| First Author | Boehme SA | Year | 2004 |
| Journal | J Immunol | Volume | 173 |
| Issue | 6 | Pages | 3599-603 |
| PubMed ID | 15356103 | Mgi Jnum | J:92758 |
| Mgi Id | MGI:3054477 | Doi | 10.4049/jimmunol.173.6.3599 |
| Citation | Boehme SA, et al. (2004) Cutting edge: serotonin is a chemotactic factor for eosinophils and functions additively with eotaxin. J Immunol 173(6):3599-603 |
| abstractText | Elevated levels of serotonin (5-hydroxytryptamine, 5-HT) are observed in the serum of asthmatics. Herein, we demonstrate that 5-HT functions independently as an eosinophil chemoattractant that acts additively with eotaxin. 5-HT2A receptor antagonists (including MDL-100907 and cyproheptadine (CYP)) were found to inhibit 5-HT-induced, but not eotaxin-induced migration. Intravital microscopy studies revealed that eosinophils roll in response to 5-HT in venules under conditions of physiological shear stress, which could be blocked by pretreating eosinophils with CYP. OVA-induced pulmonary eosinophilia in wild-type mice was significantly inhibited using CYP alone and maximally in combination with a CCR3 receptor antagonist. Interestingly, OVA-induced pulmonary eosinophilia in eotaxin-knockout (Eot-/-) mice was inhibited by treatment with the 5-HT2A but not CCR3 receptor antagonist. These results suggest that 5-HT is a potent eosinophil-active chemoattractant that can function additively with eotaxin and a dual CCR3/5-HT2A receptor antagonist may be more effective in blocking allergen-induced eosinophil recruitment. |
