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Koushki, K.; Shahbaz, S.K.; Keshavarz, M.; Bezsonov, E.E.; Sathyapalan, T.; Sahebkar, A. Multifaceted Roles of Gold Nanoparticles. Encyclopedia. Available online: https://encyclopedia.pub/entry/49411 (accessed on 18 May 2024).
Koushki K, Shahbaz SK, Keshavarz M, Bezsonov EE, Sathyapalan T, Sahebkar A. Multifaceted Roles of Gold Nanoparticles. Encyclopedia. Available at: https://encyclopedia.pub/entry/49411. Accessed May 18, 2024.
Koushki, Khadijeh, Sanaz Keshavarz Shahbaz, Mohsen Keshavarz, Evgeny E. Bezsonov, Thozhukat Sathyapalan, Amirhossein Sahebkar. "Multifaceted Roles of Gold Nanoparticles" Encyclopedia, https://encyclopedia.pub/entry/49411 (accessed May 18, 2024).
Koushki, K., Shahbaz, S.K., Keshavarz, M., Bezsonov, E.E., Sathyapalan, T., & Sahebkar, A. (2023, September 20). Multifaceted Roles of Gold Nanoparticles. In Encyclopedia. https://encyclopedia.pub/entry/49411
Koushki, Khadijeh, et al. "Multifaceted Roles of Gold Nanoparticles." Encyclopedia. Web. 20 September, 2023.
Multifaceted Roles of Gold Nanoparticles
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This entry is adapted from the peer-reviewed paper 10.3390/biom11091289

Gold nanoparticles (GNPs) have been recently applied for various diagnostic and therapeutic purposes. The unique properties of these nanoparticles (NPs), such as relative ease of synthesis in various sizes, shapes and charges, stability, high drug-loading capacity and relative availability for modification accompanied by non-cytotoxicity and biocompatibility, make them an ideal field of research in bio-nanotechnology. Moreover, their potential to alleviate various inflammatory factors, nitrite species, and reactive oxygen production and the capacity to deliver therapeutic agents has attracted attention for further studies in inflammatory and autoimmune disorders. Furthermore, the characteristics of GNPs and surface modification can modulate their toxicity, biodistribution, biocompatibility, and effects. 

gold nanoparticles autoimmune diseases

1. Introduction

The immune system is a complex network including immune cells and molecules that protect against various infections and diseases. However, sometimes the immune system loses its self-tolerance following specific conditions. This leads to the immune system attacking and damaging multiple tissues in the body and eventually leading to autoimmune disorders (Ads). These diseases are characterized by the improper activation of excessive and pathological immune responses to self-antigens, a specific organ or tissue in the absence of any tissue or cell injury, toxins exposure, or microbial attack [1]. The prevalence of autoimmune diseases is increasing [2]. The most common ADs include systemic lupus erythematosus (SLE), type 1 diabetes (T1DM), rheumatoid arthritis, psoriasis, multiple sclerosis (MS), celiac disease (CD), and inflammatory bowel diseases (IBD).
Although the exact etiology of many autoimmune diseases remains unknown, most studies suggest that it has probably genetic factors combined with environmental and epigenetic factors resulting in the breakdown of immune system homeostasis, contributing to the development of autoimmune diseases [3][4]. Among the environmental factors, three significant socioeconomic status-related factors are assumed to drive these conditions, including infections, ecology, and nutrition [5]. Unfortunately, there has been a considerable increase in the global frequency and the prevalence of ADs in the West over the last decades. This is due to notable changes in lifestyle habits such as diet and eating habits, environmental and occupational exposure to a high degree of air pollutants, and infectious disease (ID) [6]. It is estimated that AD affects around 5–7% of the global population. The prevalence is rising globally, with an onset often during adulthood nearby 40–50 years of age. ADs also have a higher incidence in women compared with men [7][8]. According to the National Institute of Health (NIH) reports, about 23.5 million people in the USA suffered from ADs and are among the top 10 leading causes of mortality in females aged up to 64 years. In addition, approximately 10 percent of the adult population in European countries was diagnosed with AD in 2018 [2][9]. The economic and societal burden of ADs results in a high medical cost for providing patient care, and relapsing AD conditions often result in reduced quality of patient life. The estimated annual cost of patients treated with ADs is approximately 100 billion dollars. Moreover, standard treatments are not very sufficient and commonly cause various unwanted side effects [10].
The application of nanoparticles (NPs) for modulating the immune system is currently an attractive field. Increasingly, some metal nanoparticles, mainly gold nanoparticles (GNPs), are used to manage various medical conditions because of their unique properties. GNPs with unique optical and chemical properties are attractive metal nanoparticles in the nanoscience field. They are most frequently applied in different biomedical purposes due to their stability, biocompatibility, and inert nature. Additionally, studies have shown that GNPs exhibit anti-inflammatory and anti-oxidant properties. Therefore, they are characterized as active therapeutic agents to diagnose and treat different ADs such as T1D, RA, and IBD. Since some nanocomposites and nanomaterials are immunomodulatory or immunotoxic, a comprehensive review of the interactions between nanomaterials and the immune system would be greatly useful to the design of various research studies. This research aims to outline the interactions of immune systems with GNPs and drugs-based GNPs in managing different ADs. Researchers discussed the toxicity, anti-inflammatory, and antioxidative potential of GNPs and subsequently selected and reviewed various investigations of GNP-based drugs and their potential as therapeutic applications in ADs.

