ArticleInternational forum of allergy & rhinology2015
Topical cathelicidin (LL-37) an innate immune peptide induces acute olfactory epithelium inflammation in a mouse model.
Article in International forum of allergy & rhinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Immune responses in the injured olfactory and gustatory systems: a role in olfactory receptor neuron and taste bud regeneration?Chemical senses · 2022Review
- Gastric alarmin release: A warning signal in the development of gastric mucosal diseases.Frontiers in immunology · 2022Review
- Cathelicidin-mediated lipopolysaccharide signaling via intracellular TLR4 in colonic epithelial cells evokes CXCL8 production.Gut microbes · 2020Article
- The Network of Colonic Host Defense Peptides as an Innate Immune Defense Against Enteropathogenic Bacteria.Frontiers in immunology · 2020Review
- Prevention of sinonasal inflammation by a synthetic glycosaminoglycan.International forum of allergy & rhinology · 2017Article
- LL-37 causes cell death of human nasal epithelial cells, which is inhibited with a synthetic glycosaminoglycan.PloS one · 2017Article
- Alarmins and Antitumor Immunity.Clinical therapeutics · 2016Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCathelicidin (LL-37) is an endogenous innate immune peptide that is elevated in patients with chronic rhinosinusitis (CRS). The role of LL-37 in olfactory epithelium (OE) inflammation remains unknown. We hypothesized that: (1) LL-37 topically delivered would elicit profound OE inflammation; and (2) LL-37 induced inflammation is associated with increased infiltration of neutrophils and mast cells.
methodsTo test our hypothesis we challenged C57BL/6 mice intranasally with increasing concentrations of LL-37. At 24 hours tissues were examined histologically and scored for inflammatory cell infiltrate, edema, and secretory hyperplasia. In separate experiments, fluorescently conjugated LL-37 was instilled and tissues were examined at 0.5 and 24 hours. To test our last hypothesis, we performed tissue myeloperoxidase (MPO) assays for neutrophil activity and immunohistochemistry for tryptase to determine the mean number of mast cells per mm(2) .
resultsLL-37 caused increased inflammatory cell infiltrate, edema, and secretory cell hyperplasia of the sinonasal mucosa, with higher LL-37 concentrations yielding significantly more inflammatory changes (p < 0.01). Fluorescent LL-37 demonstrated global sinonasal epithelial binding and tissue distribution. Further, higher concentrations of LL-37 led to significantly greater MPO levels with dose-dependent increases in mast cell infiltration (p < 0.01).
conclusionLL-37 has dramatic inflammatory effects in the OE mucosa that is dose-dependent. The observed inflammatory changes in the olfactory mucosa were associated with the infiltration of both neutrophils and mast cells. Our biologic model represents a new model to further investigate the role of LL-37 in OE inflammation.
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