Int J Sports Med 2018; 39(02): 133-140
DOI: 10.1055/s-0043-121147
Immunology
© Georg Thieme Verlag KG Stuttgart · New York

Exercise Performed Concomitantly with Particulate Matter Exposure Inhibits Lung Injury

Adriano Silva-Renno
Nove de Julho University (UNINOVE), Laboratory of Pulmonary and Exercise Immunology (LABPEI) and Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), Sao Paulo, Brazil
,
Guilherme Crisitanini Baldivia
Nove de Julho University (UNINOVE), Laboratory of Pulmonary and Exercise Immunology (LABPEI) and Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), Sao Paulo, Brazil
,
Manoel C. Oliveira-Junior
Nove de Julho University - UNINOVE, MSc and PhD Program in Rehabilitation Sciences and MSc in Medicine, São Paulo, Brazil
,
Maysa Alves Rodrigues Brandao-Rangel
Nove de Julho University (UNINOVE), Laboratory of Pulmonary and Exercise Immunology (LABPEI) and Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), Sao Paulo, Brazil
,
Elias El-Mafarjeh
Nove de Julho University (UNINOVE), Laboratory of Pulmonary and Exercise Immunology (LABPEI) and Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), Sao Paulo, Brazil
,
Marisa Dolhnikoff
School of Medicine, Sao Paulo University, Pathology, Sao Paulo, Brazil
,
Thaís Mauad
School of Medicine, Sao Paulo University, Pathology, Sao Paulo, Brazil
,
Jôse Mára Britto
Pathology (LIM 5), Universidade de Sao Paulo Faculdade de Medicina, Sao Paulo, Brazil
,
Paulo Hilário Nascimento Saldiva
Pathology, University of Sao Paulo, São Paulo, Brazil
,
Luis Vicente Franco Oliveira
Nove de Julho University (UNINOVE), Laboratory of Pulmonary and Exercise Immunology (LABPEI) and Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), Sao Paulo, Brazil
,
Ana P. Ligeiro-Oliveira
Nove de Julho University - UNINOVE, MSc and PhD Program in Rehabilitation Sciences and MSc in Medicine, São Paulo, Brazil
,
Gustavo Silveira Graudenz
Nove de Julho University (UNINOVE), Laboratory of Pulmonary and Exercise Immunology (LABPEI) and Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), Sao Paulo, Brazil
,
Rodolfo Paula Vieira
Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), School of Medical Sciences of São José dos Campos Humanitas and Universidade Brasil, Laboratory of Pulmonary and Exercise Immunology (LABPEI), São José dos Campos, Brazil
› Author Affiliations
Further Information

Correspondence

Prof. Rodolfo Paula Vieira
Brazilian Institute of Teaching and Research in Pulmonary
and Exercise Immunology (IBEPIPE)
School of Medical Sciences of São José dos Campos
Humanitas and Universidade Brasil
Laboratory of Pulmonary and Exercise Immunology (LABPEI)
Rua Pedro Ernesto 240
12245-520, São José dos Campos
Brazil   
Phone: +55/12/3303 8390   
Fax: +55/12/3303 8390   

Publication History



accepted 19 September 2017

Publication Date:
21 November 2017 (eFirst)

 

Abstract

Air pollution is a growing problem worldwide, inducing and exacerbating several diseases. Among the several components of air pollutants, particulate matter (PM), especially thick (10–2.5 µm; PM 10) and thin (≤2.5 µm; PM 2.5), are breathable particles that easily can be deposited within the lungs, resulting in pulmonary and systemic inflammation. Although physical activity is strongly recommended, its effects when practiced in polluted environments are questionable. Therefore, the present study evaluated the pulmonary and systemic response of concomitant treadmill training with PM 2.5 and PM 10 exposure. Treadmill training inhibited PM 2.5- and PM 10-induced accumulation of total leukocytes (p<0.001), neutrophils (p<0.001), macrophages (p<0.001) and lymphocytes (p<0.001) in bronchoalveolar lavage (BAL), as well as the BAL levels of IL-1beta (p<0.001), CXCL1/KC (p<0.001) and TNF-alpha (p<0.001), whereas it increased IL-10 levels (p<0.05). Similar effects were observed on accumulation of polymorphonuclear (p<0.01) and mononuclear (p<0.01) cells in the lung parenchyma and in the peribronchial space. Treadmill training also inhibited PM 2.5- and PM 10-induced systemic inflammation, as observed in the number of total leukocytes (p<0.001) and in the plasma levels of IL-1beta (p<0.001), CXCL1/KC (p<0.001) and TNF-alpha (p<0.001), whereas it increased IL-10 levels (p<0.001). Treadmill training inhibits lung and systemic inflammation induced by particulate matter.


