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Acta toxicológica argentina

versión On-line ISSN 1851-3743

Acta toxicol. argent. vol.25 no.1 Ciudad Autónoma de Buenos Aires mayo 2017



Particulate matter inside of the alveolar macrophage

Material particulado dentro del macrófago alveolar


Falcon-Rodriguez, Carlos Ivan1,2,3*; García-Alonso, Larisa Idania2,3; Segura-Medina, Patricia2.

1Posgrado en Ciencias Biológicas, Universidad Nacional Autónoma de México, UNAM. Av. Universidad 3000, Ciudad Universitaria. Delegación Coyoacán. Código Postal 04510. México, Ciudad de México. 2Departamento de Investigación en Hiperreactividad Bronquial, Instituto Nacional de Enfermedades Respiratorias, INER. Dr. Ismael Cosío Villegas, Secretaria de Salud. Calz. de Tlalpan 4502. Col. Belisario Domínguez Sección XVI. Delegación Tlalpan. Código Postal 14080. México, Ciudad de México. 3Facultad de Ciencias, Universidad Nacional Autónoma de México, UNAM. Ciudad Universitaria, Circuito Exterior s/n, Coyoacán, Cd. Univer­sitaria, 04510. Ciudad de México, México.

Recibido: 23 de septiembre de 2016
Aceptado: 25 de mayo de 2017


The inhalation of toxic environmental particles is a worldwide public health issue. To avoid the pulmonary damage, the lungs contain the alveolar macrophages, which are the primary defense of the innate immune system, since it engulfs the toxic or allergic particles. Morphologically, particulate matter inside of macrophage is observed as numerous round dark granules of vari­ous size. In guinea pig, the inhalation of fine particles in real time showed single round dark granules inside of the macrophages. After particles exposure, the alveolar macrophage can activate some cytokines such as TNF-α, IL-1β, IL-6, IL-8, and GM-CSF, which increases the inflammatory response or to activate the Th2 response. The alveolar macrophage interacts with bronchial and bronchiolar epithelium, heart, and blood vessels producing a variety of problems, such as nonfatal heart attacks, irregular heartbeat, decreased lung function, and increases respiratory symptoms such as irritation of the airways, coughing or difficulty breathing, ag­gravated asthma, and produce premature death in people with heart or lung disease.

Keywords: Bronchoalveolar lavage; Phagocytosis; Particulate matter; Air pollution.


La inhalación de partículas tóxicas ambientales es un problema de salud pública en todo el mundo. Para prevenir el daño, los pulmones contienen a los macrófagos alveolares, los cuales son la defensa primaria del sistema inmune, ya que fagocitan los tóxicos o partículas alérgicas. Morfológicamente, el material particulado dentro de los macrófagos alveolares se observa como numerosos gránulos redondos de varios tamaños. En cobayos, la inhalación de partículas finas en tiempo real mostró gránulos re­dondos oscuros dentro de los macrófagos. Después de la exposición a las partículas, el macrófago alveolar puede activar algunas citocinas como TNF-α, IL-1β, IL-6, IL-8, and GM-CSF, las cuales incrementan la respuesta inflamatoria o activan la respuesta Th2. El macrófago alveolar interactúa con el epitelio bronquial y bronquiolar, corazón y vasos sanguíneos, produciendo una variedad de problemas, tales como afecciones cardíacas, arritmias, disminución de la función pulmonar, e incrementa los síntomas res­piratorios como irritación de las vías respiratorias, tos, dificultad para respirar, agrava el asma y produce muertes prematuras en personas con enfermedades cardiacas y pulmonares.

Palabras clave: Lavado broncoalveolar; Fagocitosis; Material particulado; Contaminación atmosférica.


The inhalation of toxic environmental particles is a world-wide public health issue (Hiraiwa and van Eeden 2013). These particles may be made up metals, metalloids, nonmetals, internal transitional elements (Kleeman et al. 1999; Minguillón et al. 2012), sulfate, nitrate, and ammonium ion (Kleeman et al. 1999), or­ganic and elemental carbon (Simoneit et al. 2004), lipids, endotoxins, fungal spores, pol­lens (Monn and Koren 1999) and viruses (Pha­len and Phalen 2012). To avoid the pulmonary damage, the lung presents various cells, the most important is the alveolar macrophage, since is the primary defense of the innate im­mune system, keep the alveolar-blood barrier interface, clearing the air spaces of infectious, and engulfs toxic or allergic particles (Rubins 2003). In the alveolar region, particles whose diameter is >8 μm are phagocytized, this size range is efficient for uptake a bacteria (Pha­len and Phalen 2012). Furthermore, fine par­ticles (>100 nm or >0.1 μm) are also readily phagocytized by alveolar macrophage (Tak­enaka et al. 2001). However, previous studies showed that instilled colloidal carbon particles (30 nm or 0.03 μm) can be present in the mac­rophages (Takenaka et al. 2001). Interestingly, it was evidenced that ultrafine particles small­er than 0.1 μm in diameter are not efficiently phagocytized. This effect is due to their small­er chemical or physical signals. What is certain is that, the macrophage must recognize a cer­tain particles size to initiate engulfment (Phalen and Phalen 2012). Morphologically, particulate matter inside of the macrophage is observed as numerous round dark granules of various size (aggregated) (Gottipolu et al. 2009). This event occurs when agglomerated ultrafine particles are administrated intratracheally or high concentrations are inhaled; then PM is phagocytized by alveolar macrophages. In a guinea pig model, the inhalation during 36 h (4 h/9 days) of fine particles from México City in real time showed single round dark granules inside of the macrophage in the bronchoalveo­lar lavage (Figure 1). Also, the number of the alveolar macrophages increased in the pulmo­nary alveolus in these animals.

Figure 1.
The macrophages in the bronchoalveolar lavage. A) Guinea pigs who inhaled filtered air. B) Guinea pig exposed to fine particles from México City. Green arrows show the fine particles inside of macrophages. 850X. Original images obtained of our research.

After PM exposure, the macrophage is ca­pable of producing pulmonary inflammatory mediators such as TNF-α, IL-1β, IL-6, IL-8, and GM-CSF (Hiraiwa and van Eeden 2013). Human acute exposure of PM showed in­creased levels of IL-1 and IL-6. These cyto­kines are similar to those produces by the al­veolar macrophage exposed to PM both ex vivo and in vivo (Hiraiwa and van Eeden 2013). Mediators such as GM-CSF, IL-1, and IL-6 in­creases the inflammatory response character­ized by an increase in circulating leukocytes, platelets, and proinflammatory and prothrom­botic proteins (Hiraiwa and van Eeden 2013). In sometimes, the alveolar macrophage is activated to “M2 polarization,” which induce Th2 cytokines (IL-4 and IL-13) (Hiraiwa and van Eeden 2013), this response is associated with the allergic disease as asthma. The al­veolar macrophage interacts with bronchial, bronchiolar, and alveolar epithelium, produc­ing a variety of problems, such as aggravated asthma, decreased lung function, as well as, increased respiratory symptoms, as irritation of the airways, coughing or difficulty breath­ing or to increase other pulmonary diseases. Particles also produces heart, and blood ves­sels damage, producing premature death in people with heart disease or nonfatal heart at­tacks, (EPA 2016).


The first author wishes to thank CONACyT for the Ph.D. scholarship #233789, and Posgrado en Ciencias Bi­ológicas, UNAM, for the training received during doctoral stud­ies and to thank the Secretaría de Ciencia y Tecnología (SECITI) of CDMX, grant numbers 014/2014. Authors want to thank to Jonathon Shacat B.A. for his English editing.


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