The acute pulmonary toxicity in mice induced by <i>Staphylococcus aureus</i>, particulate matter, and their combination

Abstract

Inhalation of pathogenic bacteria transported by particulate matter (PM) presents an important potential threat to human health. Therefore, the pulmonary toxicity in mice caused by Staphylococcus aureus ( S. aureus ) and PM as individual matter and mixtures was studied. PM and S. aureus were instilled intratracheally into Kunming mice at doses of 0.2 mg/mouse and 5.08 × 10 6 CFU /mouse, respectively, as individual matter and in combination two times at 5-day intervals. After the exposure period, oxidative stress markers and nitric oxide (NO) in the lung, cellular infiltration, neurotrophins, chemokines, and cytokines in bronchoalveolar lavage fluid (BALF), and immunoglobulin (Ig) in sera were examined. Exposure to the combination of PM and S. aureus caused significant increases in malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and NO and significant decreases in total antioxidant capacity (T-AOC) and the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG) in the lung. Meanwhile, the ratio of interleukin (IL)-4 to interferon (INF)-γ, the IL-4 level in BALF, and the IgE concentration in sera were significantly increased in the groups exposed to S . aureus or the combination of PM and S . aureus. Substance P and IL-8 in BALF were significantly increased in mice exposed to PM, S. aureus or their combination. In addition, PM, S. aureus , and their combination caused infiltration of leukocytes into the alveolar tissue spaces. The results suggested that exposure to the combination of PM and S. aureus induced a lung inflammatory response that was at least partly caused by oxidative stress and mediators from the activated eosinophils, neutrophils, alveolar macrophages, and epithelial cells.

ROCK inhibitor attenuates carbon blacks‐induced pulmonary fibrosis in mice via Rho/ROCK/NF‐kappa B pathway

“…Previous studies also suggested that some external stimulations, such as particular matter and carbon nanotubes, could increase the various types of inflammatory cells in BALF 25,26 . In our study, the number of inflammatory cells in BALF were also increased in CBs treated mice and Y‐27632 could appear to suppress the increase of inflammatory cells caused by CBs.…”

Protective Role of Peroxiredoxin I in Heat-KilledStaphylococcus Aureus-infected Mice

“…In the present study, we analyzed the regulatory function of Prx I on both lethal shock reaction and host immune response to S. aureus infection in mice. Several studies have previously shown that S. aureus promotes a host immune response from minor skin infections to severe systemic inflammations, including septic lethal shock (17,18). TLR2 is known as a key molecule to contribute to host immune response against S. aureus infections (19,20), and deletion of TLR2 increases the mortality of mice during S. aureus infection (15,(21)(22)(23) combined with impaired cytokines production and severe inflammatory burden.…”

Expectorant Effects of Immature Asian Pear Extract on PM2.5-Induced Subacute Pulmonary Injury in Mice

“…Te initiation of an infammatory response is marked by an increase in infammatory mediators and proinfammatory cytokines [11]. Reactive oxygen species (ROS), catalase (CAT), heme oxygenase-1 (HO-1), superoxide dismutase (SOD), and glutathione peroxidase (GPX) [12] are factors infuencing oxidative stress.…”