#

Introduction

Air pollution is a growing problem worldwide, inducing and exacerbating several diseases [12] [18]. Air pollution is composed of a combination of solid particles with different aerodynamic diameters and of toxic gases [17]. The most common pollutants found in the atmosphere are the particulate matter (PM) and the gases ozone (O3), sulfur dioxide (SO2), carbon monoxide (CO) and nitrogen oxide (NOx) [17]. Among these several components of air pollutants, particulate matter (PM), especially thick (10–2.5 µm, PM 10) and thin (≤2.5 µm, PM 2.5), are breathable particles that easily can be deposited into the lungs, resulting in pulmonary and systemic inflammation [18]. The aerodynamic diameter of the particles is particularly important because their deposition in different regions of the lungs is finely related to particle size as well as to mortality [12] [17]. The deposition of PM in the respiratory tract, which as the respiratory system’s line of defense has a large surface area, can cause injury and result in an impaired immune response [13]. This impaired immune response of the respiratory tract can be mediated by an increase in oxidative stress, apoptosis, and a release of pro-inflammatory mediators, which are mediated by hyperactivation of transcription factors such as nuclear factor kB (NF-kB) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) [13].

Although air pollution can induce a microenvironment for development of several diseases, it represents a serious health risk especially for susceptible individuals [12]. In this way, situations that could increase the exposure and potentiate deposition of air pollutants into the lungs should be avoided [20]. Therefore, although physical activity is strongly recommended for all its well-known health benefits, its effects when practiced in polluted environments are questionable [3] [5] [8] [16]. For instance, although Jacobs et al. (2010) demonstrated that acute cycling in an air-polluted area results in impaired systemic inflammatory response, Giles et al. (2014) demonstrated that different exercise intensities can result in different responses when practiced in polluted areas [3] [5]. On the other hand, a mouse experimental study showed that chronic exercise during diesel exhaust particle (DEP) exposure significantly inhibits the DEP-induced inflammatory response [16].

The present study investigated for the first time the pulmonary and systemic inflammatory response to low-intensity aerobic exercise performed concomitantly with two different particulate matter exposures, PM 2.5 and PM 10.


#

Material and Methods

This study was approved by the review board for human and animal studies of the School of Medicine of the University of São Paulo and by Nove de Julho University (1225/09). The study was conducted ethically in accordance with international standards and as required by the International Journal of Sports Medicine [4].

Particulate matter 2.5 (PM 2.5) and 10 (PM 10) collection and separation

The particulate matter was collected in polycarbonate filters and separated by particle size (PM 2.5 and PM 10) using a gravimetric collector. After separation, PM 2.5 and PM 10 were suspended in 0.9% NaCl at a final concentration of 1 mg/mL.


#

Animals and experimental protocol

Forty-eight male C57Bl/6 mice (6–8 weeks age) were obtained from the Central Animal Facility of the School of Medicine of the University of Sao Paulo and maintained in the Animal Facility of Nove de Julho University, under controlled conditions of humidity, temperature and luminosity. The animals were distributed into six groups (n=8 in each group) as follows: Control (non-exercised and non-PM-instilled), Exercise (Exe; exercised and non-PM-instilled), PM 2.5 (non-exercised and PM 2.5-instilled), PM 10 (non-exercised and PM 10-instilled), PM 2.5+Ex (exercised and PM 2.5-instilled) and PM 10+Ex (exercised and PM 10-instilled).

Each mouse received 10 μL PM 2.5 or PM 10 by nasal drop instillation, and non-PM groups received only the vehicle (0.9% NaCl) [16]. For exercised groups, the animals received the nasal drop instillation 10 min after the beginning of treadmill training to simulate the pollutant’s inhalation during exercise. The instillations were administered 5x/week during the 5 weeks of the experimental protocol [16].

Before the beginning of treadmill training, the animals were adapted to the treadmill for rodents (Super ATL, Inbramed, RS, Brazil) during 3 consecutive days (15 min, 25% inclination, 0.2 km/h) [16]. After that, a maximal exercise capacity test was performed to allow us to determine the intensity of exercise training, which was set to low intensity, corresponding to 50% of maximal exercise capacity reached in the initial test [16]. Treadmill training was performed 5x/week, 60 min per session, for 5 weeks. A final exercise test was performed 24 h before the animals’ euthanasia [16].