2. Pathogenesis of Autoimmune Diseases

Autoimmune disease results from dysregulation of the immune system and losing tolerance, which leads to excessive and pathologic innate and adaptive immune responses against cellular or organ-specific self-antigens, subsequently resulting in tissue destruction and dysfunction through inducing inflammation and injury in affected systems [1]. The hyper-activation of the innate immune responses and failure in T- and B-cell repertoire selection or a failure to regulate activated T- and B-cells can trigger the initiation of autoimmunity in susceptible individuals. In addition, the presence of autoreactive B- and T-cells several years before the appearance of clinical diseases indicates that multiple triggers could act sequentially to promote disorders [4]. Autoimmune inflammations are directed by cognate interactions between antigen-presenting cells (APCs) and self-reactive T-cells [11]. In this regard, although immune tolerance is induced by presenting self-peptide–MHC (pMHC) complexes by APCs to non-inflammatory lymphocyte cells in steady-state, the recognition and engagement of pMHC by autoreactive lymphocyte cells in the context of inflammation lead to the activation of T- and B-cell and autoimmune disorders [12][13][14]. Therefore, the main purpose of autoimmune therapeutic strategies is to promote tolerance through targeting APC–autoreactive cells interaction. Furthermore, despite the essential role of dendritic cells (DCs) and maybe macrophages (MQs), especially in the initial activation of autoreactive T- and B-cells, evidence suggests cognate T/B-cell interactions are vital in this event. Some studies via elimination of T-cell populations using thymectomy and or anti-T-cell antibodies have shown the vital roles of cellular immunity in the development of some ADs marked by autoantibody production, and B-cell dysregulation is supposed to play a key role [15][16]. Eventually, T- or B-cell genetic knockouts revealed that both cell subsets are required to develop certain autoimmune diseases such as SLE [17][18].
Overall, these mechanisms and affected organs via autoimmunity are broadly varied. For example, in multi-organ ADs such as RA, inflammation is mainly localized to the joints following immune cell infiltration of the synovial membrane [19]. This category generally involves a strong autoantibody (Th2) component. However, in organ-specific cases, autoinflammatory responses occur against a specific organ such as T1DM, which destroys β-islet cells of the pancreas and eventually leads to insulin deficiency [20]. Similarly, autoimmune diseases of the gastrointestinal (GI) tract seen in IBDs subsets, including ulcerative colitis (UC) and Crohn’s disease (CD) [21], are generally T-cell-mediated (Th1 or Th17 subsets) processes [22]. Furthermore, some cases such as MS exhibit both systemic and organ-specific characteristics. For example, MS is characterized by inflammation in the brain and spinal cord, resulting in axon and myelin damage, which results in central nervous system disturbance [23].

