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Article ; Online: First contact: the role of respiratory cilia in host-pathogen interactions in the airways.

Kuek, Li Eon / Lee, Robert J

American journal of physiology. Lung cellular and molecular physiology

2020 Volume 319, Issue 4, Page(s) L603–L619

Abstract: Respiratory cilia are the driving force of the mucociliary escalator, working in conjunction with secreted airway mucus to clear inhaled debris and pathogens from the conducting airways. Respiratory cilia are also one of the first contact points between ... ...

Abstract	Respiratory cilia are the driving force of the mucociliary escalator, working in conjunction with secreted airway mucus to clear inhaled debris and pathogens from the conducting airways. Respiratory cilia are also one of the first contact points between host and inhaled pathogens. Impaired ciliary function is a common pathological feature in patients with chronic airway diseases, increasing susceptibility to respiratory infections. Common respiratory pathogens, including viruses, bacteria, and fungi, have been shown to target cilia and/or ciliated airway epithelial cells, resulting in a disruption of mucociliary clearance that may facilitate host infection. Despite being an integral component of airway innate immunity, the role of respiratory cilia and their clinical significance during airway infections are still poorly understood. This review examines the expression, structure, and function of respiratory cilia during pathogenic infection of the airways. This review also discusses specific known points of interaction of bacteria, fungi, and viruses with respiratory cilia function. The emerging biological functions of motile cilia relating to intracellular signaling and their potential immunoregulatory roles during infection will also be discussed.
MeSH term(s)	Bacteria/immunology ; Cilia/metabolism ; Epithelial Cells/metabolism ; Fungi/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate/immunology ; Mucociliary Clearance/physiology ; Mucus/metabolism ; Respiratory System/immunology ; Viruses/immunology
Keywords	covid19
Language	English
Publishing date	2020-08-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00283.2020
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Article ; Online: Savory Signaling: T1R Umami Receptor Modulates Endoplasmic Reticulum Calcium Store Content and Release Dynamics in Airway Epithelial Cells.

McMahon, Derek B / Jolivert, Jennifer F / Kuek, Li Eon / Adappa, Nithin D / Palmer, James N / Lee, Robert J

Nutrients

2023 Volume 15, Issue 3

Abstract: T1Rs are expressed in solitary chemosensory cells of the upper airway where they detect apical glucose levels and repress bitter taste receptor ... ...

Abstract	T1Rs are expressed in solitary chemosensory cells of the upper airway where they detect apical glucose levels and repress bitter taste receptor Ca
MeSH term(s)	Calcium ; Receptors, G-Protein-Coupled/metabolism ; Taste/physiology ; Amino Acids/metabolism ; Calcium, Dietary ; Epithelial Cells/metabolism ; Glucose ; Endoplasmic Reticulum/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Receptors, G-Protein-Coupled ; Amino Acids ; Calcium, Dietary ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-01-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu15030493
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Article: First contact: the role of respiratory cilia in host-pathogen interactions in the airways

Kuek, Li Eon / Lee, Robert J

Am J Physiol Lung Cell Mol Physiol

Abstract	Respiratory cilia are the driving force of the mucociliary escalator, working in conjunction with secreted airway mucus to clear inhaled debris and pathogens from the conducting airways. Respiratory cilia are also one of the first contact points between host and inhaled pathogens. Impaired ciliary function is a common pathological feature in patients with chronic airway diseases, increasing susceptibility to respiratory infections. Common respiratory pathogens, including viruses, bacteria, and fungi, have been shown to target cilia and/or ciliated airway epithelial cells, resulting in a disruption of mucociliary clearance that may facilitate host infection. Despite being an integral component of airway innate immunity, the role of respiratory cilia and their clinical significance during airway infections are still poorly understood. This review examines the expression, structure, and function of respiratory cilia during pathogenic infection of the airways. This review also discusses specific known points of interaction of bacteria, fungi, and viruses with respiratory cilia function. The emerging biological functions of motile cilia relating to intracellular signaling and their potential immunoregulatory roles during infection will also be discussed.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #817848
Database	COVID19

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Article ; Online: Utilizing the Off-Target Effects of T1R3 Antagonist Lactisole to Enhance Nitric Oxide Production in Basal Airway Epithelial Cells.

