The epithelial-derived cytokine, thymic stromal lymphopoietin (TSLP), has been identified as an important cytokine in allergic inflammation. Various studies demonstrated elevate levels and expression of TSLP in airways of asthmatic. Environmental factors such as toll-like receptor ligands, viruses, microbes, allergen sources, diesel exhaust and cigarette smoke trigger TSLP production by epithelial cells. It has been described that TSLP amplifies the differentiation of peritoneal macrophages and bone marrow derived macrophages in M2-type in mice. Our aims were to investigate the role of TSLP in the M1/M2 polarization of human lung macrophages (LM).

Lung macrophages were isolated from tissues obtained after surgical resection for cancer. Macrophages were treated with LPS (10ng/mL) or IL-4 (10ng/mL) in presence or not of TSLP (10–30ng/mL) for 24h or 48h. Production of cytokines of the M1-type (TNF-α, CCL-2, CXCL-8 and CXCL-1) and the M2-type (CCL-13, CCL-17, CCL-18 and CCL-22) was determined by ELISA and cytokine expression by RT-qPCR.

Exposure to TSLP did not alter the production of TNF-α, CXCL-8 and CXCL-1 either in unstimulated LM or in LPS-stimulated LM. However, CCL-2 production was increased by TSLP at 20ng/mL in unstimulated LM. In addition, TSLP (10ng/mL but not 30ng/mL) increased M2-type cytokine production (CCL-13 and CCL-17, but did not CCL-18 and CCL-22). TSLP also increased IL4-induced CCL-17 and CCL-22. Expression of CCL-17 and CCL-13 was also increased by TSLP in unstimulated LM, and expression of CCL-17 and CCL-22 was increased in IL-4-stimulantes LM.

Our results show that TSLP can activate unstimulated LM and modulate the IL-4-induced polarization of LM in the M2 subtype.