1998Journal of Leukocyte BiologyRequires access

Resident mast cells are important for eotaxin-induced eosinophil accumulation in vivo

Anuk Das, Roderick J. Flower, Mauro Perretti

Open publisher page 33 citations

Abstract

Eotaxin administration intraperitoneally, but not into dorsal air-pouches, of ovalbumin-sensitized mice exhibiting blood eosinophilia induced a threefold increase in eosinophil (E phi s) infiltration. Transfer of 1 x 10(6) mixed peritoneal cavity cells (PCC), containing 3.5 to 4.5 x 10(4) mast cells (MC), from donor mice to air-pouches of sensitized (but not unsensitized) recipient mice, established an E phi infiltration to eotaxin (vehicle, 0.86 +/- 0.27 x 10(6); eotaxin, 1.63 +/- 0.16 x 10(6) E phi s/air-pouch). Neutrophil numbers were also increased. When MC-depleted (-93%) PCC were injected into air-pouches of recipient animals, E phi infiltration was not supported (-52%). Injection of macrophage-depleted (-99%) PCC into air-pouches elicited a full E phi response to eotaxin but not neutrophil infiltration (-81%). Systemic dexamethasone treatment of recipient mice reduced E phi accumulation; treatment of donor mice only reduced neutrophil accumulation. Our study points to a crucial role for MC in E phi recruitment by eotaxin.

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What this paper is about

Eotaxin administration intraperitoneally, but not into dorsal air-pouches, of ovalbumin-sensitized mice exhibiting blood eosinophilia induced a threefold increase in eosinophil (E phi s) infiltration. Transfer of 1 x 10(6) mixed peritoneal cavity cells (PCC), containing 3.5 to 4.5 x 10(4) mast cells (MC), from donor mice to air-pouches of sensitized (but not unsensitized) recipient mice, established an E phi infiltration to eotaxin (vehicle, 0.86 +/- 0.27 x 10(6); eotaxin, 1.63 +/- 0.16 x 10(6) E phi s/air-pouch). Neutrophil numbers were also increased. When MC-depleted (-93%) PCC were injected into air-pouches of recipient animals, E phi infiltration was not supported (-52%). Injection of macrophage-depleted (-99%) PCC into air-pouches elicited a full E phi response to eotaxin but not neutrophil infiltration (-81%). Systemic dexamethasone treatment of recipient mice reduced E phi accumulation; treatment of donor mice only reduced neutrophil accumulation. Our study points to a crucial role for MC in E phi recruitment by eotaxin.

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Available abstract

Eotaxin administration intraperitoneally, but not into dorsal air-pouches, of ovalbumin-sensitized mice exhibiting blood eosinophilia induced a threefold increase in eosinophil (E phi s) infiltration. Transfer of 1 x 10(6) mixed peritoneal cavity cells (PCC), containing 3.5 to 4.5 x 10(4) mast cells (MC), from donor mice to air-pouches of sensitized (but not unsensitized) recipient mice, established an E phi infiltration to eotaxin (vehicle, 0.86 +/- 0.27 x 10(6); eotaxin, 1.63 +/- 0.16 x 10(6) E phi s/air-pouch). Neutrophil numbers were also increased. When MC-depleted (-93%) PCC were injected into air-pouches of recipient animals, E phi infiltration was not supported (-52%). Injection of macrophage-depleted (-99%) PCC into air-pouches elicited a full E phi response to eotaxin but not neutrophil infiltration (-81%). Systemic dexamethasone treatment of recipient mice reduced E phi accumulation; treatment of donor mice only reduced neutrophil accumulation. Our study points to a crucial role for MC in E phi recruitment by eotaxin.

Key concepts: Eotaxin, Eosinophil, Infiltration (HVAC), Peritoneal cavity, Eosinophilia, Ovalbumin, Dexamethasone, Immunology

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