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Self-assembled chitosan nanoparticles for intranasal delivery of recombinant protein interleukin-17 receptor C (IL-17RC): preparation and evaluation in asthma mice.

ABSTRACT: Asthma is mentioned as a chronic airway inflammatory disease, whose pathogenesis is complicated. The promotion of inflammation in asthma by IL-17A and IL-17F has been confirmed. In addition to covalent homodimers, both cytokines are also able to form heterodimers, further inducing downstream pathways via binding to the IL-17RA and IL-17RC receptor complex. In recent years, IL-17RA and its signal transduction pathway have been extensively researched. IL-17RC, however, remains relatively unexplored. In the present study, we self-assembled chitosan (CS) nanoparticles for intranasal delivery of recombinant protein IL-17RC (rIL-17RC) and preliminarily investigated its effect on a murine model of allergic asthma induced by ovalbumin (OVA). rIL-17RC was produced by the prokaryotic expression system and encapsulated into the CS nanoparticles via ionic cross-linking technique. The results showed that CS-RC nanoparticles via intranasal intervention significantly caused inhibition of mucus secretion and airway inflammatory cell infiltration, and reduced IL-4, IL-17, IL-17F levels in BALF. Hence, delivering receptor proteins such as IL-17RC, through CS nanoparticles as a carrier, could be an attractive therapeutic intervention for asthma.

SUBMITTER: Lv Y

PROVIDER: S-EPMC8806589 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature

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Self-assembled chitosan nanoparticles for intranasal delivery of recombinant protein interleukin-17 receptor C (IL-17RC): preparation and evaluation in asthma mice.

Lv Yongli Y Zhang Jianhua J Wang Chaoying C

Bioengineered 20211201 1

Asthma is mentioned as a chronic airway inflammatory disease, whose pathogenesis is complicated. The promotion of inflammation in asthma by IL-17A and IL-17F has been confirmed. In addition to covalent homodimers, both cytokines are also able to form heterodimers, further inducing downstream pathways via binding to the IL-17RA and IL-17RC receptor complex. In recent years, IL-17RA and its signal transduction pathway have been extensively researched. IL-17RC, however, remains relatively unexplore ...[more]

PMID: 34180764

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Project description:IL-17 is a modulator of the inflammatory response and is implicated in lung remodeling in both asthma and chronic obstructive pulmonary disease (COPD). Well as and probably in patients with asthma-COPD overlap (ACO). In this study, we evaluated the response of the airways and alveolar septa to anti-IL-17 treatment in an ACO model. Fifty-six male BALB/c mice were sensitized with ovalbumin (OVA group), received porcine pancreatic elastase (PPE group), or both (ACO group). Mice were then treated with either anti-IL-17 monoclonal antibody or saline. We evaluated hyperresponsiveness, bronchoalveolar lavage fluid (BALF) cell counts, and mean alveolar diameter. We quantified inflammatory, response, extracellular matrix remodeling, oxidative stress markers, and signaling pathway markers. Anti-IL-17 treatment in the ACO anti-IL-17 group reduced the maximum response of respiratory system Rrs, Ers, Raw, Gtis, this when compared to the ACO group (p<0.05). There was a reduction in the total number of inflammatory cells, neutrophils, and macrophages in the BALF in the ACO anti-IL-17 group compared to the ACO group (p<0.05). There was attenuated dendritic cells, CD4+, CD8+, FOXP3, IL-1β, IL-2, IL-6, IL-13, IL-17, IL-33 in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p<0.05). We observed a reduction of MMP-9, MMP-12, TIMP-1, TGF-β, collagen type I in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p < 0.05). We also observed a reduction of iNOS and 8-iso-PGF2α in the airways and in the alveolar septum was reduced in the ACO anti-IL-17group compared to the ACO group (p < 0.05). Regarding the signaling pathways, NF-kB, ROCK-1, and ROCK-2 in the airway and alveolar septum were attenuated in the ACO anti-IL-17 group when compared to the ACO group (p<0.05). Our results suggest that inhibiting IL-17 modulates cell-associated cytokine production in lung tissue, extracellular matrix remodeling, and oxidative stress in ACO through the modulation of NF-kB and FOXP3.

Dataset Information

Self-assembled chitosan nanoparticles for intranasal delivery of recombinant protein interleukin-17 receptor C (IL-17RC): preparation and evaluation in asthma mice.

Publications

Self-assembled chitosan nanoparticles for intranasal delivery of recombinant protein interleukin-17 receptor C (IL-17RC): preparation and evaluation in asthma mice.

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