McMahon, Derek B / Jolivert, Jennifer F / Kuek, Li Eon / Adappa, Nithin D / Palmer, James N / Lee, Robert J

Nutrients

2023 Volume 15, Issue 3

Abstract: Human airway sweet (T1R2 + T1R3), umami (T1R1 + T1R3), and bitter taste receptors (T2Rs) are critical components of the innate immune system, acting as sensors to monitor pathogenic growth. T2Rs detect bacterial products or bitter compounds to drive ... ...

Abstract	Human airway sweet (T1R2 + T1R3), umami (T1R1 + T1R3), and bitter taste receptors (T2Rs) are critical components of the innate immune system, acting as sensors to monitor pathogenic growth. T2Rs detect bacterial products or bitter compounds to drive nitric oxide (NO) production in both healthy and diseased epithelial cell models. The NO enhances ciliary beating and also directly kills pathogens. Both sweet and umami receptors have been characterized to repress bitter taste receptor signaling in healthy and disease models. We hypothesized that the sweet/umami T1R3 antagonist lactisole may be used to alleviate bitter taste receptor repression in airway basal epithelial cells and enhance NO production. Here, we show that lactisole activates cAMP generation, though this occurs through a pathway independent of T1R3. This cAMP most likely signals through EPAC to increase ER Ca
MeSH term(s)	Humans ; Nitric Oxide/pharmacology ; Receptors, G-Protein-Coupled/metabolism ; Taste/physiology ; Epithelial Cells/metabolism
Chemical Substances	lactisole (ZU3D90W5GZ) ; Nitric Oxide (31C4KY9ESH) ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2023-01-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu15030517
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Article ; Online: Small-molecule Akt-activation in airway cells induces NO production and reduces IL-8 transcription through Nrf-2.

Gopallawa, Indiwari / Kuek, Li Eon / Adappa, Nithin D / Palmer, James N / Lee, Robert J

Respiratory research

2021 Volume 22, Issue 1, Page(s) 267

Abstract: Background: The non-cancerous functions of Akt in the airway are understudied. In some tissues, Akt phosphorylates and activates endothelial nitric oxide synthase (eNOS) to produce nitric oxide (NO) that has anti-inflammatory effects. NO production has ... ...

