The Effects of Particulate Matter on C57BL/6 Peritoneal and Alveolar Macrophages

  • Hoda Rahmani ORCID GS PM Department of Immunology, Medicine Faculty, Shahid Beheshti University of Medical Science, Tehran, Iran
  • Somaye Sadeghi ORCID GS PM Department of Immunology, Medicine Faculty, Shahid Beheshti University of Medical Science, Tehran, Iran
  • Niloofar Taghipour ORCID GS PM Department of Tissue Engineering and Applied Cell Science, School of Advanced Technologies in Medicine, Shahid Beheshti University of medical science, Tehran. Iran
  • Mohsen Roshani ORCID GS PM Tehran Air Quality Control Company (AQCC), Tehran, Iran
  • Davar Amani ORCID GS PM Department of Immunology, Medicine Faculty, Shahid Beheshti University of Medical Science, Tehran, Iran
  • Tooba Ghazanfari ORCID GS PM Department of Immunology, School of Medicine, Shahed University of Medical Science, Tehran, Iran
  • Nariman Mosaffa ORCID GS PM Mail Department of Immunology, Medicine Faculty, Shahid Beheshti University of Medical Science, Tehran, Iran
Inflammation, Macrophages, Particulate matter


The presence of ambient particulate matter (PM) poses more dangers to human health than that of other common air pollutants such as Carbon dioxide (Co2) and ozone.  Epidemiologic studies show a direct correlation between PM and the risk of respiratory and cardiovascular diseases. The immune system seems to play a critical role in the process of these diseases. The main goal of this study was to investigate the effect of Tehran particulate matter in two aerodynamic diameters (PM2.5 and PM10) on alveolar macrophages (AM) from C57/BL6 mice. To evaluate the inflammatory effects of PMs, cultured alveolar, and peritoneal macrophages were treated with PM2.5 and PM10 (concentrations of 5 µg/mL and 10 µg/mL). Tumor necrosis factor-alpha (TNF-α) and IL-10 (representatives of inflammatory and anti-inflammatory cytokines, respectively) were assessed in the culture supernatant by ELISA. Expression of arginase and inducible nitric oxide synthase (iNOS) genes was carried out by quantitative real-time PCR. Different functional types of cultured alveolar macrophages (M1, M2) were also determined in this study. Our results suggest that PM2.5 induces M1 inflammatory phenotype in comparison with PM10. We found Also, an increase in TNF-α and M1-related gene expression (iNOS), as well as a decrease in both IL-10 and M2 phenotype genes (Arginase). Moreover, a reduction in phagocytic capacity and increased apoptosis function of macrophage cells were detected. PM2.5 as a major component in hydrocarbons has a considerable effect on polarizing the alveolar macrophages to an inflammatory phenotype and eliciting lung inflammation in mice.


1. Anderson JO, Thundiyil JG, Andrew Stolbach. Clearing the Air : A Review of the Effects of Particulate Matter Air Pollution on Human Health. J Med Toxicol.2012;166–75.
2. Kelly FJ, Fussell JC, Julia C. Size, source and chemical composition as determinants of toxicity attributable to ambient particulate matter. Atmospheric Envir. 2012;60:504–26.
3. Kopf M, Schneider C, Nobs SP. The development and function of lung-resident macrophages and dendritic cells. Nat Immunol. 2014;16(1):36–44.
4. Hussell T, Bell TJ. Alveolar macrophages: plasticity in a tissue-specific context. Nat Rev Immunol. 2014;14(2):81–93.
5. Hiraiwa K, Van Eeden SF. Contribution of lung macrophages to the inflammatory responses induced by exposure to air pollutants. Mediators Inflamm. 2013 2013:10.
6. Miyata R, Eeden SF Van. The innate and adaptive immune response induced by alveolar macrophages exposed to ambient particulate matter. Toxicol Applied Pharmacol, 2011;257:209–26.
