AI Article Synopsis
- Asthma triggers severe leukocyte infiltration into the lungs, primarily facilitated by the interaction between sialyl Lewis X (sLe) glycans on leukocytes and E-and P-selectins on endothelial cells during inflammation.
- In a mouse model of asthma, an anti-sLe monoclonal antibody (mAb F2) significantly reduced eosinophil levels, serum IgE, and T helper type 2 (Th2) cytokines, suggesting a decrease in allergic responses.
- The study highlights mAb F2's potential as a new therapeutic option for allergic asthma by targeting sLe glycans for improved treatment outcomes.
Article Abstract
Asthma is an allergic disease that causes severe infiltration of leukocytes into the lungs. Leukocyte infiltration is mediated by the binding of sialyl Lewis X (sLe) glycans present on the leukocytes to E-and P-selectins present on the endothelial cells at the sites of inflammation. Here, we found that mouse eosinophils express sLe glycans, and their infiltration into the lungs and proliferation in the bone marrow were significantly suppressed by an anti-sLe monoclonal antibody (mAb) F2 in a murine model of ovalbumin-induced asthma. The percentage of eosinophils in the bronchoalveolar lavage fluid and bone marrow and serum IgE levels decreased significantly in the F2-administered mice. Levels of T helper type 2 (Th2) cytokines and chemokines, involved in IgE class switching and eosinophil proliferation and recruitment, were also decreased in the F2-administered mice. An ex vivo cell rolling assay revealed that sLe glycans mediate the rolling of mouse eosinophils on P-selectin-expressing cells. These results indicate that the mAb F2 exerts therapeutic effects in a murine model of allergen-induced asthma, suggesting that sLe carbohydrate antigen could serve as a novel therapeutic target for allergic asthma.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8471066 | PMC |
| http://dx.doi.org/10.3390/ijms22189961 | DOI Listing |
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