#

Pulmonary inflammation

Pulmonary inflammation was assessed through the total and differential cellular counting in bronchoalveolar lavage (BAL) and by quantitative image analysis of the number of polymorphonuclear (PMN) and mononuclear (MN) cells in the lung parenchyma and in the peribronchial space [9] [14] [15] [16].

For BAL collection and analysis, mice were cannulated and the lungs gently washed for 3 times by using 0.5 mL of phosphate-buffered saline (PBS) [9] [11]. The volume collected was centrifuged and the supernatant stored at −80°C for cytokine analysis [9] [11]. The cell pellet was resuspended in 1 mL of PBS and the cells were counted using a hematocytometer (Neubauer chamber, Carl Roth GmbH, Karlsruhe, Germany) [9] [11]. An aliquot of the resuspended cell pellet was used to prepare cytospin slides, which were stained with Diff Quick (Medion Diagnostics, Düdigen, Switzerland), and 300 cells were counted, in a blinded fashion for the group description, using the hematological criteria [9] [11].

For quantitative histological analysis, the lungs were removed in block and fixed in 10% formalin for 24 h and then submitted to histological routine. Four micrometer thick slides were stained with hematoxylin and eosin and the number of PMN and MN cells was counted in the lung parenchyma and in the peribronchial space. The results were expressed as the number of cells/mm2 of lung tissue for lung parenchyma [9] [15] [16] and the number of cells/mm2 of peribronchial area. All lungs of all mice from all experimental groups were used; 15 random fields of lung parenchyma were assessed [9] [15] [16] and 5 peribronchial spaces were assessed at 400x magnification [14].


#

Pulmonary and systemic cytokines

The supernatant of bronchoalveolar lavage (BAL) and the plasma were used to quantify the levels of IL-1beta, CXCL1/KC, IL-10 and TNF-alpha by ELISA, according the manufacturer’s instructions (R&D Systems, MN, USA) [9] [16].


#

Statistical analysis

Graph Pad Prism 5.0 software was used to perform the statistical analysis and to build the graphs. The one-way analysis of variance was applied followed by a Bonferroni post hoc test for comparison between the groups for all data because all data presented parametric distribution. All data were presented as mean ± standard error (SE). Furthermore, a multivariate ANOVA was used to better understand and interpret the effects of exercise, PM 2.5 and PM 10 alone and in combination, and whether these variables influence each other.


#
#

Results

Particulate matter (PM) exposure did not inhibit physical capacity development in mice

[Fig. 1] shows the initial and final time for the physical test. The results demonstrated that all groups submitted to exercise improved exercise capacity, demonstrated by increased time during the treadmill physical test, independently of exposure to PM. On the other hand, non-exercised mice did not present any improvement in exercise capacity. In addition, the multivariate ANOVA analysis revealed that exercise training significantly increased exercise capacity (F=52,153, p<0.03), whereas PM 2.5 and PM 10 did not affect exercise capacity significantly. Furthermore, no interaction between exercise and particulate matter (both PM 2.5 and PM 10) was observed.

Zoom Image
Fig. 1 Comparison between initial and final time of treadmill physical test in each group. ** p<0.01 when final versus initial time compared for Exe, PM 2.5+Exe and PM 10+Exe groups. Data are presented as mean ± standard error.

#

Low-intensity treadmill training inhibits particulate matter-induced pulmonary inflammation

[Fig. 2] shows the inflammatory profile in BAL ([Fig. 2a–d]) and the levels of cytokines in BAL ([Fig. 2e–h]). The results demonstrated that chronic exposure to PM 2.5 and to PM 10 resulted in an increased number of total cells in BAL [PM 2.5 (p<0.001) and to PM 10 (p<0.001)] compared to the Control, Exe, PM 2.5+Exe and PM 10+Exe groups ([Fig. 2a]). Similarly, chronic exposure to PM 2.5 and to PM 10 resulted in an increased number of neutrophils ([Fig. 2b]), macrophages ([Fig. 2c]) and lymphocytes ([Fig. 2d]) in BAL [PM 2.5 (p<0.001) and PM 10 (p<0.001)] compared to the Control, Exe, PM 2.5+Exe and PM 10+Exe groups. Multivariate ANOVA analysis showed that aerobic training in PM 2.5- and PM 10-exposed mice respectively reduced the particulate matter-induced increases in the number of total cells (F=54,352, p<0.000; F=37,189, p<0.000); neutrophils (F=35,213, p<0.000; F=44,049, p<0.000), macrophages (F=33,631, p<0.000; F=30,040, p<0.000) and lymphocytes (F=8,334, p<0.008; F=20,162, p<0.000) in BAL. Concerning a possible interaction between exercise and particulate matter PM 2.5 and PM 10, no interaction effects between PM and exercise were observed. These results reinforce the pro-inflammatory effects of PM and also the protective and anti-inflammatory effects of low-intensity aerobic exercise.