7. Pozzi R, De Berardis B, Paoletti L, Guastadisegni C. Inflammatory mediators induced by coarse (PM2. 5–10) and fine (PM2. 5) urban air particles in RAW 264.7 cells. Toxicology. 2003;183(1):243–254.
8. Park E, Roh J, Kim Y, Park K, Kim D, Yu S. PM 2 . 5 collected in a residential area induced Th1-type inflammatory responses with oxidative stress in mice. Envir Res. 2011 111(3):348–55.
9. Beamish LA, Osornio-Vargas AR, Wine E. Air pollution: An environmental factor contributing to intestinal disease. Journal of Crohn’s& Colitis. 2011; 5(4):279–86.
10. Kaplan GG, Hubbard J, Korzenik J, Sands BE, Panaccione R, Ghosh S, et al. The Inflammatory Bowel Diseases and Ambient Air Pollution: A Novel Association. Am J Gastroenterol. 2010;105(11):2412–9.
11. Cassado A, Lima M, Bortoluci K. Revisiting mouse peritoneal macrophages : heterogeneity, development, and function. Front Immunol. 2015;6(21):1–9.
12. Varol C, Mildner A, Jung S. Macrophages : Development and Tissue Specialization. Ann Rev Immunol. 2015;33:643-75.
13. Schins RPF, Lightbody JH, Borm PJA, Shi T, Donaldson K, Stone V. Inflammatory effects of coarse and fine particulate matter in relation to chemical and biological constituents. Toxicol Applied Pharmacol. 2004;195:1–11.
14. Kocbach A, Namork E, Schwarze PE. Pro-inflammatory potential of wood smoke and traffic-derived particles in a monocytic cell line.Toxicology. 2008;247(2–3):123–32.
15. Mosser DM, Edwards JP Exploring the full spectrum of macrophage activation. Nat Rev Immunol. 2009; 8(12):958–69.
16. Xia Zhang, Ricardo Goncalves, and David M. Mosser.The Isolation and Characterization of Murine Macrophages. Curr Protocol Immunol. 2010 1–18.
17. Martinelli N, Olivieri O, Girelli D. Air particulate matter and cardiovascular disease : A narrative review. Eur J Int Med. 2013;24(4):295–302.
18. Sean H Ling, Stephan F van Eeden. Particulate matter air pollution exposure : role in the development and exacerbation of chronic obstructive pulmonary disease. Int J Chron Obstruct Pulmon Dis. 2009;233–43.
19. Happo MS, Jalava PI, Pennanen AS, Salonen RO. Seasonal variation in chemical composition of size-segregated urban air particles and the inflammatory activity in the mouse lung. Inhal Toxicology.2010;22(128):17–32.
20. Tan H, Wang N, Li S, Hong M, Wang X, Feng Y. The Reactive Oxygen Species in Macrophage Polarization : Human Diseases. Oxid Med Cell Longev. 2016; 2016:16.
21. Zhao Q, Chen H, Yang T, Rui W, Liu F, Zhang F, et al. Direct effects of airborne PM 2 .5 exposures on macrophage polarizations. Biochim Biophysica Acta. 2016; 1860(12):2835–43.
22. Murray PJ, Allen JE, Biswas SK, Fisher EA, Gilroy DW, Goerdt S, et al. Perspective Macrophage Activation and Polarization : Nomenclature and Experimental Guidelines. Immunity. 2014; 41(1):14–20.
23. Labranche N, Khattabi C El, Berkenboom G, Pochet S. Effects of diesel exhaust particles on macrophage polarization. Hum Exp toxicol; 2016;1–9.
24. Eeden SF Van, Tan WANC, Suwa T, Mukae H, Terashima T, Fujii T, et al. Cytokines Involved in the Systemic Inflammatory Response Induced by Exposure to Particulate Matter Air Pollutants ( PM 10 ). Am j Res Crit care med. 2001; 164(5):826-30.
25. Turner MD, Nedjai B, Hurst T, Pennington DJ. Cytokines and chemokines : At the crossroads of cell signalling and inflammatory disease. . BiochimicaetBiophysicaActa 2014; 1843(11):2563–82.
