Abstract
Free radicals are important antimicrobial effectors that cause damage to DNA, membrane lipids, and proteins. Professional phagocytes produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) that contribute towards the destruction of pathogens. Toll-like receptors (TLRs) play a fundamental role in the innate immune response and respond to conserved microbial products and endogenous molecules resulting from cellular damage to elicit an effective defense against invading pathogens, tissue injury, or cancer. In recent years, several studies have focused on how the TLR-mediated activation of innate immune cells leads to the production of pro-inflammatory factors upon pathogen invasion. Here, we review recent findings that indicate that TLRs trigger a signaling cascade that induces the production of reactive oxygen and nitrogen species.
Highlights
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are recognized for their dual role as both deleterious and beneficial species
In research on TLR4 overexpressing ovine macrophages, TLR4 initially promoted the production of proinflammatory cytokines TNFα and IL-6 by activating TLR4-mediated interleukin-1 receptor-associated kinase 4 (IRAK4)-dependent NF-κB and mitogen-activated protein kinase (MAPK) (JNK and ERK1/2) signaling
Toll-like receptors (TLRs) act as immune receptors to initiate innate immunity and acquired immunity. They play an important role in the development of oxidative stress in the body
Summary
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are recognized for their dual role as both deleterious and beneficial species. The salutary effects of ROS/RNS occur at low/moderate concentrations in cellular responses, including in defense against infectious agents, in the function of a number of cellular signaling pathways, and the induction of a mitogenic response [1]. Neutrophils, monocytes, and macrophages are the most prominent immune cell types that release various pro- and anti-inflammatory mediators for both host defense and inflammatory responses [4]. Oxidation intermediates are essential activators of oxidative stress This is because low levels of free radicals, including ROS and RNS, form a stressful oxidative environment that can clear invading pathogens and maintain physiological homeostasis [5]. There have been a significant number of discoveries regarding how the TLR-mediated activation of innate immune cells leads to the production of pro-inflammatory factors upon pathogen invasion. We discuss recent research findings on TLR activities, with a particular focus on TLR-mediated signaling pathways that are activated during nitroxidative stress
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