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In vivo short‐term exposure to residual oil fly ash impairs pulmonary innate immune response against environmental mycobacterium infection
Author(s) -
Delfosse Verónica C.,
Tasat Deborah R.,
Gioffré Andrea K.
Publication year - 2015
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.21936
Subject(s) - bronchoalveolar lavage , proinflammatory cytokine , immune system , immunology , innate immune system , in vivo , respiratory system , microbiology and biotechnology , ex vivo , lung , medicine , biology , inflammation
Epidemiological studies have shown that pollution derived from industrial and vehicular transportation induces adverse health effects causing broad ambient respiratory diseases. Therefore, air pollution should be taken into account when microbial diseases are evaluated. Environmental mycobacteria (EM) are opportunist pathogens that can affect a variety of immune compromised patients, which impacts significantly on human morbidity and mortality. The aim of this study was to evaluate the effect of residual oil fly ash (ROFA) pre‐exposure on the pulmonary response after challenge with opportunistic mycobacteria by means of an acute short‐term in vivo experimental animal model. We exposed BALB/c mice to ROFA and observed a significant reduction on bacterial clearance at 24 h post infection. To study the basis of this impaired response four groups of animals were instilled with (a) saline solution (Control), (b) ROFA (1 mg kg −1 BW), (c) ROFA and EM‐infected ( Mycobacterium phlei , 8 × 10 6 CFU), and (d) EM‐infected. Animals were sacrificed 24 h postinfection and biomarkers of lung injury and proinflammatory madiators were examined in the bronchoalveolar lavage. Our results indicate that ROFA was able to produce an acute pulmonary injury characterized by an increase in bronchoalveolar polymorphonuclear (PMN) cells influx and a rise in O 2 − generation. Exposure to ROFA before M. phlei infection reduced total cell number and caused a significant decline in PMN cells recruitment ( p < 0.05), O 2 − generation, TNFα ( p < 0.001), and IL‐6 ( p < 0.001) levels. Hence, our results suggest that, in this animal model, the acute short‐term pre‐exposure to ROFA reduces early lung response to EM infection. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 589–596, 2015.