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Li, C.;  Tsai, M.;  Chiou, H.(.;  Lin, Y.;  Liao, W.;  Hung, C. Heavy Metals for Macrophage Polarization in Asthma. Encyclopedia. Available online: https://encyclopedia.pub/entry/31663 (accessed on 11 May 2024).
Li C,  Tsai M,  Chiou H(,  Lin Y,  Liao W,  Hung C. Heavy Metals for Macrophage Polarization in Asthma. Encyclopedia. Available at: https://encyclopedia.pub/entry/31663. Accessed May 11, 2024.
Li, Chung-Hsiang, Mei-Lan Tsai, Hsin-Ying (Clair) Chiou, Yi-Ching Lin, Wei-Ting Liao, Chih-Hsing Hung. "Heavy Metals for Macrophage Polarization in Asthma" Encyclopedia, https://encyclopedia.pub/entry/31663 (accessed May 11, 2024).
Li, C.,  Tsai, M.,  Chiou, H.(.,  Lin, Y.,  Liao, W., & Hung, C. (2022, October 27). Heavy Metals for Macrophage Polarization in Asthma. In Encyclopedia. https://encyclopedia.pub/entry/31663
Li, Chung-Hsiang, et al. "Heavy Metals for Macrophage Polarization in Asthma." Encyclopedia. Web. 27 October, 2022.
Heavy Metals for Macrophage Polarization in Asthma
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This entry is adapted from the peer-reviewed paper 10.3390/ijms232012337

Asthma is a chronic inflammatory airway disease characterized by variable airflow obstruction, bronchial hyper-responsiveness, and airway inflammation. The chronic inflammation of the airway is mediated by many cell types, cytokines, chemokines, and inflammatory mediators. Research suggests that exposure to air pollution has a negative impact on asthma outcomes in adult and pediatric populations. Air pollution is one of the greatest environmental risks to health, and it impacts the lungs’ innate and adaptive defense systems. A major pollutant in the air is particulate matter (PM), a complex component composed of elemental carbon and heavy metals. According to the WHO, 99% of people live in air pollution where air quality levels are lower than the WHO air quality guidelines. This suggests that the effect of air pollution exposure on asthma is a crucial health issue worldwide. Macrophages are essential in recognizing and processing any inhaled foreign material, such as PM. Alveolar macrophages are one of the predominant cell types that process and remove inhaled PM by secreting proinflammatory mediators from the lung.

asthma air pollution particulate matter heavy metals macrophages

1. Macrophage Polarization in Asthma

Asthma is a common, complex respiratory disease that is characterized by recurrent symptoms of wheeze, cough, chest tightness, and dyspnea. There is growing evidence of environmental triggers that exacerbate the disease, especially inhaled agents such as allergens, pollutants, and viruses [1]. Depending on the microenvironment of the lung, macrophages can change their gene expression to two polarized macrophage profiles, M1 (proinflammatory) and M2 (anti-inflammatory) [2]. These cells play important roles in the protection against various respiratory pathogens, partly by tightly regulated NLRP3 inflammasome-dependent mechanisms [3]. In animal models, it was revealed that the mostly immunosuppressive function of AMs in airway allergies is partially mediated by CD40, TNF-α, PGE2, and the secretion of exosomes and may be defective in asthmatic patients [4][5]. The depletion of resident AMs led to significant worsening of allergic airway inflammation in mice [6]. The bronchial macrophages in asthmatic patients expressed less CD16 and CD64 and showed decreased phagocytic activities and anti-inflammatory capabilities [7]. The activated M2 macrophages were proposed to mediate type 2 immunity. However, their exact contribution to disease pathogenesis is still under investigation [8]. Importantly, some experiments also demonstrated a proinflammatory role for AMs in the context of allergic airway inflammation. In mouse models, AMs were found to be significant sources of IL-17, and their depletion prevented the development of allergic inflammation and airway hyper-responsiveness [9]. Moreover, the researchers previously used a new macrophage marker, PM-2K, to analyze the association of macrophage polarization in the peripheral blood with the severity of adult and childhood asthma. The researchers found that PM-2K+ macrophages were significantly lower, particularly the CD14−PM-2K+ subset and M2b (PM-2K+CCR7−CD86+) cells, in subjects with poor lung function compared to normal subjects and asthmatics with normal lung function, whereas the frequency of fibrocytes was higher in asthmatics, and the M2b subset distributions were significantly different in subjects with varying severities [10]. In contrast, the PM-2K+CD14+ but not PM-2K+CD14− was lower in asthmatic children than in healthy children. In asthmatic children, the M2a (CCR7−CXCR1+), M2b (CCR7−CD86+), and M2c (CCR7−CCR2+) subsets, but not M1 (CCR7+CD86+), were higher in asthmatic children than in healthy children. Significantly, the percentage of the M2c subset was positively associated with asthmatic children requiring hospitalization during exacerbations. It was demonstrated that macrophage polarization is involved in the pathogenesis of adult and childhood asthma and is a potential biomarker of asthma disease severity [11].

