Pivotal Advance: Eosinophil infiltration of solid tumors is an early and persistent inflammatory host response (original) (raw)

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Divisions of Hematology and Oncology

, Washington, DC

Department of Biological Sciences, Louisiana State University

, Baton Rouge, Washington, DC

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Pulmonary Medicine

, Washington, DC

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Pulmonary Medicine

, Washington, DC

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Divisions of Hematology and Oncology

, Washington, DC

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,

Divisions of Hematology and Oncology

, Washington, DC

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,

Divisions of Hematology and Oncology

, Washington, DC

Search for other works by this author on:

,

Pulmonary Medicine

, Washington, DC

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,

Pulmonary Medicine

, Washington, DC

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,

Divisions of Hematology and Oncology

, Washington, DC

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,

Divisions of Hematology and Oncology

, Washington, DC

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Received:

13 January 2006

Revision received:

07 February 2006

Accepted:

28 February 2006

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Stephania A Cormier, Anna G Taranova, Carrie Bedient, Thanh Nguyen, Cheryl Protheroe, Ralph Pero, Dawn Dimina, Sergei I Ochkur, Katie O’Neill, Dana Colbert, Theresa R Lombari, Stephanie Constant, Michael P McGarry, James J Lee, Nancy A Lee, Pivotal Advance: Eosinophil infiltration of solid tumors is an early and persistent inflammatory host response, Journal of Leukocyte Biology, Volume 79, Issue 6, Jun 2006, Pages 1131–1139, https://doi.org/10.1189/jlb.0106027
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Abstract

Tumor-associated eosinophilia has been observed in numerous human cancers and several tumor models in animals; however, the details surrounding this eosinophilia remain largely undefined and anecdotal. We used a B16-F10 melanoma cell injection model to demonstrate that eosinophil infiltration of tumors occurred from the earliest palpable stages with significant accumulations only in the necrotic and capsule regions. Furthermore, the presence of diffuse extracellular matrix staining for eosinophil major basic protein was restricted to the necrotic areas of tumors, indicating that eosinophil degranulation was limited to this region. Antibody-mediated depletion of CD4+ T cells and adoptive transfer of eosinophils suggested, respectively, that the accumulation of eosinophils is not associated with T helper cell type 2-dependent immune responses and that recruitment is a dynamic, ongoing process, occurring throughout tumor growth. Ex vivo migration studies have identified what appears to be a novel chemotactic factor(s) released by stressed/dying melanoma cells, suggesting that the accumulation of eosinophils in tumors occurs, in part, through a unique mechanism dependent on a signal(s) released from areas of necrosis. Collectively, these studies demonstrate that the infiltration of tumors by eosinophils is an early and persistent response that is spatial-restricted. It is more important that these data also show that the mechanism(s) that elicit this host response occur, independent of immune surveillance, suggesting that eosinophils are part of an early inflammatory reaction at the site of tumorigenesis.

© 2006 Society for Leukocyte Biology

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