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ISSN : 1226-7155(Print)
ISSN : 2287-6618(Online)
International Journal of Oral Biology Vol.51 No.2 pp.9-15
DOI : https://doi.org/10.11620/IJOB.2026.51.2.9

Low-dose fine particulate matter induces inflammatory responses in primary macrophages and increases systemic nitric oxide production in mice

Hye Young Mun1, Septika Prismasari1,2, Jung Yun Kang1*
1Department of Dental Hygiene, College of Health Sciences, Yonsei University, Wonju 26493, Republic of Korea
2Department of Preventive and Community Dentistry, Faculty of Dentistry, Universitas Gadjah Mada, Yogyakarta 55281, Indonesia
*Correspondence to: Jung Yun Kang, hannahkang@yonsei.ac.krhttps://orcid.org/0000-0003-3725-8868
March 13, 2026 April 10, 2026 April 13, 2026

Abstract


Airborne fine particulate matter (FPM) is a major environmental health threat associated with inflammatory responses. Although previous studies have reported FPM-induced inflammation in macrophage cell lines, the effects of FPM on primary bone marrow-derived macrophages (BMMs) and systemic nitric oxide metabolite (NOx) levels have not been fully characterized. This study evaluated whether low-dose FPM exposure induces inflammatory responses in vitro and in vivo. BMMs isolated from ICR mice were treated with FPM (0.0–12.5 µg/mL), and proinflammatory cytokine production was measured by enzyme-linked immunosorbent assay. For in vivo assessment, mice were administered FPM (7.5 mg/kg) by intraperitoneal injection under short-term exposure conditions, and serum NOx levels were quantified using the Griess assay. Exposure to FPM at 6.25 and 12.5 µg/mL significantly increased tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 production by BMMs compared with the control group (p < 0.05). In vivo, serum NOx levels were also significantly elevated in FPM-exposed mice compared with the control group (p = 0.026), consistent with results observed in the lipopolysaccharide-treated positive control group (p = 0.004). These findings suggest that low-dose transient FPM exposure activates innate immune cells and induces systemic inflammatory responses, supporting the potential role of FPM in the pathogenesis of inflammatory diseases.


Particulate matter , Macrophages , Inflammation , Nitric oxide , Cytokines

초록

    © The Korean Academy of Oral Biology. All rights reserved.

    This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

    Introduction

    Fine particulate matter (FPM) with an aerodynamic diameter of ≤2.5 μm is widely recognized as a serious global public health threat. FPM is primarily absorbed through the respiratory tract, where it can reach the alveoli and subsequently enter the bloodstream. During this process, FPM can stimulate the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which promote the release of pulmonary inflammatory mediators and contribute to the initiation or exacerbation of various diseases [1]. Although the cardiovascular and respiratory systems have been the most extensively studied target organs of FPM exposure, its toxic effects are not limited to these systems. Increasing evidence suggests that FPM can also exert toxic effects on multiple organs, including the kidneys, nervous system, gastrointestinal tract, and reproductive system [1,2].

    Inflammatory responses induced by FPM are largely mediated by innate immune cells, particularly macrophages. The inflammation and oxidative stress triggered by FPM exposure are primarily initiated and propagated through epithelial cells and innate immune cells, including neutrophils, monocytes, and macrophages. In macrophages, multiple molecular mechanisms have been implicated in this response, including inflammatory signaling pathways, chemokine signaling pathways, cytokine–cytokine receptor interactions, and mitogen activated protein kinase (MAPK) signaling pathways [3,4]. In fact, FPM treated alveolar macrophages have been shown to exhibit increased production of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, along with elevated CD80 mRNA expression, indicating polarization toward the pro-inflammatory M1 phenotype [5]. Such macrophage mediated inflammatory responses are closely associated not only with local tissue damage but also with the persistence of systemic inflammatory conditions [6].

    However, most previous studies have primarily focused on the effects of high concentrations of FPM, and the evidence regarding whether low dose FPM exposure can induce inflammatory responses in innate immune cells remains limited [7]. In particular, few studies have simultaneously evaluated whether cellular inflammatory responses translate into systemic inflammation. Although macrophage mediated propagation of low grade inflammation has been proposed as a key pathological mechanism underlying FPM exposure, integrated investigations examining this process at both the cellular and organismal levels remain scarce [8,9].