Zoom Image
Fig. 2 Lung inflammation evaluated through the bronchoalveolar lavage (BAL). For a–g, ***p<0.001 when compared with all other groups. For h, *p<0.05 when compared with all other groups. Data are presented as mean ± standard error.

The results also demonstrated that chronic exposure to PM 2.5 and to PM 10 resulted in the increased release and accumulation of pro-inflammatory cytokines IL-1β ([Fig. 2e]), CXCL1/KC ([Fig. 2f]) and TNF-α ([Fig. 2g]) in BAL [PM 2.5 (p<0.001) and PM 10 (p<0.001)] compared to the Control, Exe, PM 2.5+Exe and PM 10+Exe groups. These results also clearly demonstrate the anti-inflammatory effects of low-intensity aerobic exercise because the levels of IL-1β, CXCL1/KC and TNF-α were abrogated in exercised groups. In addition, these anti-inflammatory effects of low intensity aerobic exercise can be partially explained by the increased release of the anti-inflammatory cytokine IL-10 in the Exe (p<0.05), PM 2.5+Exe (p<0.05) and in PM 10+Exe (p<0.05) groups when compared with all other groups. Additionally, multivariate ANOVA analysis showed that aerobic training in PM 2.5- and PM 10-exposed mice, respectively reduced particulate matter-induced accumulation of IL-1β (F=29,999, p<0.000; F=12,305, p<0.001); CXCL1/KC (F=9,951, p<0.000; F=23,981, p<0.000), TNF-α (F=17,180, p<0.000; F=4,400, p<0.048), whereas exercise alone (F=8,757, p<0.006) or on PM 2.5 exposure (F=7,642, p<0.010) or on PM 10 exposure (F=8,683, p<0.007) increases IL-10 levels in BAL. Concerning a possible interaction between exercise and PM 2.5. and PM 10, no interaction effects between PM and exercise were observed.

To better discriminate the extension of the effects of low-intensity aerobic exercise in different lung compartments, a quantitative histological analysis of the density of polymorphonuclear (PMN) and mononuclear (MN) cells in the lung parenchyma and in the peribronchial space were performed ([Fig. 3a–j]). The results demonstrated that exposure to PM 2.5 and to PM 10 resulted in an increased accumulation of PMN cells (p<0.001; [Fig. 3a]) and MN cells (p<0.001, [Fig. 3b]) in the lung parenchyma and also of PMN cells (p<0.001, [Fig. 3c]) and MN cells (p<0.001, [Fig. 3d]) in the peribronchial space. [Fig. 3e–j] shows the representative photomicrographs of slides stained with hematoxylin and eosin of the Control, Exe, PM 2.5, PM 10, PM 2.5+Exe and PM 10+Exe groups, at 400x magnification. The multivariate ANOVA analysis showed that aerobic training alone increased the number of PMN cells in the lung parenchyma (F=26,475, p<0.000), whereas it decreased particulate matter-induced PMN cell accumulation in the PM 2.5 group (F=99,140, p<0.000) and PM 10 group (F=144,366, p<0.000). Regarding MN cells in the lung parenchyma, only aerobic training in PM 2.5-exposed mice (F=20,273, p<0.000) and in PM 10-exposed mice (F=20,839, p<0.000) presented a significant effect. Concerning peribronchial inflammation, the results demonstrated that aerobic training significantly reduced particulate matter-induced PMN cell accumulation (PM 2.5-exposed mice: F=8,941, p<0.006; PM 10-exposed mice: F=10,498, p<0.003) and also MN cell accumulation (PM 2.5-exposed mice: F=30,294, p<0.000; PM 10-exposed mice: F=16,704, p<0.000). Similar to the results from BAL, no interaction effects between PM and exercise were observed.