26. Soukup JM, Becker S. Human Alveolar Macrophage Responses to Air Pollution Particulates Are Associated with Insoluble Components of Coarse Material, Including Particulate Endotoxin. Toxicology and applied pharmacology, 2001; 26:20–6.
27. Bekki K, Ito T, Yoshida Y, He C, Arashidani K. PM 2.5 collected in China causes inflammatory and oxidative stress responses in macrophages through the multiple pathways. Enviro Toxicology Pharmacol. 2016; 45:362–9.
28. Arhami M, Hosseini V, Shahne MZ, Bigdeli M, Lai A, Schauer JJ. Seasonal trends, chemical speciation and source apportionment of fine PM in Tehran. Atmosph Envir. 2016;12:406.
29. Matsumura F. The significance of the nongenomic pathway in mediating inflammatory signaling of the dioxin-activated Ah receptor to cause toxic effects. Biochem Pharmacol. 2009;77:608–26.
30. Haarmann-stemmann T, Bothe H, Abel J. Growth factors, cytokines and their receptors as downstream targets of arylhydrocarbon receptor (AhR) signaling pathways. Biochem Pharmacol, 2009;77:508–20.
31. Couper KN, Blount DG, Riley EM. IL-10: The Master Regulator of Immunity to Infection. J Immunol. 2008; 180(9):5771-7
32. Rath M, Müller I, Kropf P, Closs EI, Munder M. Metabolism via arginase or nitric oxide synthase : two competing arginine pathways in macrophages. Front Immunol. 2014; 5(475):1–10.
33. Obot CJ, Morandi MT, Beebe TP, Hamilton RF, Holian A. Surface Components of Airborne Particulate Matter Induce Macrophage Apoptosis through Scavenger Receptors Surface Components of Airborne Particulate Matter Induce. Toxicol Applied Pharmacol. 2002; 106:98–106.
34. Montiel-dávalos A, Ibarra-sánchez MDJ, Ventura-gallegos JL, Alfaro-moreno E, López-marure R. Toxicology in Vitro Oxidative stress and apoptosis are induced in human endothelial cells exposed to urban particulate matter. Toxicol Vitro. 2010;24(1):135–41.
35. Li N, Hao M, Phalen RF, Hinds WC, Nel AE. Particulate air pollutants and asthma A paradigm for the role of oxidative stress in PM-induced adverse health effects. Clin Immunol. 2003; 109:250–65.
36. Wang W, Deng Z, Feng Y, Liao F, Zhou F, Feng S, et al. Chemosphere PM 2 . 5 induced apoptosis in endothelial cell through the activation of the p53-bax-caspase pathway. Chemosphere. 2017;177:135–144
37. Li H, Chen R, Meng X, Zhao Z, Cai J, Wang C, et al. Short-term exposure to ambient air pollution and coronary heart disease mortality in 8 Chinese cities. Int J cardiology . 2015;197:265–70.
38. Johard U, Gerde P, Jarstrand C, Lundborg M, and Dahle S. Aggregates of ultrafine particles impair phagocytosis of microorganisms by human alveolar macrophages. Envir Res. 2006; 100:197–204.
39. Wang C, Yu X, Cao Q, Wang Y, Zheng G, Tan TK, et al. Characterization of murine macrophages from bone marrow, spleen and peritoneum. BMC Immunology. 2013;14:6.
40. Kohler B, Moreira AR, Barros T, Castro P De, Ito T, Emı L, et al. Chronic exposure to diesel particles worsened emphysema and increased M2-like phenotype macrophages in a PPE-induced model. PLoSE One. 2020;1–18.
How to Cite
Rahmani H, Sadeghi S, Taghipour N, Roshani M, Amani D, Ghazanfari T, Mosaffa N. The Effects of Particulate Matter on C57BL/6 Peritoneal and Alveolar Macrophages. Iran J Allergy Asthma Immunol. 19(6):647-659.
Original Article(s)