The role played by granulocyte colony‐stimulating factor in hidradenitis suppurativa

Abstract

British Journal of DermatologyVolume 185, Issue 1 p. e18-e18 Plain Language Summary The role played by granulocyte colony-stimulating factor in hidradenitis suppurativa First published: 02 July 2021 https://doi.org/10.1111/bjd.20456AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat Abstract Linked Article: Wolk et al. Br J Dermatol 2021; 185:164–176. Hidradenitis suppurativa (HS) is a quite common, chronic skin disease that greatly impairs quality of life. Typically, the disease starts during early adulthood. Patients develop painful, tissue-destructive skin inflammation with abscesses and tunnels in body folds such as the armpit and groin. Certain inflammatory immune cells, called neutrophilic granulocytes, are key players in the formation of the abscesses and tunnels found in HS. Surprisingly, however, no data from investigations into these important cells have been published so far for HS. It is known that the development, function and survival of neutrophilic granulocytes is regulated by a body-own protein called granulocyte colony-stimulating factor (G-CSF). With that in mind, the authors of this German study investigated the role of G-CSF in HS, as the authors had found high levels of G-CSF in the diseased skin of patients. Laboratory experiments revealed that two specific types of skin tissue cells, called fibroblasts and keratinocytes, are the main producers of G-CSF. Proteins derived from immune cells, called interleukin (IL)-1ß and IL-17, turned out to be the major triggers of that G-CSF production. Matching these results, experimental blocking of IL-1 in collected HS skin samples reduced the G-CSF levels. Further investigations allowed the authors to suggest that in the diseased skin, G-CSF prolongs the survival of neutrophilic granulocytes and enhances their activation, induced by bacteria and damaged host cells. More importantly, G-CSF was found to stimulate the granulocytes’ production of enzymes that, via different mechanisms, digest the skin tissue. This observation is consistent with the typical destructive and progressive nature of HS. The authors have concluded that G-CSF induces a previously unknown inflammatory cascade in HS skin. Consequently, inhibition of G-CSF’s action may be a promising therapeutic approach for treatment in patients with HS. Volume185, Issue1July 2021Pages e18-e18 RelatedInformation