Abstract
BackgroundParticulate matter exposure is associated with respiratory and cardiovascular system dysfunction. Recently, we demonstrated that fine particles, also named PM2.5, modify the expression of some components of the angiotensin and bradykinin systems, which are involved in lung, cardiac and renal regulation. The endocrine kidney function is associated with the regulation of angiotensin and bradykinin, and it can suffer damage even as a consequence of minor alterations of these systems. We hypothesized that exposure to PM2.5 can contribute to early kidney damage as a consequence of an angiotensin/bradykinin system imbalance, oxidative stress and/or inflammation.ResultsAfter acute and subchronic exposure to PM2.5, lung damage was confirmed by increased bronchoalveolar lavage fluid (BALF) differential cell counts and a decrease of surfactant protein-A levels. We observed a statistically significant increment in median blood pressure, urine volume and water consumption after PM2.5 exposure. Moreover, increases in the levels of early kidney damage markers were observed after subchronic PM2.5 exposure: the most sensitive markers, β-2-microglobulin and cystatin-C, increased during the first, second, sixth and eighth weeks of exposure. In addition, a reduction in the levels of specific cytokines (IL-1β, IL-6, TNF-α, IL-4, IL-10, INF-γ, IL-17a, MIP-2 and RANTES), and up-regulated angiotensin and bradykinin system markers and indicators of a depleted antioxidant response, were also observed. All of these effects are in concurrence with the presence of renal histological lesions and an early pro-fibrotic state.ConclusionSubchronic exposure to PM2.5 induced an early kidney damage response that involved the angiotensin/bradykinin systems as well as antioxidant and immune imbalance. Our study demonstrates that PM2.5 can induce a systemic imbalance that not only affects the cardiovascular system, but also affects the kidney, which may also overall contribute to PM-related diseases.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0179-8) contains supplementary material, which is available to authorized users.
Highlights
Particulate matter exposure is associated with respiratory and cardiovascular system dysfunction
We recently demonstrated that subchronic exposure to coarse, fine and ultrafine particles increases the expression of angiotensin receptor type-1 (AT1R) in the lungs and heart
Blood pressure measurement In this study, we report the mean blood pressure (MBP) as a physiological parameter of vascular tone on the basis that it is indicative of the perfusion pressure of organs, which could be affected by exposure to PM2.5
Summary
Particulate matter exposure is associated with respiratory and cardiovascular system dysfunction. The endocrine kidney function is associated with the regulation of angiotensin and bradykinin, and it can suffer damage even as a consequence of minor alterations of these systems. We hypothesized that exposure to PM2.5 can contribute to early kidney damage as a consequence of an angiotensin/bradykinin system imbalance, oxidative stress and/or inflammation. Substantial epidemiological evidence obtained through multi-city and meta-analysis studies has indicated that medium and long-term exposure to particulate matter of less than 2.5 μm (PM2.5) is associated with an increase in the incidence of adverse respiratory and cardiovascular events [1]. The health effects reported as a consequence of PM2.5 exposure are associated with cellular and molecular inflammation and oxidative stress responses, which are considered to be the underlying mechanisms that drive. Renal dysfunction and the development of cardiovascular diseases (CVD) are closely associated. The most important causes of mortality in end-stage kidney disease are CVD and infections, where the infections are thought to be associated with disorders of the innate and adaptive immune responses [12]
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