Journal articles: 'Nasal explants'

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Anderson, Michele J., Maren L. David, Matt Scholz, Sally J. Bull, Dan Morse, Michelle Hulse-Stevens, and Marnie L. Peterson. "Efficacy of Skin and Nasal Povidone-Iodine Preparation against Mupirocin-Resistant Methicillin-Resistant Staphylococcus aureus and S. aureus within the Anterior Nares." Antimicrobial Agents and Chemotherapy 59, no. 5 (March 2, 2015): 2765–73. http://dx.doi.org/10.1128/aac.04624-14.

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ABSTRACTMupirocin decolonization of nasalStaphylococcus aureusprior to surgery decreases surgical-site infections; however, treatment requires 5 days, compliance is low, and resistance occurs. In 2010, 3M Company introduced povidone-iodine (PVP-I)-based skin and nasal antiseptic (Skin and Nasal Prep [SNP]). SNP has rapid, broad-spectrum antimicrobial activity. We tested SNP's efficacy using full-thickness tissue (porcine mucosal [PM] and human skin) explant models and human subjects. Prior to or following infection with methicillin-resistantStaphylococcus aureus(MRSA) (mupirocin sensitive and resistant), explants were treated with Betadine ophthalmic preparation (Bet), SNP, or mupirocin (Bactroban nasal ointment [BN]) or left untreated. One hour posttreatment, explants were washed with phosphate-buffered saline (PBS) plus 2% mucin. One, 6, or 12 h later, bacteria were recovered and enumerated. Alternatively, following baseline sampling, human subjects applied two consecutive applications of SNP or saline to their anterior nares. One, 6, and 12 h after application of the preparation (postprep), nasal swabs were obtained, andS. aureuswas enumerated. We observed that treatment of infected PM or human skin explants with SNP resulted in >2.0 log10CFU reduction in MRSA, regardless of mupirocin sensitivity, which was significantly different from the values for BN- and Bet-treated explants and untreated controls 1 h, 6 h, and 12 h after being washed with PBS plus mucin. Swabbing the anterior nares of human subjects with SNP significantly reduced residentS. aureuscompared to saline 1, 6, and 12 h postprep. Finally, pretreatment of PM explants with SNP, followed by a mucin rinse prior to infection, completely prevented MRSA infection. We conclude that SNP may be an attractive alternative for reducing the bioburden of anterior nares prior to surgery.

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Pol, J. M. A., W. G. V. Quint, G. L. Kok, and J. M. Broekhuysen-Davies. "Pseudorabies virus infections in explants of porcine nasal mucosa." Research in Veterinary Science 50, no. 1 (January 1991): 45–53. http://dx.doi.org/10.1016/0034-5288(91)90052-p.

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Read, R. C., A. Fox, K. Miller, T. Gray, N. Jones, R. Borrow, D. M. Jones, and R. G. Finch. "Experimental infection of human nasal mucosal explants with Neisseria meningitidis." Journal of Medical Microbiology 42, no. 5 (May 1, 1995): 353–61. http://dx.doi.org/10.1099/00222615-42-5-353.

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Trela, Bruce A., and Matthew S. Bogdanffy. "Cytotoxicity of dibasic esters (DBE) metabolites in rat nasal explants." Toxicology and Applied Pharmacology 110, no. 2 (September 1991): 259–67. http://dx.doi.org/10.1016/s0041-008x(05)80008-0.

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Constantin, Stephanie, Alain Caraty, Susan Wray, and Anne H. Duittoz. "Development of Gonadotropin-Releasing Hormone-1 Secretion in Mouse Nasal Explants." Endocrinology 150, no. 7 (February 12, 2009): 3221–27. http://dx.doi.org/10.1210/en.2008-1711.

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Pulsatile release of GnRH-1 is critical to stimulate gonadotropes of the anterior pituitary. This secretory pattern seems to be inherent to GnRH-1 neurons, however, the mechanisms underlying such episodical release remain unknown. In monkey nasal explants, the GnRH-1 population exhibits synchronized calcium events with the same periodicity as GnRH-1 release, suggesting a link, though the sequence of events was unclear. GnRH-1 neurons in mouse nasal explants also exhibit synchronized calcium events. In the present work, GnRH-1 release was assayed in mouse nasal explants using radioimmunology and its relationship with calcium signaling analyzed. GnRH-1 neurons generated episodical release as early as 3 d in vitro (div) and maintained such release throughout the period studied (3–21 div). The pulse frequency remained constant, suggesting that the pulse generator is operative at an early developmental stage. In contrast, pulse amplitude increased 2-fold between 3 and 7 div, and again between 7 and 14 div, suggesting maturation in synthesizing and/or secretory mechanisms. To evaluate these possibilities, total GnRH-1 content was measured. Only a small increase in GnRH-1 content was detected between 7 and 14 div, whereas a large increase occurred between 14 and 21 div. These data indicate that GnRH-1 content was not a limiting factor for the amplitude of the pulses at 7 div but that the secretory mechanisms mature between 3 and 14 div. The application of kisspeptin-10 revealed the ability of GnRH-1 neurons to integrate signals from natural ligands into a secretory response. Finally, simultaneous sampling of medium and calcium imaging recordings indicated that the synchronized calcium events and secretory events are congruent.