2. Effects of Heavy Metals on Macrophage Polarization

The composition of PM is complicated. It mostly contains elemental and organic carbons, heavy metals, sulfates with nitrate, and other components [12]. Earlier immunotoxicology studies focused on the influence of PM on health, as it was considered the most important component in air pollutants. However, other components in the PM may also participate in this adverse effect. It has been found that coexposure to particulate-depleted diesel exhaust and allergens dampened lung function via increased NO2 despite the absence of the particulate component [13][14]. There is growing evidence that heavy metals adsorbed to PM are crucial to the toxicity and adverse health effects of PM [15][16]. Heavy metals, as significant chemical components in PM, come from either natural sources or human sources such as industrial production, residential heating, automobile exhaust emissions, and so on [17]. The WHO published guidelines for air quality in 2000 that reported that the major heavy metals in PM included lead (Pb), vanadium (V), arsenic (As), manganese (Mn), nickel (Ni), cadmium (Cd), and chromium (Cr(VI)) [18]. In this research, the researchers focus on effects of Pb, Cd, As, Ni, and Cr (VI) on macrophage polarization. The alterations of macrophage-related cytokines after heavy metal exposure are shown in Table 1.
Table 1. The changes in macrophage-related cytokines and surface markers after exposure to heavy metals.
Pollutants M1 Phenotype M2 Phenotype
Lead (Pb) IL-1β ↑ (C) [19] CD206 ↑ (A) [20]
  IL-6 ↑ (C) [19] TGF-β1 ↑ (A) [20]
  MHC class II ↑ (A) [20]  
  IL-8 ↑ (C) [21]  
  IFN-γ ↓ (C,A) [22]  
  IL-12p40 ↓ (A) [22]  
Vanadium (V) CXCL-2 ↑ (C) [23]  
  TNF-α ↓ (C) [24]  
  IL-6 ↑ (A) [25]  
  IFN-γ ↑ (A) [25]  
Arsenic (As) TNF-α ↑ (C) [26] CD206 ↑ (C) [27]
  IL-1α ↑ (C) [28] CD163 ↑ (C) [27]
  IL-8 ↑ (C) [26] IL-10 ↑ (C) [27]
  IL-12 ↑ (C) [28] CCL-18 ↑ (C) [27]
  CXCL2 ↑ (C) [29][30] TGF-β1 ↑ (C) [27]
  CD86 ↓ (C) [28] CCL-22 ↑ (C) [29][30]
Manganese (Mn) IL-1β ↑ (C) [31]  
  IL-6 ↑ (C) [31]  
  IL-8 ↑ (C) [31]  
  TNF-α ↑ (C) [31]  
  IFN-γ ↑ (C) [31]  
Nickel (Ni) IL-2 ↑ (A) [32]  
  IL-6 ↑ (A) [32]  
  IL-12 ↑ (A) [32]  
  IFN-γ ↑ (A) [32]  
  TNF-α ↑ (A) [32]  
  CCL-2 ↑ (A) [33]  
Cadmium (Cd) IL-1β ↑ (C) [34]  
  TNF-α ↑ (C) [34], ↓ (C,A) [35]  
  CXCL2 ↑ (C) [34], ↓ (A) [35]  
  IL-6 ↓ (C,A) [35]  
  IL-8 ↓ (C) [35]  
  CXCL-9 ↓ (C) [35]  
  CXCL-10 ↓ (C) [35]  
  CXCL-11 ↓ (C) [35]  
  CCL-5 ↓ (C) [35]  
Chromium (Cr)(VI) TNF-α ↓ (C) [36]  
  IFN-γ ↑ (H) [37]  
Note: (A) indicates experimental results from animal models; (C) indicates experimental results from cell models; and (H) indicates experimental results from human subjects; ↑ indicates increased the level of cytokines or mediators; ↓ indicates decreased the level of cytokines or mediators.