3. The Role of Inflammation and Inflammatory Cytokines in Autoimmune Disorders 

Inflammation serves as a first line of physiological defense against tissue injury and infection. Unfortunately, these inflammatory responses continue in some chronic conditions and result in significant tissue or organ injury. These unusual and unregulated inflammatory responses are closely related to various autoimmune disorders, such as inflammatory bowel disease (IBD), rheumatoid arthritis (RA), diabetes, systemic lupus erythematosus (SLE), and gout [21][24][25][26]. However, the exact pathogenesis of inflammation in many autoimmune disorders has remained somewhat unknown. Therefore, increasing our knowledge of various regulating mechanisms of inflammation can lead to many remarkable clinical approaches to treating autoimmune diseases.
As mentioned before, inflammatory responses mediated by T-cells have been identified as having crucial roles in developing autoimmune disorders. Recently, many studies have shown that abnormal immune responses of T-cells, including Th1, Th2, Th17, Th22, and T-Reg cell responses, have a pivotal role in developing inflammation in autoimmune disorders [27]. The enhanced activity of CD4+ T-helper lymphocytes is one of the most common pro-inflammatory phenotypes in ADs. Three major types of CD4+ T-helper subsets are significant in this respect: Th1, Th2, and Th17 cells. As a general rule, the cell-mediated processes and dominant Th1 and their cytokines such as IL-2 and interferon-gamma (INF-γ) are involved in organ-specific ADs [28][29]. In contrast, severe humoral (antibody-based) responses and elevated Th2 cytokines levels such as IL-4, IL-5, and IL-10 are typically related to multisystem ADs [28][29]. Additionally, the Th2 responses usually lead to the exacerbation of fibrosis in many ADs by higher induction of macrophages [30]. In addition, the Th17, via producing IL-23 as a neutrophil chemotactic and activating factor phenotype, contributes to the genesis of ADs [31]. Generally, both Th17 and Th1 cells are generated parallel based on overlapping only partly in their functions [32][33]. Significantly, Th17 cells can direct ADs in the absence of a concomitant Th1 immune response [34].
In addition to T-cells, various other immune cells including B-cells are also involved in developing autoimmune diseases. The different B-cell subsets play multifaceted roles in autoimmune diseases [35]. It has been shown that the B-cells, often via the production of antibodies, play a deleterious role in developing autoimmune diseases [36]. Additionally, regulatory B-cells (Bregs) have received a great deal of attention for suppressing inflammation by repressing differentiation of the Th1 and Th17 immune responses in the development of autoimmune disorders [37]. It is important to state that B-cell subtypes and their antibody production and mechanisms are very diverse. The characteristics and effects of autoantibody-secreting plasma cells depend on their tissue localization. On the other hand, innate immune cells such as monocyte and macrophage cells have been considered major regulators in the inflammation of the liver and other organs. A study by H. Li et al. demonstrated that M1-polarized macrophages could promote generating hepatic progenitor cells (HPC) with the self-renewing phenotype, which is associated with activation of the Notch signaling HPCs in primary sclerosing cholangitis [38]. Toll-like receptors (TLRs) are a group of pattern recognition receptors (PRRs) that play a crucial role in the innate immune response [39], which by activating the innate immune cells play a key role in developing autoimmune diseases. APCs, particularly DCs, are crucially involved in autoimmunity disorders through their capability in priming and activation of autoreactive T-cells and subsequently breaking immune tolerance [40]. Moreover, it has been shown that human amnion mesenchymal cells (hAMC) could be promising cells for MS therapy via reducing inflammation and developing remyelination in EAE models [41].

