Squamous carcinoma cells influence monocyte phenotype and suppress lipopolysaccharide-induced TNF-alpha in monocytes

Inflammation. 2010 Aug;33(4):207-23. doi: 10.1007/s10753-009-9175-6.

Abstract

Bacteria and chronic inflammation are present in squamous cell carcinoma of the head and neck (HNSCC), but their roles in the pathogenesis of HNSCC are unclear. Our studies described here revealed that human monocytes co-cultured short term with HNSCC cells were more likely to express CD16, and CD16(+) small mononuclear cells were common in HNSCC specimens. In addition, we identified monocytes as the primary source of LPS-induced IL-6 and TNF-alpha in the monocyte-HNSCC co-cultures. Remarkably, relative to LPS-stimulated monocytes cultured alone, HNSCC cells profoundly suppressed LPS-induced TNF-alpha in monocytes, without compromising IL-6 production. High levels of cytoprotective factors like IL-6 and low levels of TNF-alpha are important for the tumor microenvironment that enables tumor cell survival, affects monocyte differentiation and may contribute to tumor colonization by bacteria. This study provides novel observations that HNSCC cells affect monocyte phenotype and function, which are relevant to the regulation of the HNSCC microenvironment.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Squamous Cell / immunology
  • Carcinoma, Squamous Cell / pathology*
  • Cell Line, Tumor / cytology
  • Cells, Cultured / cytology
  • Cells, Cultured / drug effects
  • Cells, Cultured / metabolism
  • Coculture Techniques
  • Disease Progression
  • GPI-Linked Proteins
  • Head and Neck Neoplasms / immunology
  • Head and Neck Neoplasms / pathology*
  • Humans
  • Inflammation
  • Interleukin-6 / biosynthesis
  • Interleukin-6 / metabolism
  • Keratinocytes / cytology
  • Lipopolysaccharides / pharmacology*
  • Monocytes / cytology
  • Monocytes / drug effects
  • Monocytes / immunology*
  • Monocytes / metabolism
  • Mouth Mucosa / pathology
  • Phagocytosis
  • Phenotype
  • Receptors, IgG / biosynthesis
  • Receptors, IgG / immunology*
  • Stomatitis / pathology
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • FCGR3B protein, human
  • GPI-Linked Proteins
  • IL6 protein, human
  • Interleukin-6
  • Lipopolysaccharides
  • Receptors, IgG
  • Tumor Necrosis Factor-alpha
  • lipopolysaccharide, E. coli O26-B6