Congresos y reuniones científicas
Título:
ROLE OF SPHINGOSINE‐1‐PHOSPHATE IN NEUTROPHIL TRAFFICKING TO LYMPH NODES IN AN IMMUNE INFLAMMATION MODEL
Autor/es:
GORLINO, CAROLINA; RANOCCHIA, ROMINA; HARMAN, FLORENCIA; MORÓN, GABRIEL; MALETTO, BELKYS; PISTORESI, MARÍA CRISTINA
Reunión:
Congreso; 1º Congreso Franco Argentino de Inmunología. Bs. As.; 2010
Resumen:
We previously demonstrated that when OVA-FITC was injected into the footpad of OVA/CFA immunized
mice, the main OVA-FITC+ cells recruited in draining popliteal lymph nodes were neutrophils and this influx
was dependent on an antigen-specific response. Moreover, we showed that neutrophils entered into lymph
nodes through afferent lymphatics and blood and that this migration was dependent on the presence of
immune complexes as well as on an inflammatory condition. On the basis of these findings, we
investigated if the phospholipid sphingosine-1-phosphate (S1P) is involved in this traffic. Treatment with
the S1P receptor modulator FTY720 inhibited neutrophil influx in draining popliteal lymph nodes of mice
immunized with OVA (43±3% vs 9±4%; p=0.02) but not its recruitment to the site of inflammation (23±2%
vs 16±3%; p=0.19). To further characterize the role of S1P in neutrophil trafficking from skin (by lymph
vessels) or from blood into reactive lymph nodes, we performed adoptive transfer experiments. Bone
marrow neutrophils incubated with immune complexes (anti-OVA rabbit sera plus OVA) were differentially
labeled either with DiIC(18)-DS or DiOC(18)-SP and simultaneously injected i.v. and s.c. into the footpads,
respectively, of FTY720 treated OVA/CFA-immunized mice. The administration of FTY720 caused
impaired migration of transferred neutrophils from footpad to popliteal lymph nodes (0.44±0.08% vs
0.21±0.04%; p<0.05) and from blood to lymph nodes (0.56±0.09% vs 0.26±0.07%; p<0.05). In summary,
these data suggest that S1P participates in neutrophil migration from a peripheral tissue (by lymph
vessels) and from blood into lymph nodes in an immune inflammation model.