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Updated: Aug 24, 2026
Protective Efficacy and Pulmonary Immune Response Following Subcutaneous and Intranasal BCG Administration in Mice
Published on: September 19, 2016
[The effect of BCG on airway inflammatory reaction of experimental asthma mice]
Jin-Bao Liu1, Nan-Shan Zhong, Shu-Nong Li
1Department of Pathophysiology, Department of Histology and Embryology, Institute of Respiratory Diseases, Guangzhou Medical College, Guangzhou 510182,China.
Aim:
To explore in-vivo regulation of T cells in pulmonary tissues of ovalbumin(OVA)-sensitized mice by BCG and its effect on airway inflammatory reaction.
Methods:
Thirty BALB/c mice (male and female, 6 to 8 weeks of age) were divided into 3 groups. For the mice of first group, aerosol OVA was inhaled daily for 20 minutes once for 10 days running, so as to establish a OVA-sensitized mouse model. In the mice of second group, aerosol normal solution was inhaled according to the time and frequency of the first group. In the third group, the mice were intradermally injected with BCG of 0.04 to 0.06 mg on 10 and 14 days before OVA sensitization, respectively, and then aerosol purified protein derivative (PPD) was inhaled to the mice on 6 days after OVA sensitization. The changes in the number of CD4(+), CD8(+) and IFN-gamma(+) T cells in the inflammatory tissues and changes in the inflammatory cells in the inflammatory tissues and broncho-alveolar lavage fluid (BALF) were detected by SABC immuno-histochemical staining.
Results:
The number of CD4(+) T cells significantly increased in the pulmonary tissues of OVA-sensitized mice, which mainly was the increased number of CD4(+)/IFN-gamma(-) T cells, While the number of CD8(+) T cells had no notable variation, thus the ratio of CD4(+)/IFN-gamma(+) T cells descended. After BCG treatment, the number of CD8(+) T cells markedly increased, so the ratio of CD4(+)/ IFN-gamma(+) T cells variously rose, whereas the number of inflammatory cells decreased in BALF.
Conclusion:
BCG can upregulate the number of Th1 cells and lighten the airway inflammatory reaction of experimental asthma mice.
