The acute pulmonary toxicity in mice induced by Staphylococcus aureus, particulate matter, and their combination.

The acute pulmonary toxicity in mice induced by Staphylococcus aureus, particulate matter, and their combination.

PMID: 

Exp Anim. 2019 May 8 ;68(2):159-168. Epub 2018 Dec 10. PMID: 30531117

Abstract Title: 

The acute pulmonary toxicity in mice induced by Staphylococcus aureus, 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× 10CFU /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.

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