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Boosting innate immune mechanisms could be one attractive alternative in the defence against infectious diseases. The cholesterol-lowering drugs, statins, have been demonstrated to also affect the immune system. Here we investigate the effect of statins on the expression of the human cathelicidin anti-microbial peptide (CAMP) LL-37\/hCAP-18 [encoded by the CAMP gene] and explore the underlying mechanisms in four epithelial cell lines of different origin. Simvastatin induced CAMP expression in bladder epithelial cells telomerase-immortalized uroepithelial cells (TERT-NHUCs), intestinal cells HT-29 and keratinocytes HEKa, but not in airway epithelial cells A549. Gene induction in HEKa cells was reversible by mevalonate, while this effect was independent of the cholesterol biosynthesis pathway in TERT-NHUCs. Instead, inhibition of histone deacetylases by simvastatin seems to be involved. For HT-29 cells, both mechanisms may contribute. In addition, simvastatin increased transcription of the vitamin D-activating enzyme CYP27B1 which, in turn, may activate LL-37\/hCAP-18 production. Taken together, simvastatin is able to promote the expression of LL-37\/hCAP-18, but cell line-specific differences in efficacy and the involved signalling pathways exist.<\/jats:p>","DOI":"10.1111\/cei.13217","type":"journal-article","created":{"date-parts":[[2018,9,16]],"date-time":"2018-09-16T05:05:32Z","timestamp":1537074332000},"page":"265-276","source":"Crossref","is-referenced-by-count":8,"title":["Statins influence epithelial expression of the anti-microbial peptide LL-37\/hCAP-18 independently of the mevalonate pathway"],"prefix":"10.1093","volume":"195","author":[{"given":"P","family":"L\u00fcthje","sequence":"first","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden"},{"name":"Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden"},{"name":"Division of Clinical Microbiology, Karolinska University Hospital, Stockholm, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S","family":"Walker","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden"},{"name":"Division of Clinical Microbiology, Karolinska University Hospital, Stockholm, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W","family":"Kamolvit","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden"},{"name":"Division of Clinical Microbiology, Karolinska University Hospital, Stockholm, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S","family":"Mohanty","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden"},{"name":"Division of Clinical Microbiology, Karolinska University Hospital, Stockholm, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K","family":"P\u00fctsep","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A","family":"Brauner","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden"},{"name":"Division of Clinical Microbiology, Karolinska University Hospital, Stockholm, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2018,10,11]]},"reference":[{"key":"2021121023244014600_cei13217-bib-0001","doi-asserted-by":"crossref","first-page":"165","DOI":"10.1097\/MOL.0b013e3283453e41","article-title":"Mechanisms for the anti-inflammatory effects of statins","volume":"22","author":"Bu","year":"2011","journal-title":"Curr Opin 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