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Published on: March 17, 2014
Lactobacillus HY2782 and Bifidobacterium HY8002 Decrease Airway Hyperresponsiveness Induced by Chronic PM2.5
Woo Nam1, Hyeonji Kim1, Chuhyun Bae1
1R&D Center, Korea Yakult Co. Ltd., Yongin, Korea.
Abstract:
Epidemiological studies have shown that exposure to particulate matter (PM) is associated with adverse health effects. Inhalation of fine particulate matter (PM2.5) is associated with elevated pulmonary diseases. However, the molecular mechanism underlying the initiation of lung inflammation following inhalation is unclear. In this study, we investigated the beneficial effects of two probiotics, Lactobacillus casei HY2782 and Bifidobacterium lactis HY8002, against PM-induced pulmonary inflammation. Model mice were subjected to chronic exposure of PM2.5. The results showed that PM2.5 enhanced oxidative stress and led to Th2 cytokine responses in the mice. PM2.5-exposed mice were orally administered with HY2782 and HY8002 from the day of first exposure to the end point of the study. The results showed that HY2782 ameliorated PM 2.5 exposure-enhanced leukocyte migration and activation of proinflammatory cytokines. HY2782 and HY8002 also prevented exacerbation of eosinophil and neutrophil infiltration in the bronchoalveolar lavage fluid. HY2782 and HY8002 significantly increased scavenging of PM2.5-induced reactive oxygen species and activated superoxide dismutase and catalase activity in the blood. These results indicate that the probiotics HY2782 and HY8002 protect against PM-induced pulmonary inflammation.
Insights
Two probiotics, Lactobacillus casei HY2782 and Bifidobacterium lactis HY8002, were found to protect against lung inflammation caused by fine particulate matter (PM2.5) exposure in mice. These probiotics reduced oxidative stress and inflammatory responses, offering a potential therapeutic strategy.
Area of Science:
- Environmental Health
- Microbiology
- Immunology
Background:
- Particulate matter (PM) exposure is linked to adverse health outcomes, particularly pulmonary diseases from fine particulate matter (PM2.5).
- The precise molecular mechanisms driving lung inflammation after PM inhalation remain incompletely understood.
Purpose of the Study:
- To investigate the protective effects of Lactobacillus casei HY2782 and Bifidobacterium lactis HY8002 against PM2.5-induced pulmonary inflammation.
- To elucidate the impact of these probiotics on oxidative stress and inflammatory markers in a mouse model.
Main Methods:
- Mice were chronically exposed to PM2.5 and orally administered with either HY2782 or HY8002 probiotics.
- Assessed leukocyte migration, pro-inflammatory cytokine activation, and immune cell infiltration (eosinophils, neutrophils) in bronchoalveolar lavage fluid.
- Measured reactive oxygen species (ROS) scavenging and antioxidant enzyme activities (superoxide dismutase, catalase) in blood.
Main Results:
- PM2.5 exposure increased oxidative stress and Th2 cytokine responses in mice.
- Oral administration of HY2782 and HY8002 ameliorated PM2.5-induced leukocyte migration and pro-inflammatory cytokine activation.
- Both probiotics prevented increased eosinophil and neutrophil infiltration and enhanced ROS scavenging and antioxidant enzyme activity.
Conclusions:
- Lactobacillus casei HY2782 and Bifidobacterium lactis HY8002 demonstrate significant protective effects against PM2.5-induced pulmonary inflammation.
- These probiotics mitigate oxidative stress and modulate immune responses, suggesting their potential as a therapeutic intervention for air pollution-related lung conditions.