4. Clinical Management of Autoimmune Disorders

There is a lack of sufficient knowledge about the etiologies of different ADs. Therefore, the current clinically relevant treatments are focused on symptom management and control of disease to reduce the number of relapsing events [42][43][44] until the detection of effective targeted therapies. For example, the application of insulin for T1DM patients to maintain blood glucose homeostasis [42][43][45] or the use of tear and saliva replacements as the main treatment of Sjögren’s syndrome (SS) patients, accompanied by supplemental medications to address additional complications. Recently, biological therapies such as proteins and antibodies have been developed as an alternative option to treating ADs, such as modulating the expression of tumor necrosis factor-alpha (TNF-α) used to manage patients with IBDs [46][47]. Interferon-beta (IFN-β) also is widely used in the management of MS [48]. However, these biological drugs are only effective in some of the patients [49]. As a result, the next generation of ADs therapies should focus on precise medical approaches to dampen disease-propagating agents’ effects rather than relieve the symptoms as they arise.
Recently, NPs have shown many advantages in treating inflammatory and autoimmune diseases, which offer some innovative strategies to improve the therapeutic efficacy compared to traditional therapies. Numerous studies have indicated that NP-based drug delivery could enhance the treatment efficacy in comparison to current therapies through more specific targeting of infected tissues than normal, which significantly reduces prescribed drug dosage and reduces drug adverse side effects. The NPs also could improve the bioavailability and pharmacokinetics of therapeutic agents. Furthermore, the functionalization of the NP surface with diverse immunomodulators and antigens can optimize their functions by delivering coordinated messages into the immune system. Therefore, NP-based therapies are promising agents to transform a multifaceted program for the pharmaceutical industry.