Abstract	Background: The non-cancerous functions of Akt in the airway are understudied. In some tissues, Akt phosphorylates and activates endothelial nitric oxide synthase (eNOS) to produce nitric oxide (NO) that has anti-inflammatory effects. NO production has antibacterial and antiviral effects in the airway, and increasing NO may be a useful anti-pathogen strategy. Akt also stimulates the nuclear factor erythroid 2-related factor 2 (Nrf-2) transcription factor, which transcribes antioxidant genes. Therefore, we hypothesized that activation of the Akt/eNOS pathway, which also activates Nrf-2, may have protective effects in human airway cells against injury. Methods: To directly test the effects of Akt signaling in the airway, we treated A549 and 16HBE cells as well as primary bronchial, nasal, and type II alveolar epithelial cells with small molecule Akt activator SC79. We examined the effects of SC79 on eNOS activation, NO production, Nrf-2 target levels, and interleukin-8 (IL-8) transcription during exposure to TNF-α or Pseudomonas flagellin (TLR5 agonist). Additionally, air-liquid interface bronchial cultures were treated with cadmium, an oxidative stressor that causes airway barrier breakdown. Results: SC79 induced a ~ twofold induction of p-eNOS and Nrf-2 protein levels blocked by PI3K inhibitor LY294002. Live cell imaging revealed SC79 increased acute NO production. Quantitative RT-PCR showed a ~ twofold increase in Nrf-2 target gene transcription. TNF-α or flagellin-induced IL-8 levels were also significantly reduced with SC79 treatment. Moreover, the transepithelial electrical resistance decrease observed with cadmium was ameliorated by SC79, likely by an acute increase in tight junction protein ZO-1 levels. Conclusions: Together, the data presented here demonstrate SC79 activation of Akt induces potentially anti-pathogenic NO production, antioxidant gene transcription, reduces IL-8 transcription, and may protect against oxidative barrier dysfunction in a wide range of airway epithelial cells.
MeSH term(s)	A549 Cells ; Acetates/pharmacology ; Anti-Inflammatory Agents/pharmacology ; Benzopyrans/pharmacology ; Electric Impedance ; Enzyme Activation ; Enzyme Activators/pharmacology ; Epithelial Cells/drug effects ; Epithelial Cells/enzymology ; Epithelial Cells/immunology ; Humans ; Interleukin-8/genetics ; Interleukin-8/metabolism ; Lung/drug effects ; Lung/enzymology ; Lung/immunology ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Phosphorylation ; Pneumonia/enzymology ; Pneumonia/genetics ; Pneumonia/immunology ; Pneumonia/prevention & control ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Transcription, Genetic ; Zonula Occludens-1 Protein/metabolism
Chemical Substances	2-amino-6-chloro-alpha-cyano-3-(ethoxycarbonyl)-4H-1-benzopyran-4-acetic acid ethyl ester ; Acetates ; Anti-Inflammatory Agents ; Benzopyrans ; CXCL8 protein, human ; Enzyme Activators ; Interleukin-8 ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; TJP1 protein, human ; Zonula Occludens-1 Protein ; Nitric Oxide (31C4KY9ESH) ; NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2021-10-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-993X
ISSN (online)	1465-993X
ISSN	1465-993X
DOI	10.1186/s12931-021-01865-y
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Article: Cilia Stimulatory and Antibacterial Activities of T2R Bitter Taste Receptor Agonist Diphenhydramine: Insights into Repurposing Bitter Drugs for Nasal Infections.

Kuek, Li Eon / McMahon, Derek B / Ma, Ray Z / Miller, Zoey A / Jolivert, Jennifer F / Adappa, Nithin D / Palmer, James N / Lee, Robert J

Pharmaceuticals (Basel, Switzerland)

2022 Volume 15, Issue 4

Abstract: T2R bitter taste receptors in airway motile cilia increase ciliary beat frequency (CBF) and nitric oxide (NO) production. Polymorphisms in some T2Rs are linked to disease outcomes in chronic rhinosinusitis (CRS) and cystic fibrosis (CF). We examined the ... ...

Abstract	T2R bitter taste receptors in airway motile cilia increase ciliary beat frequency (CBF) and nitric oxide (NO) production. Polymorphisms in some T2Rs are linked to disease outcomes in chronic rhinosinusitis (CRS) and cystic fibrosis (CF). We examined the expression of cilia T2Rs during the differentiation of human nasal epithelial cells grown at air-liquid interface (ALI). The T2R expression increased with differentiation but did not vary between CF and non-CF cultures. Treatment with Pseudomonas aeruginosa flagellin decreased the expression of diphenhydramine-responsive T2R14 and 40, among others. Diphenhydramine increased both NO production, measured by fluorescent dye DAF-FM, and CBF, measured via high-speed imaging. Increases in CBF were disrupted after flagellin treatment. Diphenhydramine impaired the growth of lab and clinical strains of
Language	English
Publishing date	2022-04-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph15040452
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Article ; Online: The MS4A family: counting past 1, 2 and 3.

Eon Kuek, Li / Leffler, Melanie / Mackay, Graham A / Hulett, Mark D

Immunology and cell biology

2015 Volume 94, Issue 1, Page(s) 11–23

Abstract: The MS4A (membrane-spanning 4-domain family, subfamily A) family of proteins contains some well-known members including MS4A1 (CD20), MS4A2 (FcɛRIβ) and MS4A3 (HTm4). These three MS4A family members are expressed on the cell surface of specific leukocyte ...