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BOTTOMLEY, Kevin M., Neera BORKAKOTI, David BRADSHAW, Paul A. BROWN, Michael J. BROADHURST, John M. BUDD, Lucy ELLIOTT, et al. "Inhibition of bovine nasal cartilage degradation by selective matrix metalloproteinase inhibitors." Biochemical Journal 323, no. 2 (April 15, 1997): 483–88. http://dx.doi.org/10.1042/bj3230483.

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N-terminal analysis of aggrecan fragments lost from bovine nasal cartilage cultured in the presence of recombinant human interleukin 1α revealed a predominant ARGSVIL sequence with an additional ADLEX sequence. Production of the ARGSVIL-containing fragments has been attributed to the action of a putative proteinase, aggrecanase. The minor sequence (ADLEX) corresponds to a new reported cleavage product; comparison of this sequence with the available partial sequence of bovine aggrecan indicates that this is the product of a cleavage occurring towards the C-terminus of the protein. Matrix metalloproteinase (MMP) inhibitors inhibited aggrecan loss from bovine nasal explants incubated in the presence of recombinant human interleukin 1α. A strong correlation between inhibition of aggrecan metabolism and inhibition of stromelysin 1 (MMP 3) (r = 0.93) suggests a role for stromelysin or a stromelysin-like enzyme in cartilage aggrecan metabolism. However, the compounds were approx. 1/1000 as potent in inhibiting aggrecan loss from the cartilage explants as they were in inhibiting stromelysin. There was little or no correlation between inhibition of aggrecan metabolism and inhibition of gelatinase B (MMP 9) or inhibition of collagenase 1 (MMP 1). Studies with collagenase inhibitors with a range of potencies showed a correlation between inhibition of collagenase activity and inhibition of collagen degradation in the cartilage explant assay. This indicates that in interleukin 1α-driven bovine nasal cartilage destruction, stromelysin (or a closely related enzyme) is involved in aggrecan metabolism, whereas collagenase is principally responsible for collagen degradation.

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Trela, Bruce A., and Matthew S. Bogdanffy. "Carboxylesterase-dependent cytotoxicity of dibasic esters (DBE) in rat nasal explants." Toxicology and Applied Pharmacology 107, no. 2 (February 1991): 285–301. http://dx.doi.org/10.1016/0041-008x(91)90209-w.

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Tulinski, Pawel, Ad C. Fluit, Jos P. M. van Putten, Alain de Bruin, Sarah Glorieux, Jaap A. Wagenaar, and Birgitta Duim. "An Ex Vivo Porcine Nasal Mucosa Explants Model to Study MRSA Colonization." PLoS ONE 8, no. 1 (January 11, 2013): e53783. http://dx.doi.org/10.1371/journal.pone.0053783.

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Baraniuk, J. N., J. D. Lundgren, J. Goff, J. Mullol, S. Castellino, M. Merida, J. H. Shelhamer, and M. A. Kaliner. "Calcitonin gene-related peptide in human nasal mucosa." American Journal of Physiology-Lung Cellular and Molecular Physiology 258, no. 2 (February 1, 1990): L81—L88. http://dx.doi.org/10.1152/ajplung.1990.258.2.l81.

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To explore the potential range of functions for calcitonin gene-related peptide (CGRP) in human mucosa, we quantified human inferior turbinate nasal mucosal CGRP content by radioimmunoassay, localized CGRP-immunoreactivity by immunohistochemistry, detected 125I-CGRP binding sites by autoradiography, and tested the ability of CGRP to induce submucosal gland secretion in short-term explant culture of human nasal mucosa. Nasal mucosa contained 0.45-0.54 pmol CGRP/g wet wt (n = 18). Immunoreactive CGRP was found in nerve fibers that densely innervated the walls of small muscular arteries arterioles. Venules and venous sinusoids were innervated by individual CGRP staining fibers. Occasional CGRP-containing nerve fibers were also noted adjacent to submucosal gland acini, near the epithelial basement membrane, and between epithelial cells. Specific 125I-CGRP binding sites were concentrated on small muscular arteries and arterioles. CGRP (4 microM) did not stimulate glycoconjugate or lactoferrin release from mucosal explants. These results indicate that in the human nasal mucosa, CGRP is present in nerve fibers, which most likely represent nociceptive sensorimotor nerves that innervate vascular structures (muscular arteries, arterioles, veins and venous sinusoids). It is likely that CGRP release from sensory neurons may play a role in the regulation of vasomotor responses, but no evidence for a role of CGRP in glandular secretion was found.

