Vesicular acetylcholine transport deficiency potentiates some inflammatory responses induced by diesel exhaust particles
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Citações na Scopus
14
Tipo de produção
article
Data de publicação
2019
Título da Revista
ISSN da Revista
Título do Volume
Editora
ACADEMIC PRESS INC ELSEVIER SCIENCE
Autores
SANTANA, Fernanda P. R.
BITTENCOURT-MERNAK, Marcia I.
PRADO, Marco Antonio M.
Citação
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY, v.167, p.494-504, 2019
Resumo
Endogenous acetylcholine (ACh), which depends of the levels of vesicular ACh transport (VAChT) to be released, is the central mediator of the cholinergic anti-inflammatory system. ACh controls the release of cytokine in different models of inflammation. Diesel exhaust particles (DEP) are one of the major environmental pollutants produced in large quantity by automotive engines in urban center. DEP bind the lung parenchyma and induce inflammation. We evaluated whether cholinergic dysfunction worsens DEP-induced lung inflammation. Male mice with decreased ACh release due to reduced expression of VAChT (VAChT-KD mice) were submitted to DEP exposure for 30 days (3 mg/mL of DEP, once a day, five days a week) or saline. Pulmonary function and inflammation as well as extracellular matrix fiber deposition were evaluated. Additionally, airway and nasal epithelial mucus production were quantified. We found that DEP instillation worsened lung function and increased lung inflammation. Higher levels of mononuclear cells were observed in the peripheral blood of both wild-type (WT) and VAChT-KD mice. Also, both wild-type (WT) and VAChT-KD mice showed an increase in macrophages in bronchoalveolar lavage fluid (BALF) as well as increased expression of IL-4, IL-6, IL-13, TNF-alpha, and NF-kappa B in lung cells. The collagen fiber content in alveolar septa was also increased in both genotypes. On the other hand, we observed that granulocytes were increased only in VAChT-KD peripheral blood. Likewise, increased BALF lymphocytes and neutrophils as well as increased elastic fibers in alveolar septa, airway neutral mucus, and nasal epithelia acid mucus were observed only in VAChT-KD mice. The cytokines IL-4 and TNF-alpha were also higher in VAChT-KD mice compared with WT mice. In conclusion, decreased ability to release ACh exacerbates some of the lung alterations induced by DEP in mice, suggesting that VAChT-KD animals are more vulnerable to the effects of DEP in the lung.
Palavras-chave
Air pollution, Acetylcholine, Pulmonary inflammation, Cholinergic anti-inflammatory system, VAChT
Referências
- Araujo BB, 2008, EUR RESPIR J, V32, P61, DOI 10.1183/09031936.00147807
- Bai N, 2013, INHAL TOXICOL, V25, P725, DOI 10.3109/08958378.2013.844749
- Barton DB, 2014, CELL TISSUE RES, V358, P229, DOI 10.1007/s00441-014-1905-x
- Behndig AF, 2006, EUR RESPIR J, V27, P359, DOI 10.1183/09031936.06.00136904
- Belmonte Kristen E, 2005, Proc Am Thorac Soc, V2, P297, DOI 10.1513/pats.200504-043SR
- Bernik TR, 2002, J EXP MED, V195, P781, DOI 10.1084/jem.20011714
- BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
- Brook RD, 2010, CIRCULATION, V121, P2331, DOI 10.1161/CIR.0b013e3181dbece1
- Brunekreef B, 2002, LANCET, V360, P1233, DOI 10.1016/S0140-6736(02)11274-8
- Chen ZY, 2017, EXP THER MED, V14, P3485, DOI 10.3892/etm.2017.4937
- Daviskas E, 2006, J AEROSOL MED, V19, P100, DOI 10.1089/jam.2006.19.100
- de Castro BM, 2009, MOL CELL BIOL, V29, P5238, DOI 10.1128/MCB.00245-09
- DOCKERY DW, 1993, NEW ENGL J MED, V329, P1753, DOI 10.1056/NEJM199312093292401
- Gavett SH, 2003, ENVIRON HEALTH PERSP, V111, P1471, DOI 10.1289/ehp.6300
- Ghio AJ, 2001, AM J RESP CRIT CARE, V164, P704, DOI 10.1164/ajrccm.164.4.2011089
- Gosens R, 2018, EUR RESPIR J, V52, DOI 10.1183/13993003.01247-2017
- Gundavarapu S, 2012, J ALLERGY CLIN IMMUN, V130, P770, DOI 10.1016/j.jaci.2012.04.002
