Tirza Timmerman1, Jôse Mára de Brito2, Natalia Madureira de Almeida3, Francine Maria de Almeida4, Fernanda Magalhães Arantes-Costa5, Eliane Tigre Guimaraes6, Ana Julia Faria Coimbra Lichtenfels7, Dolores Helena Rodriguez Ferreira Rivero8, Regiani Carvalho de Oliveira9, João Paulo Amorim de Lacerda10, Jamille Moreira Moraes11, Danilo Augusto Pimental12, Beatriz Mangueira Saraiva-Romanholo13, Paulo Hilário Nascimento Saldiva14, Rodolfo de Paula Vieira15, Thais Mauad16. 1. Department of Pathology, Experimental Air Pollution Laboratory, LIM 05 - Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: t.timmerman87@gmail.com. 2. Department of Pathology, Experimental Air Pollution Laboratory, LIM 05 - Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: josemarabrito@usp.br. 3. Department of Pathology, Experimental Air Pollution Laboratory, LIM 05 - Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: nabiologa@gmail.com. 4. Department of Clinical Medicine, Laboratory of Experimental Therapeutics - LIM 20, Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: francinealmeida@usp.br. 5. Department of Clinical Medicine, Laboratory of Experimental Therapeutics - LIM 20, Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: fernanda.arantes@fm.usp.br. 6. Department of Pathology, Experimental Air Pollution Laboratory, LIM 05 - Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: etigre2211@gmail.com. 7. Department of Pathology, Experimental Air Pollution Laboratory, LIM 05 - Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: ana.lichtenfels@hc.fm.usp.br. 8. Department of Pathology, Experimental Air Pollution Laboratory, LIM 05 - Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: dohelena@usp.br. 9. Department of Pathology, Experimental Air Pollution Laboratory, LIM 05 - Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: regianic@gmail.com. 10. Technological Research Institute of São Paulo - IPT, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: jpaulo@ipt.br. 11. Technological Research Institute of São Paulo - IPT, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: jamille@ipt.br. 12. Technological Research Institute of São Paulo - IPT, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: dpimentel@ipt.br. 13. Department of Clinical Medicine, Laboratory of Experimental Therapeutics - LIM 20, Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: beatriz.msaraiva@fm.usp.br. 14. Department of Pathology, Experimental Air Pollution Laboratory, LIM 05 - Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: pepino@usp.br. 15. Brazil University, Post-graduation Program in Bioengineering, Sao Paulo, SP, Brazil; Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology, Sao Jose dos Campos, SP, Brazil. Electronic address: rodrelena@yahoo.com.br. 16. Department of Pathology, Experimental Air Pollution Laboratory, LIM 05 - Faculdade de Medicina FMUSP, Universidade de Sao Paulo, Sao Paulo, SP, Brazil. Electronic address: tmauad@usp.br.
Abstract
Many cities fail to meet air quality standards, which results in increased risk for pulmonary disorders, including asthma. Human and experimental studies have shown that diesel exhaust (DE) particles are associated with worsening of allergic asthma. Biodiesel (BD), a cleaner fuel from renewable sources, was introduced in the eighties. Because of the reduction in particulate matter (PM) emissions, BD was expected to cause fewer adverse pulmonary effects. However, only limited data on the effect of BD emissions in asthma are available. OBJECTIVE: Determine whether BD exhaust exposure in allergic sensitized mice leads to different effects on inflammatory and functional responses compared to DE exposure. METHODS: Balb/C mice were orotracheally sensitized with House Dust Mite (HDM) or a saline solution with 3 weekly instillations. From day 9 until day 17 after sensitization, they were exposed daily to filtered air (FA), DE and BD exhaust (concentration: 600 μg/m3 PM2.5). Lung function, bronchoalveolar lavage fluid (BALF) cell counts, cytokine levels (IL-2, IL-4, IL-5, IL-17, TNF-α, TSLP) in the BALF, peribronchiolar eosinophils and parenchymal macrophages were measured. RESULTS: HDM-sensitized animals presented increased lung elastance (p = 0.046), IgG1 serum levels (p = 0.029), peribronchiolar eosinophils (p = 0.028), BALF levels of total cells (p = 0.020), eosinophils (p = 0.028), IL-5 levels (p = 0.002) and TSLP levels (p = 0.046) in BALF. DE exposure alone increased lung elastance (p = 0.000) and BALF IL-4 levels (p = 0.045), whereas BD exposure alone increased BALF TSLP levels (p = 0.004). BD exposure did not influence any parameters after HDM challenge, while DE exposed animals presented increased BALF levels of total cells (p = 0.019), lymphocytes (p = 0.000), neutrophils (p = 0.040), macrophages (p = 0.034), BALF IL-4 levels (p = 0.028), and macrophagic inflammation in the lung tissue (p = 0.037), as well as decreased IgG1 (p = 0.046) and IgG2 (p = 0.043) levels when compared to the HDM group. CONCLUSION: The results indicate more adverse pulmonary effects of DE compared to BD exposure in allergic sensitized animals.
Many cities fail to meet air quality standards, which results in increased risk for pulmonary disorders, including asthma. Human and experimental studies have shown that diesel exhaust (DE) particles are associated with worsening of allergic asthma. Biodiesel (BD), a cleaner fuel from renewable sources, was introduced in the eighties. Because of the reduction in particulate matter (PM) emissions, BD was expected to cause fewer adverse pulmonary effects. However, only limited data on the effect of BD emissions in asthma are available. OBJECTIVE: Determine whether BD exhaust exposure in allergic sensitized mice leads to different effects on inflammatory and functional responses compared to DE exposure. METHODS: Balb/C mice were orotracheally sensitized with House Dust Mite (HDM) or a saline solution with 3 weekly instillations. From day 9 until day 17 after sensitization, they were exposed daily to filtered air (FA), DE and BD exhaust (concentration: 600 μg/m3 PM2.5). Lung function, bronchoalveolar lavage fluid (BALF) cell counts, cytokine levels (IL-2, IL-4, IL-5, IL-17, TNF-α, TSLP) in the BALF, peribronchiolar eosinophils and parenchymal macrophages were measured. RESULTS: HDM-sensitized animals presented increased lung elastance (p = 0.046), IgG1 serum levels (p = 0.029), peribronchiolar eosinophils (p = 0.028), BALF levels of total cells (p = 0.020), eosinophils (p = 0.028), IL-5 levels (p = 0.002) and TSLP levels (p = 0.046) in BALF. DE exposure alone increased lung elastance (p = 0.000) and BALF IL-4 levels (p = 0.045), whereas BD exposure alone increased BALF TSLP levels (p = 0.004). BD exposure did not influence any parameters after HDM challenge, while DE exposed animals presented increased BALF levels of total cells (p = 0.019), lymphocytes (p = 0.000), neutrophils (p = 0.040), macrophages (p = 0.034), BALF IL-4 levels (p = 0.028), and macrophagic inflammation in the lung tissue (p = 0.037), as well as decreased IgG1 (p = 0.046) and IgG2 (p = 0.043) levels when compared to the HDM group. CONCLUSION: The results indicate more adverse pulmonary effects of DE compared to BD exposure in allergic sensitized animals.