The Relationship between the M1/M2 Macrophage Polarization and the Degree of Ossicular Erosion in Human Acquired Cholesteatoma: An Immunohistochemical Study.

J Clin Med

Institute of Pathology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 10117 Berlin, Germany.

Published: August 2022


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Article Abstract

The differential involvement of the macrophage activation phenotypes (M1 vs. M2) has been linked to disease severity in various chronic inflammatory disorders. Pharmacologic manipulation of the M1/M2 macrophage polarization has shown therapeutic potential. Cholesteatoma is a destructive chronic middle ear disease with potentially life-threatening complications. The distribution of macrophage polarization phenotypes in middle ear cholesteatoma has not been described. In the present study, human cholesteatoma specimens acquired during tympanomastoidectomy were retrospectively retrieved and immunohistochemically characterized using a combination of antibodies labeling M1 macrophages (CD80), M2 macrophages (CD163), and total macrophages (CD68). The correlations between the immunohistochemical findings and clinical presentation were assessed. The findings revealed that cholesteatomas with more extensive ossicular erosion demonstrated a significantly higher number of M1 (CD80+) cells and a higher M1/M2 ratio than less invasive cholesteatomas (Wilcoxon test, p < 0.05). The extent of ossicular erosion correlated significantly with the M1/M2 ratio (Spearman correlation coefficient ρ = 0.4, p < 0.05). Thus, the degree of ossicular erosion in human acquired cholesteatoma appears to be related to the M1/M2 macrophage polarization. The investigation of macrophage polarization and functions in various clinical presentations of middle ear cholesteatoma is of great interest since it may contribute to the development of pharmaceutical treatment approaches.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9410162PMC
http://dx.doi.org/10.3390/jcm11164826DOI Listing

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