    Therefore, the present study aimed to evaluate whether low dose FPM exposure can induce inflammatory responses using both cellular and animal models. In the in vitro experiments, bone marrow-derived macrophages (BMMs) were treated with different concentrations of FPM to examine changes in the secretion of pro-inflammatory cytokines, TNF-α, IL-1β, and IL-6. In the in vivo experiments, serum nitric oxide metabolites (NOx) levels were measured in mice following repeated intraperitoneal administration of FPM to evaluate the potential induction of systemic inflammatory responses. The findings of this study are expected to provide evidence supporting the activation of innate immune responses and the potential induction of systemic inflammation following low dose FPM exposure.

    Materials and Methods

    1. Experimental animals and reagents

    Six-week-old male ICR mice were obtained from KOATECH and maintained under controlled conditions with a 12 hours light/dark cycle, temperature, and humidity until use. FPM was purchased from the National Institute of Standards and Technology (NIST SRM 2786). Lipopolysaccharide (LPS; Escherichia coli 0111:B4; EMD Millipore) was dissolved in phosphate buffered saline (PBS; Welgene) immediately prior to use. Macrophage colony stimulating factor (M-CSF; PeproTech) was used for the culture of BMMs. In addition, fetal bovine serum (FBS), penicillin–streptomycin, and trypan blue (0.4%) were purchased from Gibco-BRL, and minimum essential medium alpha modification (α-MEM) was obtained from Cytiva-HyClone.

    2. Experimental design

    All animal experiments were approved by the Institutional Animal Care and Use Committee of Yonsei University (approval number: YWCI-202308-015-02). All animals used in this study received appropriate humane care, including measures to minimize pain and distress. Six-week-old male mice were randomly assigned to three groups based on body weight: a control group (PBS, 10 mL/kg, n = 5), an FPM treated group (7.5 mg/kg, n = 5), and an LPS treated group (5 mg/kg, n = 4). Each substance was administered by intraperitoneal injection (i.p.) every three days from day 0 to day 15, and all mice were sacrificed on day 19.

    The i.p. was selected to provide reproducible and controlled systemic exposure the short-term experimental period. Although this route does not replicate direct inhalation exposure, it is commonly used in particulate matter toxicology to examine extrapulmonary and systemic biological effects after circulation-mediated distribution [10,11]. Thus, i.p. administration was considered appropriate for the present study, which was designed to evaluate early systemic inflammatory and tissue responses rather than localized respiratory toxicity. The FPM dose (7.5 mg/kg) used in this study was selected as a relatively low experimental dose compared with those doses used in previous particulate matter studies designed to induce more overt toxic or inflammatory responses [12,13]. This dose was chosen to evaluate early biological changes and low-grade inflammation rather than acute severe toxicity. Likewise, the in vitro FPM concentrations also set at relatively low levels to maintain consistency with the in vivo dosing and to allow more coherent interpretation across cellular and organismal responses.

    3. Cell culture

    BMMs were isolated from the femurs and tibias of 6 week old male ICR mice. Bone marrow cells were obtained using Histopaque density gradient centrifugation and cultured according to previously established methods [14]. The isolated cells were cultured in α-MEM complete medium supplemented with 10% FBS and 1% penicillin–streptomycin, in the presence of M-CSF (30 ng/mL). The culture medium was replaced every two days.

    For experiments, BMMs were seeded in 96 well plates at a density of 5 × 104 cells/well, treated with FPM (0, 3.125, 6.25, and 12.5 μg/mL), and incubated at 37°C in a humidified atmosphere containing 5% CO2.

    4. Enzyme-linked immunosorbent assay

    BMMs treated with FPM (0, 3.125, 6.25, and 12.5 μg/mL) or PBS were cultured for 3 days, and the cell culture supernatants were collected. The secretion levels of TNF-α, IL-1β, and IL-6 were quantified using enzyme-linked immunosorbent assay (ELISA) kits (R&D Systems) according to the manufacturer’s instructions. The absorbance was measured at 450 nm using a microplate reader (SpectraMax® ABS; Molecular Devices).

    5. Measurement of serum nitric oxide metabolites

    Blood samples were directly collected from the hearts of mice. The collected blood was centrifuged at 4,000 rpm for 10 minutes at 4°C to obtain serum. Prior to nitric oxide (NO) measurement, serum samples were subjected to protein precipitation. Serum was mixed with acetonitrile (Sigma-Aldrich) at a 1:1 (v/v) ratio, followed by centrifugation to collect the supernatant. Subsequently, chloroform (Sigma-Aldrich) was added to the supernatant at twice the sample volume, thoroughly mixed, and centrifuged. The aqueous phase was then collected for further analysis.

