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Host-derived interleukin-5 promotes adenocarcinoma-induced malignant pleural effusion
Georgios T Stathopoulos1, Taylor P Sherrill, Sophia P Karabela
1Vanderbilt University School of Medicine, Nashville, Tennessee, USA. gstathop@med.uoa.gr
Rationale:
IL-5 is a T helper 2 cytokine important in the trafficking and survival of eosinophils. Because eosinophils can be found in malignant pleural effusions (MPE) from mice and humans, we asked whether IL-5 is involved in the pathogenesis of MPE.
Objectives:
To determine the role of IL-5 in MPE formation.
Methods:
The effects of IL-5 on experimental MPE induced in C57BL/6 mice by intrapleural injection of syngeneic lung (Lewis lung cancer [LLC]) or colon (MC38) adenocarcinoma cells were determined using wild-type (il5(+/+)) and IL-5-deficient (il5⁻(/)⁻) mice, exogenous administration of recombinant mouse (rm) IL-5, and in vivo antibody-mediated neutralization of endogenous IL-5. The direct effects of rmIL-5 on LLC cell proliferation and gene expression in vitro were determined by substrate reduction and microarray.
Measurements And Main Results:
Eosinophils and IL-5 were present in human and mouse MPE, but the cytokine was not detected in mouse (LLC) or human (A549) lung and mouse colon (MC38) adenocarcinoma-conditioned medium, suggesting production by host cells in MPE. Compared with il5(+/+) mice, il5⁻(/)⁻ mice showed markedly diminished MPE formation in response to both LLC and MC38 cells. Exogenous IL-5 promoted MPE formation in il5(+/+) and il5⁻(/)⁻ mice, whereas anti-IL-5 antibody treatment limited experimental MPE in il5(+/+) mice. Exogenous IL-5 had no effects on LLC cell proliferation and gene expression; however, IL-5 was found to be responsible for recruitment of eosinophils and tumor-promoting myeloid suppressor cells to MPE in vivo.
Conclusions:
Host-derived IL-5 promotes experimental MPE and may be involved in the pathogenesis of human MPE.
Insights
Interleukin-5 (IL-5) promotes malignant pleural effusion (MPE) formation by recruiting eosinophils and myeloid suppressor cells. Blocking IL-5 reduces MPE development, suggesting its role in human MPE pathogenesis.
Area of Science:
- Immunology
- Oncology
- Cell Biology
Background:
- Interleukin-5 (IL-5) is a T helper 2 cytokine crucial for eosinophil trafficking and survival.
- Eosinophils are present in malignant pleural effusions (MPE) in both mice and humans.
- The role of IL-5 in the pathogenesis of MPE remains to be elucidated.
Purpose of the Study:
- To investigate the role of IL-5 in the formation of malignant pleural effusions (MPE).
Main Methods:
- Experimental MPE was induced in wild-type and IL-5-deficient mice using Lewis lung cancer (LLC) or MC38 adenocarcinoma cells.
- Effects of exogenous recombinant mouse (rm) IL-5 and anti-IL-5 antibodies were assessed.
- In vitro studies evaluated rmIL-5's direct effects on LLC cell proliferation and gene expression.
Main Results:
- IL-5 deficiency significantly reduced MPE formation in mice.
- Exogenous IL-5 administration enhanced MPE development, while IL-5 neutralization limited it.
- IL-5 promoted the recruitment of eosinophils and myeloid suppressor cells to MPE, but did not directly affect tumor cell proliferation or gene expression in vitro.
Conclusions:
- Host-derived IL-5 plays a key role in promoting experimental MPE.
- IL-5 may be involved in the pathogenesis of human malignant pleural effusions.
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