{'fraction_non_alphanumeric': 0.015644820295983086, 'fraction_numerical': 0.024101479915433405, 'mean_word_length': 5.429347826086956, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Letter to the Editor

To the Editor, With great interest we have read the recent article by Dahlstrand Rudin and colleagues addressing CD177+ and CD177− neutrophilic granulocyte subset accumulation in human periodontitis.1 We would like to discuss a possible additional explanation of these findings beyond differential recruitment. The flow cytometric histogram in figure 2E appears to depict an upward shift in the CD177mean fluorescence intensity (MFI) of the CD177 negative population. This is somewhat reminiscent of an earlier report of enhanced neutrophil CD177 expression in sternal wounds after cardiac surgery.2 An elevated CD177-MFI on the negative subpopulation could point at transfer of CD177 from cell to cell. Transfer of a large range of functional proteins has been described in the form of extracellular vesicles as well as smaller membrane particles.3,4 We would therefore like to ask the authors for systematic analysis of the CD177 MFI in the negative populations, both in vivo and after the in vitro migration assays. This first step to address this hypothesis could in future studies be complemented by confocal microscopy to discern granulocytes with CD177 exclusively on the surface from cells that also contain CD177 in their preformed intracellular granules. Extracellular vesicles can transfer functional receptors and mediate cell activation and cellular interactions in many types of inflammation.3,4 Transfer of CD177 could therefore be relevant for neutrophil interactions, for example, with its binding partner CD31/PECAM on the endothelium.5 Determination whether such a transfer occurs in their system could also be helped by analysis of neutrophil subsets and their MFIs in both the upper and lower well of the transwell migration system (figure 5A and B) and the in vivo measurements (figure 2D and E). It is conceivable that extracellular vesicle formation depends on composition of the local inflammatory milieu. In our own study on CD177+ neutrophil migration in highly acute, mostly bacterial peritonitis, we did not observe a change in CD177 MFI of the CD177negative neutrophil subpopulation.6 Possibly, formation of membrane vesicles that mediate receptor transfer is favored in more chronic inflammatory processes investigated in the present publication and earlier.1,2 Sincerely, Julia Volkmann, Sibylle von Vietinghoff