    Total NOx were quantified using a Griess Reagent System (Promega). To convert nitrate (NO3−) to nitrite (NO2−), vanadium(III) chloride (Sigma-Aldrich) was added to the samples prior to the Griess reaction. The reaction product was measured at an absorbance of 540 nm using a microplate reader (SpectraMax® ABS). Total NOx concentrations were calculated based on a standard curve generated with sodium nitrite (NaNO2).

    6. Statistical analysis

    All data are presented as mean ± standard deviation. The normality of the data distribution was assessed using the Shapiro–Wilk test. As the assumption of normality was satisfied, one-way analysis of variance (ANOVA) was performed to evaluate differences among the experimental groups, followed by Tukey’s post hoc test for multiple comparisons. Changes in body weight among groups were analyzed using two-way repeated measures ANOVA. All statistical analyses and graphical representations were performed using GraphPad Prism 8 software (GraphPad Software Inc.). Statistical significance was defined as *p < 0.05, **p < 0.01, and ***p < 0.001.

    Results

    1. Low dose fine particulate matter exposure promotes inflammatory cytokine secretion in innate immune cells

    To evaluate the effects of low dose FPM on inflammatory responses in innate immune cells, BMMs were exposed to FPM, and the changes in pro-inflammatory cytokine production were analyzed. The results showed that TNF-α secretion was significantly increased in the 6.25 and 12.5 µg/mL FPM treated groups compared with the control group (p < 0.001, Fig. 1A). For IL-1β, a significant increase was observed at 6.25 µg/mL (p = 0.016), and the elevated level was also maintained at 12.5 µg/mL (p = 0.002, Fig. 1B). Similarly, IL-6 levels were significantly increased in the 6.25 and 12.5 µg/mL FPM treated groups compared with the control (p = 0.002 and p < 0.001, respectively, Fig. 1C). These findings suggest that even low concentrations of FPM are sufficient to activate inflammatory responses in macrophages.

    2. Low dose fine particulate matter exposure induces systemic inflammatory response in mice

    To evaluate whether low dose FPM exposure induces systemic inflammatory responses, mice were subjected to repeated i.p. administration of FPM for a short period. The body weights of all mice remained within the normal range, and no significant differences in body weight changes were observed among the groups (Fig. 2A).

    Serum levels of NOx were measured to assess systemic inflammatory responses. The results showed that serum NOx levels were significantly increased in the FPM treated group compared with the control group. Similarly, a significant increase in NOx levels was also observed in the LPS treated positive control group (p = 0.026 and p = 0.004, respectively, Fig. 2B). NO is a major inflammatory mediator produced during inflammatory responses, and increased serum NOx levels are indicative of the induction of systemic inflammation. These findings suggest that even short-term exposure to low dose FPM can trigger systemic immune activation and inflammatory responses.

    Discussion

    In this study, both in vitro and in vivo mouse models were employed to evaluate whether the selected FPM exposure induces inflammatory responses at the cellular and systemic levels. In the in vitro experiments, treatment of BMMs with increasing concentrations of FPM resulted in significant increases in TNF-α, IL-1β, and IL-6 at concentrations of 6.25 and 12.5 µg/mL. This dose-dependent increase reflects the classical activation (M1 polarization) of macrophages induced by FPM exposure. Notably, no significant increase in cytokine production was observed at 3.125 µg/mL, whereas all three cytokines showed significant elevation at 6.25 µg/mL or higher concentrations. These findings indicate that the pro-inflammatory effects of FPM emerge above a certain threshold concentration and highlight the need for further studies to determine the threshold level of FPM required to trigger inflammatory responses. FPM exposure induces oxidative stress, inflammatory responses, and immune activation, and cytokines such as IL-6 and TNF-α have been recognized as potential biomarkers of exposure and inflammation [15]. In particular, these pro-inflammatory cytokines contribute to the persistence of systemic inflammatory states beyond local inflammatory responses, and circulating IL-6, TNF-α, and IL-1β are associated with cardiovascular diseases and neurodegenerative disorders [16-18].

    The observed increase in serum NOx levels suggests that FPM exposure may induce systemic inflammatory responses beyond localized cellular inflammation. The in vitro and in vivo experiments were designed to assess cellular and systemic inflammation, respectively; accordingly, pro-inflammatory cytokines were measured in BMMs, whereas serum NOx was measured in mice. The present data thus provide complementary evidence of inflammation at both the cellular and systemic levels, though a direct correlation between these markers was not established. In the present study, NOx was measured because NO itself is highly reactive and short-lived in vivo, whereas its stable oxidative metabolites, nitrite and nitrate, provide a practical indirect indicator of inflammatory NO production. In inflammatory conditions, pro-inflammatory cytokines such as TNF-α and IL-1β can activate NF-κB signaling and induce inducible nitric oxide synthase (iNOS), thereby increasing NO generation and its downstream metabolites [19]. In addition, these cytokines may further interact with oxidative stress pathways, contributing to sustained systemic inflammatory responses, oxidative stress amplification, and endothelial dysfunction [20,21].