5. Gold Nanoparticles, Characterization, and Immune Stimulation

Gold nanoparticles (GNPs) are attractive NPs with unique physical, chemical, and optical properties in nanotechnology and bio-nanotechnology fields. Due to many advantageous and unique properties of GNPs, such as easy and controllable fabrication, high stability, oxidation resistance, water-solubility, plasmon resonance, high surface reactivity, high drug-loading capacity, low cytotoxicity, and cost–benefits, they have been widely investigated and have shown potential applications in various engineering, chemistry, and biomedical fields [50][51]. In particularly, GNPs have become one of the ideal metal nanomaterials for medical purposes because of their biocompatibility and inert nature. In addition, GNPs offers other therapeutic options than traditional gold salts, such as radiotherapy enhancement due to the preferential absorption of x-rays via high-atomic-number GNPs [52].
Apart from numerous advantages, easily functionalization of GNPs with different molecules can offer entirely new therapeutic options for combination therapy [52] and also combined therapy and diagnostics (theranostics). It has been demonstrated that GNPs are an efficient carrier with a controllable release for diverse therapeutic agents such as antineoplastic medications [53], antioxidants [54], antibiotics [55], proteins [56][57], nucleic acids [58], and glucose [59]. The nanospheres and nanorods shapes of GNPs are the most-favored gold structures that have been investigated for biomedical purposes due to their well-characterized synthesis. In addition, GNPs offer other therapeutic options than traditional gold salts, such as radiotherapy enhancement due to the preferential absorption of x-rays via high-atomic-number GNPs [52]. Therefore, the GNPs’ functionalization with various therapeutic and targeting led to further growth of their applications. Wide successful usage of GNPs in many biomedical fields such as diagnostics [60], therapeutics and vaccine development [60][61], drug, gene delivery and imaging [58][62], and electrochemical biosensors [63] has been obtained through controlling the size and shape of these particles via using proper synthesis as well as modifying through suitable functionalizing groups.
The continuous rise in utilization of GNPs has increased considerations of the safety and toxicity of these NPs for possible toxicological effects. It has been evident that the cytotoxic effects of GNPs are nearly zero or at least significantly less than other NPs such as silver NPs [64]. Several studies have demonstrated that GNPs are nontoxic to mice and humans [65][66]. Non-toxic effects of 12.5 nm GNPs have been shown in the lungs, liver, spleen, kidneys, or brain [67]. However, an in vitro study showed a size-dependent toxic impact of GNP has occurred for 1.4 nm GNP but not for 15 or 0.8 nm GNP [68]. Another study in human cells has shown that GNPs are non-toxic in 250 nanometer sizes and rejected their toxicity. It has been indicated that GNPs’ toxicity increased by decreasing the diameter of NPs [69]. Chen et al. showed that GNPs with 3, 5, 50, and 100 nm (8 mg/kg/week, for three weeks) did not show any cytotoxicity and harmful effects, while 8–37 nm GNPs showed cytotoxicity effects. Interestingly, they indicated that the surface modification of the GNPs with peptides significantly ameliorated this toxicity and was associated with their ability to induce an antibody response [70]. A subsequent study in the same condition by Reeves et al. [67] showed that different doses (40, 200, and 400 μg/kg/day, for eight days) of 12.5 nm diameter GNPs did not produce any toxicity and side effects in various organs of mice. In line with this finding, another study has shown that functionalized GNPs with 13–20 nanometer diameters do not cause acute side effects [71]. Therefore, it is supposed that dosage and surface modification of GNPs are other important factors of GNPs’ cytotoxicity.
In addition to size and shape, surface modification of NPs is another important factor that can impact the biocompatibility and toxicity of GNPs, which are still being explored. It has been shown that 20 nm diameter gold nanospheres covered with mercaptopropane sulfonate have nontoxic effects on the human keratinocyte cell line, but 16.7 and 43.8 nm diameter gold nanorods functionalized with PEG could induce ROS production significantly and upregulate expression levels of genes related to cellular stress and toxicity proposing. Therefore, it seems that GNP modifications play a crucial role in GNP-mediated cellular response [72]. On the other hand, various results demonstrate that tissue distribution and accumulation of GNPs is size-dependent, and the smallest nanoparticles show the most widespread organ distribution [73][74]. For example, it has recently been shown that 50 nm diameter GNPs are more permeable to cells and more effectively accumulate into the tumor after a single IV administration. Conversely, larger GNPs were fundamentally concentrated in and around blood vessels and the periphery of the spherical tumor, preventing their deep penetration into tumors [75]. Additionally, biodistribution studies reported that PEG-GNPs with 5 and 10 nm sizes accumulate in the liver, and 30 nm diameter GNPs accumulated in the spleen, while 60 nm diameter GNPs did not significantly accumulate in mice organs. These data suggest that the toxicity of PEG-GNPs is complicated, and it cannot be concluded that smaller particles have more significant toxicities and vice versa [76]. Besides size and shape, surface modification of NPs is another important factor that can impact the biocompatibility and toxicity of GNPs. It has been reported that although 20 nm diameter gold nanospheres covered with mercaptopropane sulfonate have nontoxic effects in the human keratinocyte cell line, 16.7 and 43.8 nm diameter gold nanorods functionalized with PEG could significantly induce ROS production and upregulate expression levels of genes related to cellular stress and toxicity proposing. Therefore, it seems that GNPs modifications play a crucial role in GNP-mediated cellular response [72]. Moyano et al. [77] demonstrated the importance of hydrophobicity of engineered GNPs in immune system activation in vitro and in vivo.
Collectively, the main determinative characteristics of GNPs, including size, shape, chemical composition, surface properties and modifications, and environmental impact, could modify biodistribution, cytotoxicity, and biocompatibility of GNPs, which still need to be further evaluated. It has to be noted that although the zerovalent of GNPs can be a valuable alternative, replacing the potential of metallic gold [78], their intracellular uptake and subsequent responses could vary according to their particle characterization. Hence, a detailed assessment of the interaction between GNPs or GNP–biomolecule conjugates and the immune system can be crucial for estimating both unintended and intended effects of their applications.

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Subjects: Medicine, Research & Experimental
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Khadijeh Koushki
,
Sanaz Keshavarz Shahbaz
,
Mohsen Keshavarz
,
Evgeny E. Bezsonov
,
Thozhukat Sathyapalan
,
Amirhossein Sahebkar
View Times: 308
Entry Collection: Biopharmaceuticals Technology
Revisions: 2 times (View History)
Update Date: 20 Sep 2023
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