Abstract	The MS4A (membrane-spanning 4-domain family, subfamily A) family of proteins contains some well-known members including MS4A1 (CD20), MS4A2 (FcɛRIβ) and MS4A3 (HTm4). These three MS4A family members are expressed on the cell surface of specific leukocyte subsets and have been well characterized as having key roles in regulating cell activation, growth and development. However, beyond MS4A1-3 there are a large number of related molecules (18 to date in humans) where our understanding of their biological roles is at a relatively nascent stage. This review examines the larger MS4A family focusing on their structure, expression, regulation and characterized and/or emerging biological roles. Our own work on one family member MS4A8B, and its possible role in epithelial cell regulation, is also highlighted.
MeSH term(s)	Amino Acid Sequence ; Animals ; Cell Cycle ; Disease ; Humans ; Ion Channels/metabolism ; Membrane Proteins/chemistry ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Molecular Sequence Data ; Multigene Family ; Signal Transduction
Chemical Substances	Ion Channels ; Membrane Proteins
Language	English
Publishing date	2015-04-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1038/icb.2015.48
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Article ; Online: Cilia Stimulatory and Antibacterial Activities of T2R Bitter Taste Receptor Agonist Diphenhydramine

Li Eon Kuek / Derek B. McMahon / Ray Z. Ma / Zoey A. Miller / Jennifer F. Jolivert / Nithin D. Adappa / James N. Palmer / Robert J. Lee

Pharmaceuticals, Vol 15, Iss 452, p

Insights into Repurposing Bitter Drugs for Nasal Infections

2022 Volume 452

Abstract	T2R bitter taste receptors in airway motile cilia increase ciliary beat frequency (CBF) and nitric oxide (NO) production. Polymorphisms in some T2Rs are linked to disease outcomes in chronic rhinosinusitis (CRS) and cystic fibrosis (CF). We examined the expression of cilia T2Rs during the differentiation of human nasal epithelial cells grown at air–liquid interface (ALI). The T2R expression increased with differentiation but did not vary between CF and non-CF cultures. Treatment with Pseudomonas aeruginosa flagellin decreased the expression of diphenhydramine-responsive T2R14 and 40, among others. Diphenhydramine increased both NO production, measured by fluorescent dye DAF-FM, and CBF, measured via high-speed imaging. Increases in CBF were disrupted after flagellin treatment. Diphenhydramine impaired the growth of lab and clinical strains of P. aeruginosa , a major pathogen in CF and CF-related CRS. Diphenhydramine impaired biofilm formation of P. aeruginosa , measured via crystal violet staining, as well as the surface attachment of P. aeruginosa to CF airway epithelial cells, measured using colony-forming unit counting. Because the T2R agonist diphenhydramine increases NO production and CBF while also decreasing bacterial growth and biofilm production, diphenhydramine-derived compounds may have potential clinical usefulness in CF-related CRS as a topical therapy. However, utilizing T2R agonists as therapeutics within the context of P. aeruginosa infection may require co-treatment with anti-inflammatories to enhance T2R expression.
Keywords	Staphylococcus aureus ; Pseudomonas aeruginosa ; ciliary beat frequency ; calcium ; nitric oxide ; G protein-coupled receptors ; Medicine ; R ; Pharmacy and materia medica ; RS1-441
Subject code	610
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The bitter end: T2R bitter receptor agonists elevate nuclear calcium and induce apoptosis in non-ciliated airway epithelial cells.

McMahon, Derek B / Kuek, Li Eon / Johnson, Madeline E / Johnson, Paige O / Horn, Rachel L J / Carey, Ryan M / Adappa, Nithin D / Palmer, James N / Lee, Robert J

Cell calcium

2021 Volume 101, Page(s) 102499

Abstract: Bitter taste receptors (T2Rs) localize to airway motile cilia and initiate innate immune responses in retaliation to bacterial quorum sensing molecules. Activation of cilia T2Rs leads to calcium-driven NO production that increases cilia beating and ... ...