2.1. Lead (Pb)

Lead (Pb) is found naturally in the environment as well as in manufactured products. According to the U.S. Environmental Protection Agency, the major sources of lead in the air are ore and metal processing and piston-engine aircraft operating on leaded aviation fuel. From 1980 to 2014, the concentration of Pb in the air decreased by about 98% due to one reason: the removal of lead from motor vehicle gasoline. Because of the waste incinerators, utilities, and lead–acid battery manufacturers, lead is still an air pollutant [38]. Previously, studies suggested that Pb could result in impaired macrophage functions, including decreased chemotactic activity and phagocytosis ability in animal studies [22]. Recently research has indicated that 5 or 10 μg/dL Pb can increase the inflammation-related genes COX-1 and COX-2 and the concentrations of thromboxane B2, prostaglandin E2 (PGE-2), and proinflammatory cytokines (IL-1β and IL-6) in the human monocyte cell line THP-1 [19]. In a mouse study involving exposure to environmentally relevant concentrations of Pb (6 μg/dL), bone-marrow-derived macrophages (BMDM) were used to investigate the effects of Pb on inflammation and anti-inflammation. They found that Pb could reduce NO production and increase major histocompatibility complex class II (MHC II) expression but could not affect the production of the proinflammatory cytokines TNF-α and IL-1β or CD86 expression in LPS/IFN-γ stimulated BMDM. In contrast, Pb increased TGF-β1 and mannose receptor (CD206) expression in IL4/IL-13-stimulated BMDM. This might explain the susceptibility to allergic diseases reported in subjects exposed to Pb [20]. Another study used THP-1-derived macrophages to evaluate the cellular effects of Pb nanoparticles. They showed that Pb decreased mitochondrial activity and ROS production but increased LDH release and the production of the proinflammatory cytokine IL-8. They also indicated that Pb nanoparticles were stronger immune inducers than a Pb(NO3)2 solution. These results suggest that the inhalation of Pb nanoparticles may cause pulmonary inflammation [21].

2.2. Vanadium (V)

Vanadium (V) a widely distributed and fairly abundant element in the Earth’s crust and is commonly used to manufacture tools, orthopedic implants, and machinery due to its hardness, ability to form alloys, and high resistance to corrosion. The total emission of V is estimated to be between 71,000 and 210,000 tons per year worldwide [39]. In a previous study, the authors used 5 μg/mL sodium metavanadate (NaVO3) to observe the inflammatory effect in the RAW 264.7 macrophage cell line. The results showed that NaVO3 could increase CXC chemokine macrophage inflammatory protein-2 (MIP-2/CXCL-2) mRNA expression in a dose-dependent manner, and the expression could be suppressed by an antioxidant N-acetylcysteine treatment. These results indicated that NaVO3 induced CXCL-2 mRNA expression via increased oxidative stress [23]. Cohen et al. studied the effect of ammonium metavanadate (NH4VO3) and vanadium pentoxide (V2O3) on murine macrophage-like cells. The results indicated that V suppressed TNF-α production but increased prostaglandin E2 (PGE2) production [24]. The other study by Cohen et al. used the V-exposed rats to examine the inflammation effects. After 2 mg V/m3 (as NH4VO3) for 8 h/d for 4 d, the rats received an intratracheal (it) instillation of polyinosinic.polycytidilic acid (poly I:C) or saline, and bronchoalveolar lavage fluid (BALF) was collected for cytokine determination. The levels of IL-6 and IFN-γ in BALF were increased by V exposure alone, but TNF-α and IL-1 were not affected. The BALF IL-6 and IFN-γ levels were significantly increased by the poly l:C induced in the poly l:C and V coexposure groups. However, V-exposed rats produced significantly less cytokines when the cytokine levels were calculated with total lavaged protein [25].

