Keratinocyte chemoattractant (interleukin‐8) regulation of sinonasal cilia function in a murine model

Shen, Junhao; Chen, Bei; Cohen, Noam A.

doi:10.1002/alr.20087

Cited by 9 publications

(8 citation statements)

References 22 publications

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“…In CRS, patients may have dysfunctional ciliary beating from direct effects of the organisms or from an inappropriate inflammatory response 879–881 . Mucociliary stasis is a common finding of CRS, which propagates the disease as the stagnant mucus can harbor infection and sustain inflammatory mediators 841 .…”

Section: Chronic Rhinosinusitis Without Nasal Polyps (Crssnp)mentioning

confidence: 99%

“…An overactive inflammatory environment or defects in cellular transport may also be the cause of some CRS ciliary pathology. TNF‐α, IL‐1β, IL‐5, and IL‐8 are consistently elevated in CRS cases, 43,879,889,890 and chronic elevation of these factors often blunts ciliary response 880 . TNF‐α has been shown to prevent CBF increases in response to mechanical stimulation, 874 while cycles of inflammation can cause ciliary loss or ciliary abnormalities in a chronic setting 873 .…”

Section: Chronic Rhinosinusitis Without Nasal Polyps (Crssnp)mentioning

confidence: 99%

See 1 more Smart Citation

International consensus statement on allergy and rhinology: rhinosinusitis 2021

Orlandi

Kingdom

Smith

et al. 2021

Int Forum Allergy Rhinol

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518

479

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I. Executive Summary Background The 5 years since the publication of the first International Consensus Statement on Allergy and Rhinology: Rhinosinusitis (ICAR‐RS) has witnessed foundational progress in our understanding and treatment of rhinologic disease. These advances are reflected within the more than 40 new topics covered within the ICAR‐RS‐2021 as well as updates to the original 140 topics. This executive summary consolidates the evidence‐based findings of the document. Methods ICAR‐RS presents over 180 topics in the forms of evidence‐based reviews with recommendations (EBRRs), evidence‐based reviews, and literature reviews. The highest grade structured recommendations of the EBRR sections are summarized in this executive summary. Results ICAR‐RS‐2021 covers 22 topics regarding the medical management of RS, which are grade A/B and are presented in the executive summary. Additionally, 4 topics regarding the surgical management of RS are grade A/B and are presented in the executive summary. Finally, a comprehensive evidence‐based management algorithm is provided. Conclusion This ICAR‐RS‐2021 executive summary provides a compilation of the evidence‐based recommendations for medical and surgical treatment of the most common forms of RS.

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Section: Chronic Rhinosinusitis Without Nasal Polyps (Crssnp)mentioning

confidence: 99%

Section: Chronic Rhinosinusitis Without Nasal Polyps (Crssnp)mentioning

confidence: 99%

International consensus statement on allergy and rhinology: rhinosinusitis 2021

Orlandi

Kingdom

Smith

et al. 2021

Int Forum Allergy Rhinol

Self Cite

518

479

View full text Add to dashboard Cite

show abstract

“…The increase of serum KC with LXB 4 was unexpected and distinct from LXA 4 24 . In addition to its well defined role as a neutrophil chemoattractant, KC can modulate ciliary function of murine sinonasal epithelial cells 25 – 26 , suggesting that LXB 4 might enhance mucociliary clearance via this mechanism. In contrast to KC, serum IL-17 levels were low and significantly decreased by LXB 4 .…”

