M2 macrophages expressing CD163 are known to suppress immune responses but have been also found in biopsies of patients with chronic kidney allograft injury associated with interstitial fibrosis. The aim of our study was to evaluate the expression of CD163 in blood monocytes, precursors of tissue macrophages, in kidney allograft recipients with uncomplicated outcome (n=94) compared with those developing acute rejection (n=44). Blood samples were collected before the transplantation and at 1 week, 1 month and 1 year. The expression of CD163 increased during the first week after the transplantation not only in classical (CD14+CD16-) but also in intermediate (CD14+CD16+) and nonclassical (CD14lowCD16+) monocytes in all patients regardless of their rejection status. In patients developing acute rejection, higher pre-transplant expression of CD163 on blood monocytes was found. In vitro experiments confirmed strong induction of membrane CD163 on monocytes together with CD206 (an alternative marker of M2 macrophages) in response to IL-10. We assume from our data that dramatic upregulation of CD163 by peripheral blood monocytes may have a pathophysiological role in early phases after kidney allograft transplantation and high pre-transplant expression of CD163 on blood monocytes might be involved in events leading to acute rejection.

• MeSH
• Allografts MeSH
• CD163 Antigen MeSH
• Antigens, Differentiation, Myelomonocytic blood   MeSH
• Biomarkers blood   MeSH
• Antigens, CD blood   MeSH
• Adult MeSH
• Interleukin-10 metabolism   MeSH
• Middle Aged MeSH
• Humans MeSH
• Macrophages immunology   metabolism   MeSH
• Adolescent MeSH
• Young Adult MeSH
• Monocytes immunology   metabolism   MeSH
• Receptors, Cell Surface blood   MeSH
• Graft Rejection blood   etiology   MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Kidney Transplantation * MeSH
• Up-Regulation MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Young Adult MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• CD163 Antigen MeSH
• Antigens, Differentiation, Myelomonocytic MeSH
• Biomarkers MeSH
• Antigens, CD MeSH
• IL10 protein, human MeSH Browser
• Interleukin-10 MeSH
• Receptors, Cell Surface MeSH

Macrophages located in airways and the alveolar space are continually exposed to different signals from the respiratory mucosa. In this respect, epithelial cells represent an important source of cytokines and mediators modulating the state of activation and/or differentiation of mononuclear phagocytes. Many of the proinflammatory genes induced in macrophages during immune and immunopathological reactions are regulated by transcription factor NF kappa B. The aim of our study was to characterize changes in the expression of genes associated with NF kappa B activation and signalling in THP-1 human macrophages co-cultured with A549 respiratory epithelial cells. At least 4-fold upregulation of mRNA level was found in 29 of 84 tested genes including genes for multiple cytokines and chemokines, membrane antigens and receptors, and molecules associated with NF kappa B signalling. The mRNA induction was confirmed at the level of protein expression by evaluating the release of IL-6 and IL-8 and by ICAM-1 expression. Blocking of one NFκB subunit by p65 siRNA inhibited the production of IL-6 in both cell types while IL-8 release from THP-1 cells did not seem to be affected. We conclude from our data that unstimulated respiratory epithelial cells regulate genes associated with NF kappa B dependent immune responses in human macrophages and that these interactions may play a key role in immediate responses in the respiratory mucosa.

• MeSH
• Cell Line MeSH
• Cytokines metabolism   MeSH
• Epithelial Cells metabolism   MeSH
• Coculture Techniques MeSH
• Humans MeSH
• Macrophages immunology   metabolism   MeSH
• RNA, Messenger genetics   MeSH
• Intercellular Adhesion Molecule-1 genetics   metabolism   MeSH
• NF-kappa B antagonists & inhibitors   metabolism   MeSH
• Gene Expression Regulation * MeSH
• Respiratory Mucosa immunology   metabolism   MeSH
• Signal Transduction MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Cytokines MeSH
• RNA, Messenger MeSH
• Intercellular Adhesion Molecule-1 MeSH
• NF-kappa B MeSH