2.3. Arsenic (As)

Arsenic (As) is generally released into the environment from various natural sources such as volcanic eruptions and forest fires. Several studies have been published on the health effects of arsenic in water. However, more As is released into the atmosphere due to human activities such as coal burning and industrial waste disposal with industrial development [40]. Therefore, it is suggested that atmospheric As is a high-ranking health risk to the respiratory system.
In As-exposed (0.5 mg/kg/body weight sodium arsenite solution) Swiss albino mice, researchers gave an intravenous injection of Staphylococcus aureus and collected and cultured blood at different intervals after injection. Compared with the control group, few bacteria from the blood of As-exposed mice were still cultured, which showed slower clearance. In addition, the splenic macrophages from As-exposed mice showed reduced adhesion and migration index values [41]. After As stimulation, the adherent ability and surface marker CD86 were reduced [28], but the amount of apoptosis/necrosis in primary human monocyte-derived macrophages increased [26]. The production of NO, IL-1α, IL-8, IL-12, and TNF-α in As-induced primary human monocyte-derived macrophages was markedly higher than in the untreated group [26][28]. Emilie Bourdonnay et al. reported that As could increase CCL-22 and CXCL2 in human primary monocyte-derived macrophages, which was reversed by an N-acetylcysteine treatment. This demonstrated that arsenic alters macrophage gene expression through redox-sensitive signaling pathways [29][30]. Another study revealed that As could increase M2 markers and CD206 and CD163 expression in THP-1-derived M2 macrophages. In addition, IL-6, IL-10, TGF-β, and CCL-18 were significantly increased in As-induced THP-1-derived M2 macrophages [27].

2.4. Manganese (Mn)

Manganese (Mn), an essential trace element in humans, is naturally present in many foods and is available as a dietary supplement. However, industrial processes such as welding, mining, smelting, battery manufacturing, and steel production can lead to high Mn release into the environment from dust particles containing Mn [42].
Matlou I. Mokgobu et al. used primary human monocyte-derived macrophages to investigate the effects of MnCl2 on immune responses as a potential mechanism of MnCl2 toxicity. They found that 100 μM MnCl2 could significantly increase the inflammatory cytokines IL-1β, IL-6, IL-8, TNF-α, and IFN-γ and intracellular H2O2 production in primary human monocyte-derived macrophages. MnCl2-induced IL-6 and IL-8 were partially inhibited by p38 MAPK and NF-κB inhibitors but were abolished entirely by dithiothreitol ROS scavenger treatment. This suggested that MnCl2 causes increased primary monocyte-derived macrophage inflammatory cytokine production through oxidative stress activation [31].

2.5. Nickel (Ni)

Nickel (Ni), one of the ferromagnetic elements, is naturally present in the Earth’s crust. Due to its unique physical and chemical properties, Ni is used in a wide variety of metallurgical processes such as alloy production, electroplating, batteries, and as a catalyst in the chemical and food industries. In all stages of manufacturing, recycling, and disposal, Ni unavoidably causes pollution in the environment [43].
In a previous study, researchers found that lung inflammation and fibrosis were significantly increased, but the counts of macrophages in bronchoalveolar lavage fluid (BALF) from Ni-nanoparticle-exposed mice were significantly decreased after 21 days of exposure. The CCL-2 concentration in BALF was significantly increased in Ni-nanoparticle-exposed mice [33]. In contrast, Katherine A. Roach et al. used fine NiO particles (NiO-F, 181 nm) and ultrafine particles (NiO-UF, 42 nm) to expose BALB/cJ mice and evaluated the effect of NiO on allergies. The lactate dehydrogenase, total cells, and levels of IL-6, IFN-γ, and TNF-α in BALF from NiO-UF-exposed mice were significantly increased compared to the NiO-F-exposed or control groups after 10 days of NiO exposure. In NiO-UF-exposed mice with OVA challenge, the levels of IFN-γ and IL-2 in both BALF and serum, IL-6 in BALF, and IL-12p40 in serum were significantly increased compared to the OVA control groups. These findings demonstrated that the NiO surface area correlates best with acute pulmonary injury and inflammation following respiratory exposure [32].

