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Neonatal Bacterial Infection
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Koilmani Emmanuvel Rajan, Christopher Karen
During meningitis, TLRs play the key inflammatory mediators that trigger immune response and promote proinflammatory cytokines production, which finally causes neuronal damage (Amor et al. 2010). On the cell surface, TLRs that have been identified are TLR1, 2, 4, 5, 6, and 10, which facilitate to identify the subcapsular bacterial components; additionally, TLR3, 4, 7, 8, and 9 trigger signaling cascades. It has been reported that TLR2 along with TLR1 and CD14 recognize LTA, lipoproteins, and peptidoglycan (Hirschfeld et al. 1999; Han et al. 2003; Schröeder et al. 2003), wherein lipopolysaccharides (LPS) and PLY can be engaged by TLR4 (Poltorak et al. 1998; Malley et al. 2003) and bacterial flagellin can be recognized by TLR5 (Hayashi et al. 2001) (Table 6.3). TLRs activate mitogen activated protein kinase (MAPK) and nuclear factor κB (NF-κB). These findings suggest that TLRs have to combine to activate inflammatory response. The individuals with meningitis show general characteristics of high levels of proinflammatory cytokines like IL-1β, IL-6, and TNF-α in CSF (Dunne and O’Neill 2003; Mogensen et al. 2006).
Landscape of Papillomavirus in Human Cancers
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Susri Ray Chaudhuri (Guha), Anirban Roy, Indranil Chatterjee, Rahul Roy Chowdhury, Snehasikta Swarnakar
Eukaryotic cells express germ line-encoded receptors of the innate immune system, pathogen recognition receptors (PRRs) that recognize invariant molecular motifs known as pathogen-associated molecular patterns (PAMPs) (Medzhitov and Janeway 1997). Genital tract keratinocytes express several toll-like receptors (TLRs) located either on the cell surface (TLR1, TLR2, TLR4, TLR5, and TLR6) or in the endosome (TLR3 and TLR9) (Nasu and Narahara 2010). TLR7 expression is induced on keratinocytes by triggering TLR3 with double-stranded RNA, a feature of viral infections, thus activating IFN-responsive genes (Kalali et al. 2008). Type I IFNs that elicit predominantly Th1-type cytotoxic responses are produced by activation of TLRs on keratinocytes (Miller and Modlin 2007).
Controlling Neuroinflammation
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Constitutive expression of TLRs by microglia is localized mainly in circumventricular organs and meningea, which constitute the port of entry of blood-carried pathogens. TLR expression by microglia rises after pathogen invasion or constituents mimicking a pathogen invasion with expression of TLR1-4 being dominant (Bsibsi et al. 2002; Farina et al. 2005; Jack et al. 2005; Suh et al. 2009). Microglia express RLRs (RIG-1 and MDA5 in particular) (Furr et al. 2008), scavenger receptors (SR-A, SR-B RAGE, MARCO, TREM) (Block et al. 2007; Farina et al. 2007; Husemann et al. 2002), purinergic receptors such as P2X7 (Di Virgilio 2006; Farina et al. 2007), NLRs, NLRP3 in particular (Kummer et al. 2007), and complement factor receptors and inhibitors (Farina et al. 2007; Griffiths et al. 2009).
Difference in Host Immune response to Methicillin-Resistant and Methicillin Sensitive Staphylococcus aureus (MRSA and MSSA) Endophthalmitis
Published in Ocular Immunology and Inflammation, 2022
RNeasy Mini Kit (Qiagen Ltd., West Sussex, UK) was used to extract the total RNA from the cells following the manufacturer’s instructions. For quantitative RT-PCR, cDNA was synthesized (Verso cDNA Synthesis Kit, Thermo scientific) and amplified using StepOnePlus Real-Time PCR system (Applied Biosystems, University Park, IL, USA) with the SYBR® Master Mix (Thermo scientific). Human-specific primers were used to amplify human Toll-like receptor 1–7 (TLR-1-7, 9 and TLR 10), Interleukin-1α (IL-1α,) IL-1β, Tumor Necrosis Factor-α (TNF-α), Interferon-gamma (IFN-ϒ), macrophage colony-stimulating factor (GM-CSF), IL-6, IL-8, IL-10, Matrix MetalloProteinase-2 and −9 (MMP-2/9) and Tissue inhibitor of metalloproteinases (TIMP-1), NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) and Caspase-1.Data were analyzed by using ΔΔCT method with β-actin as the internal control and the expression levels are presented as fold induction in comparison to uninfected cells. All the above experiments were done in triplicates and the data are presented as mean± standard error of mean (SEM).
P2X1: a unique platelet receptor with a key role in thromboinflammation
Published in Platelets, 2021
Few studies indicated that the P2X1 ion channel could contribute to platelet-dependent immune responses during bacterial infection. A first study showed that antagonism of either P2X1 ion channel or P2Y12 receptor inhibited platelet release of microbicidal proteins and kinocidins, thereby mitigating platelet bactericidal activity against Staphylococcus aureus [39]. In a second study, Toll-like receptor 2 (TLR2)-dependent platelet responses involved early P2X1-mediated intracellular calcium increase, TXA2 production and activation of P2Y1 and P2Y12 receptors by ADP [40]. TLR2 forming dimers with TLR1 and TLR6 is essential for the recognition of various bacterial lipoproteins and lipopeptides by immune cells. Interestingly this TLR-induced Ca2+ response is resistant to inhibition by prostacyclin and nitric oxide and thus could occur in the intact circulation [34]. Next, Ilkan et al. demonstrated that the P2X1 ion channel was required for platelet aggregation induced upon stimulation of the FcγRIIa receptor for immunoglobulin G or by Streptococcus sanguinis bacteria [41], further suggesting that platelets could contribute to bacteria sensing and platelet-dependent immune responses via ATP-P2X1 ion channel signaling. Yet, no studies ever investigated the role of P2X1 ion channels in vivo in mouse models of bacterial infection. The respective role of platelet and neutrophil P2X1 ion channels in immune eradication of bacteria remains unknown.
Differential synovial tissue expression of TLRs in seropositive and seronegative rheumatoid arthritis: A preliminary report
Published in Autoimmunity, 2021
Alzahraa Abdelwahab, Sanna Palosaari, Soha Abdelkawy Abdelwahab, Rehab Ahmed Rifaai, Nashwa Fathy El-Tahawy, Entesar Ali Saber, Tomi Nousiainen, Maarit Valkealahti, Johanna Huhtakangas, Tuomo J. Karttunen, Petri Lehenkari
RA develops in a complex interplay between internal and external factors. Especially interesting in the context of RA are the Toll-like receptors (TLRs) that recognize either pathogen-associated molecular patterns expressed by microbial pathogens or damage-associated molecular patterns expressed by stressed cells [7]. More than 13 mammalian TLRs have been identified [8,9]. TLRs are trans-membrane proteins that are found in inflammatory and resident cells [10,11]. TLRs1, 2, 4, 5 and 6 are cell surface receptors that respond to components on the pathogen surface. TLR1 and TLR 6 are hetero-dimers of TLR2, which interacts with bacterial lipoproteins. Lipopolysaccharides are recognized by TLR 4, flagellins by TLR 5, and fungal zymosans by TLRs 2 and 6. In contrast, TLRs 3, 7, 8 and 9 are intracellular receptors present on endosomal membranes and interact with ligands taken up into the endosome. Double-stranded viral RNA is recognized by TLR 3, single-stranded RNA by TLRs 7 and 8, while TLR 9 responds to unmethylated cytosine phosphate guanine “CpG” bacterial DNA and “self-DNA” [7,10–12].