leads to delayed LR [59]. From this perspective, studies on TLR in LR might reveal an important mechanism for developing new therapeutic strategies. Similarly, the prolactin signalling pathway is also a double-edged sword with respect to cellular inflammation under some conditions [60].
Prognostic role of TLR4 and TLR2 in hepatocellular carcinoma
Published in Acta Oncologica, 2021
Valtteri Kairaluoma, Niko Kemi, Heikki Huhta, Vesa-Matti Pohjanen, Olli Helminen
The relationship between inflammatory response and cancer progression has been known for years [14]. In several animal models inflammatory cells and cytokines, such as NF-κB, TNF-α and various interleukins, have shown the ability to promote carcinogenesis with their anti-apoptotic effects, induction of oxidative damage to DNA, and the induction of tissue repair response [14–17]. Toll-like receptors are known for their role in host defense, but increasing evidence suggests also a role in cancer progression [15]. Infection, or injury can induce inflammation, which can promote tumorigenesis through chronic tissue damage and the subsequent induction of tissue repair [15]. The unregulated TLR-regulated tissue repair response can drive tumor growth and progression in a positive feedback of unregulated tissue injury and repair, which can trigger TLR-dependent inflammatory responses [15]. Multiple mechanisms for TLRs role in cancer promotion have been suggested [5,15,18–20]. Also, the potential role of TLRs in cancer immunotherapy has gained a lot of interest [21]. The underlying mechanism behind nuclear translocation of TLR4 and the correlation with prognosis is unclear. TLR4 contains several sequences indicating nuclear localization [22]. Alternatively, nuclear carrier proteins might be related to nuclear translocation, but no such proteins have been identified. Translocation of membrane-bound TLRs to nucleus might be due to an increased amount of these proteins and related to signaling activity [12].