- Gwilt CR, 2007, PHARMACOL THERAPEUT, V115, P208, DOI 10.1016/j.pharmthera.2007.05.007
- HANTOS Z, 1992, J APPL PHYSIOL, V72, P168
- Hiura TS, 1999, J IMMUNOL, V163, P5582
- Inoue K, 2009, EXP BIOL MED, V234, P200, DOI 10.3181/0809-RM-285
- Ishihara Y, 2002, INHAL TOXICOL, V14, P1049, DOI 10.1080/08958370290084773
- James AL, 2012, AM J RESP CRIT CARE, V185, P1058, DOI 10.1164/rccm.201110-1849OC
- Jeremias IC, 2016, MOL NEUROBIOL, V53, P6635, DOI 10.1007/s12035-015-9538-y
- Kampa M, 2008, ENVIRON POLLUT, V151, P362, DOI 10.1016/j.envpol.2007.06.012
- Kodavanti UP, 2013, TOXICOL APPL PHARM, V268, P232, DOI 10.1016/j.taap.2013.02.002
- Lara A, 2010, MOL CELL BIOL, V30, P1746, DOI 10.1128/MCB.00996-09
- Lehmann AD, 2009, PART FIBRE TOXICOL, V6, DOI 10.1186/1743-8977-6-26
- Leite HR, 2016, BRAIN BEHAV IMMUN, V57, P282, DOI 10.1016/j.bbi.2016.05.005
- Li DJ, 2011, HYPERTENSION, V57, P298, DOI 10.1161/HYPERTENSIONAHA.110.160077
- Li N, 2002, J IMMUNOL, V169, P4531, DOI 10.4049/jimmunol.169.8.4531
- Li P, 2016, EXP GERONTOL, V74, P43, DOI 10.1016/j.exger.2015.12.005
- Li RJ, 2007, REGUL TOXICOL PHARM, V48, P284, DOI 10.1016/j.yrtph.2007.04.009
- Lips KS, 2007, LIFE SCI, V80, P2263, DOI 10.1016/j.lfs.2007.01.026
- Massa CB, 2017, PLOS COMPUT BIOL, V13, DOI 10.1371/journal.pcbi.1005570
- Mauad T, 2007, J ALLERGY CLIN IMMUN, V120, P997, DOI 10.1016/j.jaci.2007.06.031
- Nemmar A, 2012, TOXICOLOGY, V292, P162, DOI 10.1016/j.tox.2011.12.009
- Parrish WR, 2008, MOL MED, V14, P567, DOI 10.2119/2008-00079.Parrish
- Pinheiro NM, 2015, PLOS ONE, V10, DOI 10.1371/journal.pone.0120441
- Pires-Neto RC, 2006, ENVIRON RES, V101, P356, DOI 10.1016/j.envres.2005.12.018
- Prado MAM, 2002, NEUROCHEM INT, V41, P291, DOI 10.1016/S0197-0186(02)00044-X
- Prado VF, 2013, BIOCHEM J, V450, P265, DOI 10.1042/BJ20121662
- Prado VF, 2006, NEURON, V51, P601, DOI 10.1016/j.neuron.2006.08.005
- Proskocil BJ, 2004, ENDOCRINOLOGY, V145, P2498, DOI 10.1210/en.2003-1728
- RighettI RF, 2014, RESP PHYSIOL NEUROBI, V192, P134, DOI 10.1016/j.resp.2013.12.012
- Rosas-Ballina M, 2009, J INTERN MED, V265, P663, DOI 10.1111/j.1365-2796.2009.02098.x
- Rosas-Ballina M, 2011, SCIENCE, V334, P98, DOI 10.1126/science.1209985
- Roy A, 2014, MOL MED, V20, P527, DOI 10.2119/molmed.2014.00125
- Roy A, 2013, FASEB J, V27, P5072, DOI 10.1096/fj.13-238279
- Sagai M, 1996, FREE RADICAL BIO MED, V21, P199, DOI 10.1016/0891-5849(96)00032-9
- Salvi S, 1999, AM J RESP CRIT CARE, V159, P702, DOI 10.1164/ajrccm.159.3.9709083
- Sango K, 1996, NAT GENET, V14, P348, DOI 10.1038/ng1196-348
- Schuliga M, 2015, BIOMOLECULES, V5, P1266, DOI 10.3390/biom5031266
- SCHWARTZ J, 1994, AM J RESP CRIT CARE, V150, P1234, DOI 10.1164/ajrccm.150.5.7952546
- Seriani R, 2015, ENVIRON TOXICOL, V30, P1297, DOI 10.1002/tox.22000
- Smith R, 2006, HUM MOL GENET, V15, P3119, DOI 10.1093/hmg/ddl252
- Stenfors N, 2004, EUR RESPIR J, V23, P82, DOI 10.1183/09031936.03.00004603
- Tanaka M, 2013, J TOXICOL SCI, V38, P35, DOI 10.2131/jts.38.35
- Terry AV, 2007, NEUROSCIENCE, V146, P1316, DOI 10.1016/j.neuroscience.2007.03.003
- Toledo AC, 2013, BRIT J PHARMACOL, V168, P1736, DOI 10.1111/bph.12062
- Win-Shwe TT, 2013, J TOXICOL SCI, V38, P71, DOI 10.2131/jts.38.71
- Yanamala N, 2013, TOXICOL APPL PHARM, V272, P373, DOI 10.1016/j.taap.2013.07.006
- Yang X, 2014, QJM-INT J MED, V107, P789, DOI 10.1093/qjmed/hcu005
- Yoshizaki K, 2010, INHAL TOXICOL, V22, P610, DOI 10.3109/08958371003621633
- Yoshizaki K, 2015, RESP RES, V16, DOI [10.1186/s12931-15-0172-z, 10.1186/s12931-015-0172-z]
Coleções
Artigos e Materiais de Revistas Científicas - FM/MPT
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/05
Artigos e Materiais de Revistas Científicas - LIM/20
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - HC/InCor
Artigos e Materiais de Revistas Científicas - LIM/05
Artigos e Materiais de Revistas Científicas - LIM/20