Section: Discussionmentioning

confidence: 99%

Lipoxin B4 promotes the resolution of allergic inflammation in the upper and lower airways of mice

et al. 2015

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Chronic mucosal inflammation is the hallmark of important and common airway diseases, such as allergic rhinitis and asthma. Lipoxin A4 (LXA4) is an endogenous pro-resolving mediator for mucosal inflammation that decreases allergic and asthmatic responses. Lipoxin B4 (LXB4) is a structurally distinct member of the lipoxin family that signals in a manner distinct from LXA4. LXB4 is generated by mucosal tissues, but its actions in allergic inflammation are unknown. Here, we used murine models of allergic rhinitis and asthma to investigate LXB4’s activity in mucosal inflammation. In the upper airway, LXB4 significantly decreased nasal mucosal leukocytes and degranulation of mast cells and eosinophils. In the lower airway, LXB4 significantly decreased airway inflammation, mucus metaplasia and hyper- responsiveness. Inhibition of mast cell degranulation in vivo by LXB4 was more potent than dexamethasone, and these agents displayed unique profiles for cytokine regulation; however, their overall anti-inflammatory actions were comparable. LXB4 decreased eotaxin-dependent eosinophil chemotaxis, IgE-mediated mast cell degranulation and expression of type 2 cytokine receptors. Together, these findings indicate that LXB4 carries cell type selective and mucosal protective actions that broaden the lipoxin family’s therapeutic potential for upper and lower airway catabasis.

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“…Keratinocyte chemoattractant (KC), also known as chemokine (C‐X‐C motif) ligand (CXCL1) or growth‐regulated oncogene α, is an immunoregulatory cytokine belonging to the CXC family . KC is expressed in melanoma, neutrophils, and epithelial cells , and is involved in inflammation, angiogenesis, wound healing, and tumourigenesis .…”

Section: Introductionmentioning

confidence: 99%

NLRP3 inflammasome induced liver graft injury through activation of telomere‐independent RAP1/KC axis

Liu

Yeung

et al. 2017

The Journal of Pathology

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Acute-phase inflammation plays a critical role in liver graft injury. Inflammasomes, multi-molecular complexes in the cytoplasm, are responsible for initiating inflammation. Here, we aimed to explore the role of inflammasomes in liver graft injury and further to investigate the regulatory mechanism. In a clinical liver transplant cohort, we found that intragraft expression of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasomes was significantly up-regulated post-transplantation. Importantly, overexpression of NLRP3 was strongly associated with poor liver function characterized by high levels of ALT, AST, and urea, as well as neutrophil infiltration after transplantation. The significant correlation between NLRP3 and IL-1β mRNA levels led us to focus on one of the associated upstream regulators, telomere-independent repressor activator protein 1 (RAP1), which was further proved to be co-localized with NLRP3 in neutrophils. In the liver of a mouse model (hepatic ischaemia/reperfusion and hepatectomy model) and isolated neutrophils from RAP1 mice, the expression levels of NLRP3 and keratinocyte chemoattractant (KC) were significantly down-regulated in contrast to those in wild types. The levels of ALT and AST, as well as the neutrophil infiltration, were also decreased by RAP1 deficiency. In our clinical validation, intragraft KC expression was associated with NLRP3 and co-localized with RAP1 in neutrophils. Furthermore, NLRP3 inflammasomes were up-regulated by recombinant KC in the isolated neutrophils and liver of the mouse model. Our data demonstrated that NLRP3 inflammasomes, activated by the RAP1/KC axis, played a critical role in initiating inflammation during the early stage of liver graft injury. Targeting RAP1/KC/NLRP3 inflammasomes may offer a new therapeutic strategy against liver graft injury. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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Keratinocyte chemoattractant (interleukin‐8) regulation of sinonasal cilia function in a murine model

Abstract: Our results demonstrate modulation of cilia function of murine sinonasal epithelial cells by the inflammatory cytokine KC, which acutely increases basal CBF while decreasing the response of cilia to mechanical stimulation. Prolonged KC exposure decreases basal CBF.

Cited by 9 publications

References 22 publications

International consensus statement on allergy and rhinology: rhinosinusitis 2021

International consensus statement on allergy and rhinology: rhinosinusitis 2021

Lipoxin B4 promotes the resolution of allergic inflammation in the upper and lower airways of mice

NLRP3 inflammasome induced liver graft injury through activation of telomere‐independent RAP1/KC axis

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