2.6. Cadmium (Cd)

Cadmium (Cd), a metal belonging to group IIB of the periodic table, is emitted into the environment due to natural activities such as volcanic activity. However, anthropogenic activities also release Cd pollution into the environment, including tobacco smoking, the combustion of fossil fuels, waste incineration, and releases from tailings piles and municipal landfills [44]. Marit Låg et al. used cadmium acetate to treat rat alveolar macrophages and evaluated the effect of Cd-induced lung toxicity. In low concentrations of Cd (3 μM) treatment, the expression of IL-1β, IL-6, and TNF-α mRNA was significantly decreased after 10 h of stimulation. However, the protein production of MIP-2, IL-1β, and TNF-α was significantly increased by 10 μM Cd treatment for 20 h, but the levels of IL-6 were not affected by the different doses of Cd (1, 3, 6, and 10 μM) [34]. In another study, they used a human monocyte cell line, THP-1, and THP-1-derived macrophages to investigate the effect of Cd on macrophage immune function. They found that Cd significantly increased IL-6 and TNF-α production in THP-1 cells but significantly decreased IL-6, IL-8, and TNF-α production in THP-1-derived macrophages. In Cd-exposed mice, BALF macrophages were significantly increased compared to the control group. However, the levels of IL-6, CXCL-2, and TNF-α in lipopolysaccharide-induced BALF were significantly decreased in Cd-exposed mice compared to the control group. They also found that Cd suppressed M1-related cytokine gene expression, including CXCL-9, CXCL-10, CXCL-11, and CCL-5. These results revealed that Cd exposure prior to an endotoxin challenge impaired the capacity of macrophages to elicit a proper immune response [35].

2.7. Chromium (Cr(VI))

Chromium (Cr) is the 17th most abundant element in the Earth’s mantle and is formed naturally as chromite in ultramafic and serpentine rocks. However, the environmental contamination of Cr has increased in recent years due to it being widely used in industry for plating, alloying, the tanning of animal hides, the inhibition of water corrosion, textile dyes and mordants, pigments, ceramic glazes, and refractory bricks.
Induced nitric oxide (NO) production is an important function of macrophages. Tian and Lawrence studied the effects of different metals, including chromium, and reported that chromium does not affect NO production by cytokine-stimulated (IFN-γ and TNF-α) murine macrophages. Chromium also showed a suppressed effect on inducible NO synthase expression, which suggests that it may directly modify enzyme or cofactor activity [45]. In addition to the impaired production of NO, an in vitro experiment showed that Cr also impaired the phagocytosis of bovine macrophages [46]. Jain and Kannan reported that the decreased TNF-α secretion in U937 monocytes due to chromium stimulation was mediated by its antioxidative effect [36]. The exposure of urban women to chromium from vehicular traffic affects their immune function. Serum IgE and the production of IL-4 and IFN-γ by mononuclear blood cells were increased in urban women who were exposed to vehicular traffic [37]. Several studies have investigated the effects of prostheses on the cytokine responses of the body. A previous study examined the effects of CoCr alloy particles on basic biological responses, including cell proliferation, apoptosis, cytokine mRNA expression, and protein secretion, in the J774A.1 murine macrophage cell line. The results indicated that the levels of TNF-α, IL-1α, IL-6, and IL-12 in the supernatant were not significantly different between the control group and cells stimulated with CoCr. A change in the metabolic activity of J774A.1 cells was only observed with higher concentrations of CoCr particles [47].

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Subjects: Allergy
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Chung-Hsiang Li
,
Mei-Lan Tsai
,
Hsin-Ying (Clair) Chiou
,
Yi-Ching Lin
,
Wei-Ting Liao
,
Chih-Hsing Hung
View Times: 424
Revisions: 2 times (View History)
Update Date: 31 Oct 2022
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