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The acute pulmonary toxicity in mice induced by Staphylococcus aureus, particulate matter, and their combination
Fan Wang1,2, Ruiling Wang1, Haifang Liu3
1School of Biological Science, Luoyang Normal University, No. 6 Jinqing Road, Yinbin District, Luoyang 471934, P.R. China.
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 × 106 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.
Insights
Exposure to particulate matter (PM) and Staphylococcus aureus (S. aureus) bacteria together significantly increases lung inflammation and oxidative stress in mice. This combined exposure triggers a notable inflammatory response, impacting overall pulmonary health.
Area of Science:
- Environmental Health
- Toxicology
- Immunology
Background:
- Particulate matter (PM) can transport pathogenic bacteria, posing a significant threat to respiratory health.
- Understanding the combined pulmonary toxicity of PM and bacteria like Staphylococcus aureus (S. aureus) is crucial for public health.
Purpose of the Study:
- To investigate the pulmonary toxicity of S. aureus and PM, both individually and in combination, in a mouse model.
- To assess the impact of combined exposure on oxidative stress, inflammatory markers, and immune responses in the lungs.
Main Methods:
- Kunming mice were intratracheally instilled with PM and S. aureus, individually and combined, twice over five days.
- Analysis included oxidative stress markers (MDA, CAT, SOD, T-AOC, GSH/GSSG), nitric oxide (NO), cytokines (IL-4, INF-γ, IL-8), neurotrophins (Substance P), immunoglobulins (IgE), and leukocyte infiltration in lung tissue and bronchoalveolar lavage fluid (BALF).
Main Results:
- Combined PM and S. aureus exposure significantly increased lung MDA, CAT, SOD, and NO, while decreasing T-AOC and GSH/GSSG ratio, indicating heightened oxidative stress.
- Elevated IL-4/INF-γ ratio, IL-4 in BALF, and serum IgE were observed in groups exposed to S. aureus or the combination.
- PM, S. aureus, or their combination led to increased Substance P and IL-8 in BALF and significant leukocyte infiltration into lung tissues.
Conclusions:
- Combined exposure to PM and S. aureus induces a significant lung inflammatory response in mice.
- This inflammatory response is, at least partly, mediated by oxidative stress and inflammatory mediators released from activated immune cells and epithelial cells.
- The findings highlight the synergistic detrimental effects of airborne pollutants and pathogenic bacteria on pulmonary health.
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