Elovanoids counteract inflammatory signaling, autophagy, endoplasmic reticulum stress, and eenescence gene programming in human nasal epithelial cells exposed to allergens

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dc.contributor.authorResano Lizaldre, Alfredo
dc.contributor.authorBhattacharjee, Surjyadipta
dc.contributor.authorBarajas Vélez, Miguel Ángel
dc.contributor.authorDo, Khanh V.
dc.contributor.authorAguado Jiménez, Roberto
dc.contributor.authorRodríguez, David
dc.contributor.authorPalacios Peláez, Ricardo
dc.contributor.authorBazán, Nicolás G.
dc.contributor.departmentCiencias de la Saludes_ES
dc.contributor.departmentOsasun Zientziakeu
dc.date.accessioned2022-04-07T12:10:25Z
dc.date.available2022-04-07T12:10:25Z
dc.date.issued2022
dc.description.abstractTo contribute to further understanding the cellular and molecular complexities of inflammatory-immune responses in allergic disorders, we have tested the pro-homeostatic elovanoids (ELV) in human nasal epithelial cells (HNEpC) in culture challenged by several allergens. ELV are novel bioactive lipid mediators synthesized from the omega-3 very-long-chain polyunsaturated fatty acids (VLC-PUFA,n-3). We ask if: (a) several critical signaling events that sustain the integrity of the human nasal epithelium and other organ barriers are perturbed by house dust mites (HDM) and other allergens, and (b) if ELV would participate in beneficially modulating these events. HDM is a prevalent indoor allergen that frequently causes allergic respiratory diseases, including allergic rhinitis and allergic asthma, in HDM-sensitized individuals. Our study used HNEpC as an in vitro model to study the effects of ELV in counteracting HDM sensitization resulting in inflammation, endoplasmic reticulum (ER) stress, autophagy, and senescence. HNEpC were challenged with the following allergy inducers: LPS, poly(I:C), or Dermatophagoides farinae plus Dermatophagoides pteronyssinus extract (HDM) (30 µg/mL), with either phosphate-buffered saline (PBS) (vehicle) or ELVN-34 (500 nM). Results show that ELVN-34 promotes cell viability and reduces cytotoxicity upon HDM sensitization of HNEpC. This lipid mediator remarkably reduces the abundance of pro-inflammatory cytokines and chemokines IL-1β, IL-8, VEGF, IL-6, CXCL1, CCL2, and cell adhesion molecule ICAM1 and restores the levels of the pleiotropic anti-inflammatory IL-10. ELVN-34 also lessens the expression of senescence gene programming as well as of gene transcription engaged in pro-inflammatory responses. Our data also uncovered that HDM triggered the expression of key genes that drive autophagy, unfolded protein response (UPR), and matrix metalloproteinases (MMP). ELVN-34 has been shown to counteract these effects effectively. Together, our data reveal a novel, pro-homeostatic, cell-protective lipid-signaling mechanism in HNEpC as potential therapeutic targets for allergies.en
dc.format.extent16 p.
dc.format.mimetypeapplication/pdfen
dc.format.mimetypeapplication/zipen
dc.identifier.doi10.3390/pharmaceutics14010113
dc.identifier.issn1999-4923
dc.identifier.urihttps://academica-e.unavarra.es/handle/2454/42699
dc.language.isoengen
dc.publisherMDPI
dc.relation.ispartofPharmaceutics, 14 (1), 2022
dc.relation.publisherversionhttps://doi.org/10.3390/pharmaceutics14010113
dc.rights© 2022 by the authors. Creative Commons Attribution 4.0 Internationalen
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAllergyen
dc.subjectAnti-inflammatoryen
dc.subjectElovanoidsen
dc.subjectHouse dust miteen
dc.subjectInflammationen
dc.subjectLipid mediatorsen
dc.titleElovanoids counteract inflammatory signaling, autophagy, endoplasmic reticulum stress, and eenescence gene programming in human nasal epithelial cells exposed to allergensen
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dspace.entity.typePublication
relation.isAuthorOfPublication13c062cf-7c7d-4711-9511-a4dcdc95330b
relation.isAuthorOfPublication2e998efa-ca5a-491e-9e7f-a8fbbd0094ce
relation.isAuthorOfPublication41367ea8-f3cf-4544-8cb7-fb4f57da6283
relation.isAuthorOfPublication.latestForDiscovery13c062cf-7c7d-4711-9511-a4dcdc95330b

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