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Chemuturi, Nagendra V., Patrick Hayden, Mitch Klausner, and Maureen D. Donovan. "Comparison of Human Tracheal/Bronchial Epithelial Cell Culture and Bovine Nasal Respiratory Explants for Nasal Drug Transport Studies." Journal of Pharmaceutical Sciences 94, no. 9 (September 2005): 1976–85. http://dx.doi.org/10.1002/jps.20404.

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11

Glorieux, Sarah, H. W. Favoreel, G. Meesen, W. de vos, W. Van den Broeck, and H. J. Nauwynck. "Different replication characteristics of historical pseudorabies virus strains in porcine respiratory nasal mucosa explants." Veterinary Microbiology 136, no. 3-4 (May 2009): 341–46. http://dx.doi.org/10.1016/j.vetmic.2008.11.005.

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12

Trela, Bruce A., Steven R. Frame, and Matthew S. Bogdanffy. "A microscopic and ultrastructural evaluation of dibasic esters (DBE) toxicity in rat nasal explants." Experimental and Molecular Pathology 56, no. 3 (June 1992): 208–18. http://dx.doi.org/10.1016/0014-4800(92)90037-c.

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13

Nossin, Yannick, Eric Farrell, Wendy J. L. M. Koevoet, Frank Datema, Rodrigo A. Somoza, Arnold I. Caplan, and Gerjo J. V. M. van Osch. "The Releasate of Avascular Cartilage Demonstrates Inherent Pro-Angiogenic Properties In Vitro and In Vivo." CARTILAGE 13, no. 2_suppl (September 30, 2021): 559S—570S. http://dx.doi.org/10.1177/19476035211047628.

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Objective Cartilage is avascular and numerous studies have identified the presence of single anti- and pro-angiogenic factors in cartilage. To better understand the maintenance hyaline cartilage, we assessed the angiogenic potential of complete cartilage releasate with functional assays in vitro and in vivo. Design We evaluated the gene expression profile of angiogenesis-related factors in healthy adult human articular cartilage with a transcriptome-wide analysis generated by next-generation RNAseq. The effect on angiogenesis of the releasate of cartilage tissue was assessed with a chick chorioallantoic membrane (CAM) assay as well as human umbilical vein endothelial cell (HUVEC) migration and proliferation assays using conditioned media generated from tissue-engineered cartilage derived from human articular and nasal septum chondrocytes as well as explants from bovine articular cartilage and human nasal septum. Experiments were done with triplicate samples of cartilage from 3 different donors. Results RNAseq data of 3 healthy human articular cartilage donors revealed that the majority of known angiogenesis-related factors expressed in healthy adult articular cartilage are pro-angiogenic. The releasate from generated cartilage as well as from tissue explants, demonstrated at least a 3.1-fold increase in HUVEC proliferation and migration indicating a pro-angiogenic effect of cartilage. Finally, the CAM assay demonstrated that cartilage explants can indeed attract vessels; however, their ingrowth was not observed. Conclusion Using multiple approaches, we show that cartilage releasate has an inherent pro-angiogenic capacity. It remains vessel free due to anti-invasive properties associated with the tissue itself.

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Ali, M., J. Maniscalco, and J. N. Baraniuk. "Spontaneous release of submucosal gland serous and mucous cell macromolecules from human nasal explants in vitro." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 4 (April 1, 1996): L595—L600. http://dx.doi.org/10.1152/ajplung.1996.270.4.l595.

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Respiratory epithelial and gland cells cultured in vitro demonstrate changes from differentiated serous and mucous cells toward intermediate "seromucous" cells. This spontaneous process was examined by culturing human nasal mucosal explants in CMRL 1066 medium without growth factors for 6 days and measuring the concentrations of spontaneously released serous cell products [lactoferrin, lysozyme, 7F10-immunoreactive mucoglycoconjugates (7F10-irm)] and Alcian blue-staining mucous cell products. 7F10-irm was progressively and significantly increased on each day of culture. In contrast, lysozyme, lactoferrin, and Alcian blue-staining material decreased significantly. Each had its own pattern of decreasing release. Dexamethasone (1 microM) had no effect on these trends. Phorbol myristate ester (PMA; 100 nM) reduced 7F10-irm release on days 4-6 and delayed the drop in lactoferrin release. Dexamethasone blunted these effects of PMA. These data indicate that respiratory secretory cells alter their phenotypes when cultured in vitro and progressively change the relative amounts of mucoglycoconjugates and proteins spontaneously released. These changes should be anticipated when interpreting experiments involving cultured respiratory cells.