Abstract	Bitter taste receptors (T2Rs) localize to airway motile cilia and initiate innate immune responses in retaliation to bacterial quorum sensing molecules. Activation of cilia T2Rs leads to calcium-driven NO production that increases cilia beating and directly kills bacteria. Several diseases, including chronic rhinosinusitis, COPD, and cystic fibrosis, are characterized by loss of motile cilia and/or squamous metaplasia. To understand T2R function within the altered landscape of airway disease, we studied T2Rs in non-ciliated airway cell lines and primary cells. Several T2Rs localize to the nucleus in de-differentiated cells that typically localize to cilia in differentiated cells. As cilia and nuclear import utilize shared proteins, some T2Rs may target to the nucleus in the absence of motile cilia. T2R agonists selectively elevated nuclear and mitochondrial calcium through a G-protein-coupled receptor phospholipase C mechanism. Additionally, T2R agonists decreased nuclear cAMP, increased nitric oxide, and increased cGMP, consistent with T2R signaling. Furthermore, exposure to T2R agonists led to nuclear calcium-induced mitochondrial depolarization and caspase activation. T2R agonists induced apoptosis in primary bronchial and nasal cells differentiated at air-liquid interface but then induced to a squamous phenotype by apical submersion. Air-exposed well-differentiated cells did not die. This may be a last-resort defense against bacterial infection. However, it may also increase susceptibility of de-differentiated or remodeled epithelia to damage by bacterial metabolites. Moreover, the T2R-activated apoptosis pathway occurs in airway cancer cells. T2Rs may thus contribute to microbiome-tumor cell crosstalk in airway cancers. Targeting T2Rs may be useful for activating cancer cell apoptosis while sparing surrounding tissue.
MeSH term(s)	Apoptosis ; Bronchi ; Calcium ; Epithelial Cells/cytology ; Humans ; Receptors, G-Protein-Coupled/agonists
Chemical Substances	Receptors, G-Protein-Coupled ; taste receptors, type 2 ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-11-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	757687-0
ISSN	1532-1991 ; 0143-4160
ISSN (online)	1532-1991
ISSN	0143-4160
DOI	10.1016/j.ceca.2021.102499
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Article ; Online: Identification of an Immortalized Human Airway Epithelial Cell Line with Dyskinetic Cilia.

Kuek, Li Eon / Griffin, Paul / Martinello, Paul / Graham, Alison N / Kalitsis, Paul / Robinson, Philip J / Mackay, Graham A

American journal of respiratory cell and molecular biology

2017 Volume 59, Issue 3, Page(s) 375–382

Abstract: Primary ciliary dyskinesia is an inherited, currently incurable condition. In the respiratory system, primary ciliary dyskinesia causes impaired functioning of the mucociliary escalator, leading to nasal congestion, cough, and recurrent otitis media, and ...

Abstract	Primary ciliary dyskinesia is an inherited, currently incurable condition. In the respiratory system, primary ciliary dyskinesia causes impaired functioning of the mucociliary escalator, leading to nasal congestion, cough, and recurrent otitis media, and commonly progresses to cause more serious and permanent damage, including hearing deficits, chronic sinusitis, and bronchiectasis. New treatment options for the condition are thus necessary. In characterizing an immortalized human bronchial epithelial cell line (BCi-NS1.1) grown at an air-liquid interface to permit differentiation, we have identified that these cells have dyskinetic motile cilia. The cells had a normal male karyotype, and phenotypic markers of epithelial cell differentiation emerged, as previously shown. Ciliary beat frequency (CBF) as assessed by high-speed videomicroscopy was lower than normal (4.4 Hz). Although changes in CBF induced by known modulators were as expected, the cilia displayed a dyskinetic, circular beat pattern characteristic of central microtubular agenesis with outer doublet transposition. This ultrastructural defect was confirmed by electron microscopy. We propose that the BCi-NS1.1 cell line is a useful model system for examination of modulators of CBF and more specifically could be used to screen for novel drugs with the ability to enhance CBF and perhaps repair a dyskinetic ciliary beat pattern.
MeSH term(s)	Cell Differentiation/physiology ; Cell Line ; Cells, Cultured ; Cilia/pathology ; Ciliary Motility Disorders/pathology ; Dyskinesias/pathology ; Epithelial Cells/cytology ; Humans
Language	English
Publishing date	2017-12-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2017-0188OC
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