Zoom Image
Fig. 3 Quantitative histological analysis of lung inflammation in the lung parenchyma and in the peribronchial space. a, ***p<0.001 when compared with all other groups. For bd, **p<0.01 when compared with all other groups and *p<0.05 when compared with Control and Exe groups. ej are representative photomicrographs of Control, Exe, PM 2.5, PM 10, PM 2.5+Exe and PM 10+Exe groups, respectively. Data are presented as mean ± standard error.

#

Low-intensity treadmill training inhibits particulate matter-induced systemic inflammation

[Fig. 4a–e] shows the effects of PM exposure and of aerobic exercise on systemic inflammation. [Fig. 4a] shows that compared with all groups, PM 2.5 (p<0.001) and PM 10 (p<0.001) increased the number of blood leukocytes, which was completely inhibited by aerobic exercise. The results also show that compared with all groups, PM 2.5 and PM 10 exposure similarly increased the concentrations of pro-inflammatory cytokines IL-1β (p<0.001), CXCL1/KC (p<0.001) and TNF-α (p<0.001), which were completely abrogated by aerobic exercise. On the other hand, PM 2.5 and PM 10 exposure did not influence the systemic concentration of the anti-inflammatory cytokine IL-10, which presented increased levels in the exercised groups, Exe (p<0.001), PM 2.5+Exe (p<0.001) and PM 10+Exe (p<0.001). Multivariate ANOVA analysis showed that aerobic training in PM 2.5- and PM 10-exposed mice respectively reduced particulate matter-induced accumulation of total leukocytes in the blood (F=55,383, p<0.000; F=64,201, p<0.000). Similarly, aerobic training also reduced the levels of IL-1β (F=19,777, p<0.000; F=16,645, p<0.000), CXCL1/KC (F=80,036, p<0.000; F=104,345, p<0.000), TNF-α (F=8,061, p<0.009; F=6,332, p<0.019), whereas exercise alone (F=21,410, p<0.000) or on PM 2.5 exposure (F=12,988, p<0.001) or PM 10 exposure (F=8,922, p<0.006) increases IL-10 levels in BAL. For systemic inflammation, no interaction effects between PM and exercise were observed.

Zoom Image
Fig. 4 Systemic inflammation is demonstrated by the number of blood leukocytes and by the levels of IL-1β, CXCL1/KC, TNF-α and IL-10 in serum. For a–e, ***p<0.001 when compared with all other groups. Data are presented as mean ± standard error.

#
#

Discussion

The present study showed for the first time that low-intensity aerobic exercise performed concomitantly with particulate matter (PM) exposure did not potentiate the pro-inflammatory effects of the air pollution exposure. On the contrary, low-intensity aerobic exercise inhibited the pulmonary and systemic inflammation induced by exposure to PM.

We have previously demonstrated that aerobic exercise performed concomitantly with diesel exhaust particles (DEP) can inhibit pulmonary and systemic inflammation induced by DEP [16]. However, although DEP is partially constituted by thick, fine and ultrafine particles, DEP is also made up of polycyclic aromatic hydrocarbons, organic species, metals, sulfate, nitrite and many other trace elements, resulting in variable responses when in contact with the respiratory tract [3]. In addition, particulate matter, which represents a significant component of DEP, is deposited in different lung compartments based on the aerodynamic diameter of particles suspended in the air [12] [17]. In this context, the present study showed that aerobic exercise inhibited not only the parenchymal inflammation induced by DEP, as demonstrated previously [16], but also inhibited airway inflammation when it is induced by PM 2.5 and PM 10. However, it is important to note one limitation of the present study, in that the possible effects of different ventilatory statuses, for instance induced by exercise on PM deposition, could not be evaluated.

Atmospheric air pollution is constituted by different pollutants, including PM, which are classified mainly by the aerodynamic diameter of the particles [18]. Different sizes of PM can reach different areas of the lungs, ranging from very thick particles (>10 µm), which are deposited in the upper airways; thick particles (10–2.5 µm, PM 10), which are also deposited in the upper airways and in the main bronchi; to thin (≤2.5 µm, PM 2.5) and ultra-thin (≤0.1 µm, PM 0.1) particles, which can be deposited in the distal airways and alveoli [12] [17]. In the present study, it was observed that PM 2.5 and PM 10 exposure resulted in inflammation of the airways and parenchyma, characterized by both polymorphonuclear (PMN) and by mononuclear (MN) cells. These results are particularly important because airway inflammation is closely related to airway hyper-responsiveness, especially in susceptible individuals, a phenomenon that can limit exercise practice by narrowing the airways and reducing the airflow [1] [6]. In this context, is important to note the extension of the anti-inflammatory effects of aerobic exercise in different lung compartments, which can be differentially affected by exposure to PM. In our study, low-intensity aerobic exercise was able to inhibit the accumulation of PMN and MN cells in both the lung parenchyma and in the peribronchial space, suggesting a widespread protective effect of aerobic exercise along different lung compartments.

