Recombinant Human IL-32θ Induces Polarization Into M1-like Macrophage in Human Monocytic Cells.
Hyo-Min ParkJae-Young ParkNa-Yeon KimHyemoon KimHong-Gyum KimDong-Ju SonJin Tae HongDo-Young YoonPublished in: Immune network (2024)
The tumor microenvironment (TME) is formed by several immune cells. Notably, tumor-associated macrophages (TAMs) are existed in the TME that induce angiogenesis, metastasis, and proliferation of cancer cells. Recently, a point-mutated variant of IL-32θ was discovered in breast cancer tissues, which suppressed migration and proliferation through intracellular pathways. Although the relationship between cancer and IL-32 has been previously studied, the effects of IL-32θ on TAMs remain elusive. Recombinant human IL-32θ (rhIL-32θ) was generated using an Escherichia coli expression system. To induce M0 macrophage polarization, THP-1 cells were stimulated with PMA. After PMA treatment, the cells were cultured with IL-4 and IL-13, or rhIL-32θ. The mRNA level of M1 macrophage markers (IL-1β, TNFα, inducible nitric oxide synthase) were increased by rhIL-32θ in M0 macrophages. On the other hand, the M2 macrophage markers (CCL17, CCL22, TGFβ, CD206) were decreased by rhIL-32θ in M2 macrophages. rhIL-32θ induced nuclear translocation of the NF-κB via regulation of the MAPK (p38) pathway. In conclusion, point-mutated rhIL-32θ induced the polarization to M1-like macrophages through the MAPK (p38) and NF-κB (p65/p50) pathways.
Keyphrases
- signaling pathway
- induced apoptosis
- recombinant human
- escherichia coli
- endothelial cells
- cell cycle arrest
- pi k akt
- rheumatoid arthritis
- nitric oxide
- squamous cell carcinoma
- gene expression
- poor prognosis
- long non coding rna
- pseudomonas aeruginosa
- inflammatory response
- drug induced
- liver injury
- cystic fibrosis
- transforming growth factor
- vascular endothelial growth factor
- induced pluripotent stem cells
- toll like receptor
- childhood cancer
- candida albicans