Sophorolipids Decrease Asthma Severity And Ova-specific IgE Production In A Mouse Asthma Model

Article Outline

• Rationale
• Methods
• Results
• Conclusions
• Copyright

Back to Article Outline

Rationale 

Sophorolipids are promising modulators of the immune response. We have previously demonstrated that sophorolipids decreased IgE production in vitro in U266 cells through downregulation of IgE regulatory genes. In this study we investigated if sophorolipids could decrease asthma severity in an in vivo asthma model.

Back to Article Outline

Methods 

Black c-57 mice (5/group) were challenged with ovalbumin (OVA) via IP injection/nebulization. Sophorolipids or sucrose vehicle control was administered via nebulization pre and post full OVA asthmatic insult and animals were sacrificed after 14 days. Lung tissue was obtained and assessed for asthma severity. Serum and bronchoalveolar lavage (BAL) fluid were obtained for total and OVA specific IgE analysis (ELISA). Data are reported as mean±SD and significance between groups was determined by student's t-test.

Back to Article Outline

Results 

Mice exposed to full OVA induction regimen demonstrated pulmonary evidence of asthma. Lungs obtained from these animals showed excessive leukocytic infiltration and edema. In contrast, asthmatic animals given nebulized sophorolipids had decreased leukocytic infiltrate and edema (p < 0.05) compared with vehicle control. Furthermore, sophorolipid treated animals had decreased levels of BAL fluid OVA specific IgE when compared with vehicle-treated asthmatic mice (1.6 ± 0.15 vs 0.9 ± 0.12 OD units; p < 0.05). However, serum levels of total IgE and OVA specific IgE and BAL total IgE levels did not differ between treated and control animals. No adverse effects were observed at all doses tested.

Back to Article Outline

Conclusions 

Sophorolipids decreased asthma severity in experimental asthma. These data continue to support the utility of sophorolipids as an anti-inflammatory agent and novel potential therapy in allergic asthma.