Another important effect resulting from air pollution exposure is systemic inflammation [2] [7] [10] [18] [19]. Air pollution-induced systemic inflammation has been described as an important event mediating the development and exacerbation of several diseases, such as lupus erythematosus [2], Parkinson’s disease [7], endothelial injury [10], allergy [19], as well as respiratory diseases, such as asthma and chronic obstructive pulmonary disease (COPD) [18]. The underlying mechanisms involving air pollution-induced systemic inflammation are, at least partially, attributed to activation of oxidative stress pathways and pro-inflammatory cytokines and pro-angiogenic factors release [10]. In fact, it has been described that particulate matter increases the number of monocytes, CD4+ T lymphocytes, CD8+ T lymphocytes, and the levels of IL-1β, IL-6, MCP-1/CCL2, MIP-1α/CCL3, MIP-1β/CCL4, which are cells and cytokines/chemokines involved in the atherosclerosis process, as well as in asthma and COPD pathogenesis [10]. In addition, it has been described that particulate matter also induces the increase in the number of basophils, a cell with a central role in systemic and allergic processes [19]. In the present study, it was demonstrated that PM 2.5 and PM 10 exposure induced increases in the number of total circulating leukocytes and in the levels of IL-1β, CXCL1/KC and TNF-α, which are pro-inflammatory cytokines involved in the pathophysiology of several diseases. On the other hand, it was also demonstrated that aerobic exercise was able to inhibit cytokine release by exposure to PM 2.5 and PM 10, underscoring the protective and anti-inflammatory effects of aerobic exercise. However, the effects of aerobic exercise with concomitant exposure to pollutants were not evaluated in the context of diseases, i. e., asthma and COPD, which could demonstrate whether exercise could inhibit air pollution-induced exacerbation of diseases.

In conclusion, the present study shows that the concomitant practice of low-intensity aerobic exercise with particulate matter (PM 2.5 and PM 10) exposure did not worsen the harmful effects of particulate matter exposure but, on the contrary exhibited protective effects.


#
#

Conflict of Interest

The authors have no conflict of interest to declare.

Acknowledgements

Acknowledgements This study was supported by Sao Paulo Research Foundation (FAPESP), grant 2012/15165-2. GB holds a scientific initiation scholarship from FAPESP (2015/18821-6). MCOJ holds a PhD fellowship from FAPESP (2014/14604-8). EEM holds a scientific initiation scholarship from FAPESP (2015/18821-6).


Correspondence

Prof. Rodolfo Paula Vieira
Brazilian Institute of Teaching and Research in Pulmonary
and Exercise Immunology (IBEPIPE)
School of Medical Sciences of São José dos Campos
Humanitas and Universidade Brasil
Laboratory of Pulmonary and Exercise Immunology (LABPEI)
Rua Pedro Ernesto 240
12245-520, São José dos Campos
Brazil   
Phone: +55/12/3303 8390   
Fax: +55/12/3303 8390   


Zoom Image
Fig. 1 Comparison between initial and final time of treadmill physical test in each group. ** p<0.01 when final versus initial time compared for Exe, PM 2.5+Exe and PM 10+Exe groups. Data are presented as mean ± standard error.
Zoom Image
Fig. 2 Lung inflammation evaluated through the bronchoalveolar lavage (BAL). For a–g, ***p<0.001 when compared with all other groups. For h, *p<0.05 when compared with all other groups. Data are presented as mean ± standard error.
Zoom Image
Fig. 3 Quantitative histological analysis of lung inflammation in the lung parenchyma and in the peribronchial space. a, ***p<0.001 when compared with all other groups. For bd, **p<0.01 when compared with all other groups and *p<0.05 when compared with Control and Exe groups. ej are representative photomicrographs of Control, Exe, PM 2.5, PM 10, PM 2.5+Exe and PM 10+Exe groups, respectively. Data are presented as mean ± standard error.
Zoom Image
Fig. 4 Systemic inflammation is demonstrated by the number of blood leukocytes and by the levels of IL-1β, CXCL1/KC, TNF-α and IL-10 in serum. For a–e, ***p<0.001 when compared with all other groups. Data are presented as mean ± standard error.