Chronic urban air pollution exposure aggravates myocardial infarction in mice: the role of lung inflammation and impaired cardiac mitochondrial function

MARCHINI TIMOTEO; MAGNANI N; GARCÉS M; KELLY J; PAZ M; CALTANA L; CONTIN M; LAGO N; CACERES L; MARGIOTTIE ; CALABRÓ V; VICO T; VANASCO V; TRIPODI V; ALVAREZ S; BUCHHOLZ B ; GONZÁLEZ MAGLIO D; BERRA A ; GELPI RJ; EVELSON P

Ferrara

Congreso; SFRR-E Annual Meeting 2019; 2019

Society for Free Radical Research - Europe

Urbanair pollution exposure is associated with increased mortality rates, mainly dueto myocardial infarction (MI). In order to study the mechanisms underlying thisobservation, BALB/c mice were exposed to filtered air (FA, control) or urbanair (UA) inside whole-body inhalation chambers located in Buenos Aires City,and subjected to MI after 12 weeks. Mice breathing UA showed increased BAL leucocytecount and protein concentration, together with increased TNF-α and MCP-1levels. Consistently, lung histology showed thickening of the alveolarwall and inflammatory leukocyte recruitment. BAL analysis by flow cytometry showed enhancedalveolar macrophage activation in UA-exposed mice. In this group, a significantincrease in plasma TNF-α was also observed. At this time point, UA exposurelead to enhanced ischemia/reperfusion injury. Mechanistically, UA-exposed miceshowed impaired cardiac mitochondrial function, characterized by ultrastructuralabnormalities, decreased active state respiration, inner membranedepolarization, increased O2●- and H2O2production, and decreased ATP production rate. Our results indicate that achronic exposure to UA induces a degree of lung inflammation that impairsmitochondrial function in distant organs, such as the heart, which worsens MIoutcome. Taken together, our data highlights the importance of consideringenvironmental factors in the development of cardiovascular diseases in urbanareas.