    Previous studies have reported that FPM exposure promotes endothelial dysfunction, atherosclerosis, and systemic inflammation through multiple mechanisms, including increased oxidative stress, activation of immune-mediated inflammatory pathways, and stimulation of the autonomic nervous system. Consequently, FPM exposure is associated with the development and progression of various cardiovascular diseases, including heart failure, myocardial infarction, and stroke [22]. In the present study, serum NOx levels were elevated in the FPM-treated group, and a similar direction of change was also observed in the LPS-treated group. However, because only NOx was assessed in vivo, this result should not be interpreted as evidence that the overall inflammatory effect of FPM is comparable to that of LPS. Rather, the present findings indicate that low-dose FPM is sufficient to elicit a measurable systemic inflammatory response under the current experimental conditions.

    Pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 have previously been reported to influence bone metabolism by modulating osteoclast differentiation and bone resorption pathways [23-27]. Given these previous reports, the observed increases in TNF-α, IL-1β, IL-6, and serum NOx levels in this study may reflect an inflammatory environment potentially relevant to FPM-associated osteoclast activation and bone loss. However, because no bone-related experiments were conducted in the present study, this possible link remains hypothetical and should be interpreted as a potential implication or future research direction rather than a direct conclusion of this work. Future studies incorporating bone-related endpoints will be required to determine whether the inflammatory changes observed here translate into alterations in bone metabolism.

    In summary, the present study demonstrates that low-dose FPM exposure increases pro-inflammatory cytokine secretion in innate immune cells and elevates serum NOx levels in mice. These results indicate the induction of inflammatory responses at both the cellular and systemic levels. These findings highlight the immunological risks associated with low-dose FPM exposure and suggest that it may have broader systemic inflammatory implications.

    However, the present study is limited by the experimental design, which involved short-term IP administration of FPM. Furthermore, the use of different inflammatory markers in vitro and in vivo precluded the establishment of a direct correlation between cellular cytokine responses and systemic NO-related changes. In addition, because no bone-related parameters were evaluated, the potential relevance of these inflammatory changes to bone metabolism remains hypothetical. Further studies are required to determine whether chronic inhalation exposure to FPM leads to sustained inflammation and tissue damage, and to evaluate matched inflammatory markers, such as serum cytokines, tissue iNOS expression, or cellular NOx levels, to better define the relationship between local and systemic inflammatory responses.

    Funding

    This work was supported by the National Research Foundation of Korea (NRF) grants funded by the Korean government (2022R1G1A1004843).

    Acknowledgements

    All figures are developed by the authors.

    Conflicts of Interest

    No potential conflict of interest relevant to this article was reported.

    Figure

    IJOB-51-2-9_F1.jpg

    Fine particulate matter (FPM) activates bone marrow-derived macrophages (BMMs) to produce pro-inflammatory cytokines. BMMs were treated for 3 days in the presence of M-CSF (30 ng/mL) stimulation. (A) TNF-α, (B) IL-1β, and (C) IL-6 protein levels in cell culture media of BMMs were analyzed by ELISA. Bars represent mean ± SD.

    M-CSF, macrophage colony stimulating factor; TNF-α, tumor necrosis factor-α; IL, interleukin; ELISA, enzyme-linked immunosorbent assay; SD, standard deviation; Control, phosphate buffered saline.

    *p < 0.05, **p < 0.01, ***p < 0.001 vs. Control.

    IJOB-51-2-9_F2.jpg

    Effects of fine particulate matter (FPM) exposure on body weight and serum NOx levels in mice. ICR mice were randomly assigned to three groups: Control (10 mL/kg, n = 5), FPM (7.5 mg/kg, n = 5), and LPS (5 mg/kg, n = 4), and each substance was administered via intraperitoneal injection every 3 days. All mice were sacrificed on day 19. (A) Body weight changes were monitored throughout the experiment and expressed as a percentage of the initial body weight. No significant differences were observed among groups (two-way RM ANOVA, p = 0.329). (B) Serum NOx levels were measured using the Griess reagent assay. Data are presented as mean ± SD.

    NOx, nitric oxide metabolite; LPS, lipopolysaccharide; RM ANOVA, repeated measures analysis of variance; SD, standard deviation; Control, phosphate buffered saline.

    *p < 0.05, **p < 0.01 vs. Control.

    Table

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