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Antimicrobial peptide LL-37 increases rhinovirus-induced interferon β expression in human airway epithelial cells through a Ca2+-dependent mechanism

Cerps, Samuel LU ; Ramu, Sangeetha LU ; Gidlöf, Olof LU ; Menzel, Mandy LU ; Swärd, Karl LU ; Uller, Lena LU and Nilsson, Bengt-Olof LU orcid (2025) In Biochemistry and Biophysics Reports 43.
Abstract
The human cathelicidin LL-37 is active against both bacteria and viruses, but it also shows immunomodulatory properties. Here, we assess the impact of LL-37 on viral signaling in human airway epithelial BEAS-2B cells infected with the respiratory pathogen rhinovirus (RV). We show that LL-37 (4 μM) enhances RV-induced expression of interferon β (IFNβ) transcript and reduces viral-load. LL-37-evoked potentiation of RV-stimulated IFNβ does not involve up-regulation of the classical viral TLR3, MDA5 and RIG-I receptors. Moreover, the LL-37-induced stimulation of IFNβ expression in the presence of RV is abolished by chloroquine, an inhibitor of endosomal acidification. Interestingly, RV + LL-37-induced stimulation of IFNβ is observed in the... (More)
The human cathelicidin LL-37 is active against both bacteria and viruses, but it also shows immunomodulatory properties. Here, we assess the impact of LL-37 on viral signaling in human airway epithelial BEAS-2B cells infected with the respiratory pathogen rhinovirus (RV). We show that LL-37 (4 μM) enhances RV-induced expression of interferon β (IFNβ) transcript and reduces viral-load. LL-37-evoked potentiation of RV-stimulated IFNβ does not involve up-regulation of the classical viral TLR3, MDA5 and RIG-I receptors. Moreover, the LL-37-induced stimulation of IFNβ expression in the presence of RV is abolished by chloroquine, an inhibitor of endosomal acidification. Interestingly, RV + LL-37-induced stimulation of IFNβ is observed in the absence but not in the presence of the Ca2+ chelating agent EGTA, indicating that Ca2+ is critical for this effect. Indeed, we demonstrate that LL-37 increases intracellular [Ca2+] in cells loaded with the fluorescent Ca2+ indicator Fluo-4 AM. Furthermore, we reveal that treatment with RV in combination with the Ca2+ ionophore A23187 promotes IFNβ expression, showing the importance of Ca2+. In conclusion, we demonstrate that LL-37 acts in synergy with RV to enhance IFNβ expression and that this effect involves LL-37-induced increase in intracellular [Ca2+]. (Less)
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author
; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Biochemistry and Biophysics Reports
volume
43
article number
102105
publisher
Elsevier
external identifiers
  • pmid:40612001
  • scopus:105008547651
ISSN
2405-5808
DOI
10.1016/j.bbrep.2025.102105
language
English
LU publication?
yes
id
3a3ebe4f-d129-4971-b993-dcc5fb6640cb
alternative location
https://linkinghub.elsevier.com/retrieve/pii/S240558082500192X
date added to LUP
2025-07-29 08:54:55
date last changed
2025-10-14 10:20:02
@article{3a3ebe4f-d129-4971-b993-dcc5fb6640cb,
  abstract     = {{The human cathelicidin LL-37 is active against both bacteria and viruses, but it also shows immunomodulatory properties. Here, we assess the impact of LL-37 on viral signaling in human airway epithelial BEAS-2B cells infected with the respiratory pathogen rhinovirus (RV). We show that LL-37 (4 μM) enhances RV-induced expression of interferon β (IFNβ) transcript and reduces viral-load. LL-37-evoked potentiation of RV-stimulated IFNβ does not involve up-regulation of the classical viral TLR3, MDA5 and RIG-I receptors. Moreover, the LL-37-induced stimulation of IFNβ expression in the presence of RV is abolished by chloroquine, an inhibitor of endosomal acidification. Interestingly, RV + LL-37-induced stimulation of IFNβ is observed in the absence but not in the presence of the Ca2+ chelating agent EGTA, indicating that Ca2+ is critical for this effect. Indeed, we demonstrate that LL-37 increases intracellular [Ca2+] in cells loaded with the fluorescent Ca2+ indicator Fluo-4 AM. Furthermore, we reveal that treatment with RV in combination with the Ca2+ ionophore A23187 promotes IFNβ expression, showing the importance of Ca2+. In conclusion, we demonstrate that LL-37 acts in synergy with RV to enhance IFNβ expression and that this effect involves LL-37-induced increase in intracellular [Ca2+].}},
  author       = {{Cerps, Samuel and Ramu, Sangeetha and Gidlöf, Olof and Menzel, Mandy and Swärd, Karl and Uller, Lena and Nilsson, Bengt-Olof}},
  issn         = {{2405-5808}},
  language     = {{eng}},
  month        = {{09}},
  publisher    = {{Elsevier}},
  series       = {{Biochemistry and Biophysics Reports}},
  title        = {{Antimicrobial peptide LL-37 increases rhinovirus-induced interferon β expression in human airway epithelial cells through a Ca2+-dependent mechanism}},
  url          = {{http://dx.doi.org/10.1016/j.bbrep.2025.102105}},
  doi          = {{10.1016/j.bbrep.2025.102105}},
  volume       = {{43}},
  year         = {{2025}},
}