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Casoni, F., and S. Wray. "[P2.42]: In situ visualization of GnRH‐1 neuronal migration in mouse nasal explants: Perturbation by GABA." International Journal of Developmental Neuroscience 26, no. 8 (November 25, 2008): 880–81. http://dx.doi.org/10.1016/j.ijdevneu.2008.09.167.

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Vandekerckhove, Annelies P., S. Glorieux, A. C. Gryspeerdt, L. Steukers, L. Duchateau, N. Osterrieder, G. R. Van de Walle, and H. J. Nauwynck. "Replication kinetics of neurovirulent versus non-neurovirulent equine herpesvirus type 1 strains in equine nasal mucosal explants." Journal of General Virology 91, no. 8 (August 1, 2010): 2019–28. http://dx.doi.org/10.1099/vir.0.019257-0.

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Equine herpesvirus type 1 (EHV-1) is the causative agent of equine herpes myeloencephalopathy, of which outbreaks are reported with increasing frequency throughout North America and Europe. This has resulted in its classification as a potentially emerging disease by the US Department of Agriculture. Recently, it was found that a single nucleotide polymorphism (SNP) in the viral DNA polymerase gene (ORF30) at aa 752 (N→D) is associated with the neurovirulent potential of EHV-1. In the present study, equine respiratory mucosal explants were inoculated with several Belgian isolates typed in their ORF30 as D752 or N752, to evaluate a possible difference in replication in the upper respiratory tract. In addition, to evaluate whether any observed differences could be attributed to the SNP associated with neurovirulence, the experiments were repeated with parental Ab4 (reference neurovirulent strain), parental NY03 (reference non-neurovirulent strain) and their N/D revertant recombinant viruses. The salient findings were that EHV-1 spreads plaquewise in the epithelium, but plaques never cross the basement membrane (BM). However, single EHV-1-infected cells could be observed below the BM at 36 h post-inoculation (p.i.) for all N752 isolates and at 24 h p.i. for all D752 isolates, and were identified as monocytic cells and T lymphocytes. Interestingly, the number of infected cells was two to five times higher for D752 isolates compared with N752 isolates at every time point analysed. Finally, this study showed that equine respiratory explants are a valuable and reproducible model to study EHV-1 neurovirulence in vitro, thereby reducing the need for horses as experimental animals.

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Yamagata, M., and J. R. Sanes. "Lamina-specific cues guide outgrowth and arborization of retinal axons in the optic tectum." Development 121, no. 1 (January 1, 1995): 189–200. http://dx.doi.org/10.1242/dev.121.1.189.

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In the chick, retinal axons enter the optic tectum through a superficial lamina, then branch into distinct deeper retinorecipient laminae, where they arborize and form synapses. To study factors that guide this laminar selectivity, we devised an organotypic culture system in which a transverse tectal section is overlaid with a retinal explant large enough to allow unimpeded access to all tectal laminae. Outgrowth, branching, and arborization patterns of retinal axons on tectal slices were lamina-selective, indicating the existence of localized cues that guide retinal axons. Further studies suggested that some of these cues are: (1) associated with cell membranes or extracellular matrix (because axons grew selectively on chemically fixed tectal sections); (2) intrinsic to the tectum (because axons grew selectively on tectal sections prepared from enucleated embryos); (3) distinct from topographic cues (because axons from nasal and temporal retina behaved similarly on anterior tectal slices); and (4) selective for retinal axons (because axons growing from other explants exhibited different laminar preferences).

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Hinnrasky, Jocelyne, Denis Pierrot, Claudette Fuchey, Jean-Marie Zahm, Dominique Ploton, and Edith Puchelle. "Influence of the extracellular matrix on the ciliated cells outgrowth from cultured human tracheal and nasal explants." Biology of the Cell 63, S1 (1988): 19–19. http://dx.doi.org/10.1016/0248-4900(88)90181-5.

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Golec, Anita, Iwona Pranke, Paolo Scudieri, Kate Hayes, Elise Dreano, Fiona Dunlevy, Aurelie Hatton, Damian G. Downey, Luis Galietta, and Isabelle Sermet. "Isolation, cultivation, and application of primary respiratory epithelial cells obtained by nasal brushing, polyp samples, or lung explants." STAR Protocols 3, no. 2 (June 2022): 101419. http://dx.doi.org/10.1016/j.xpro.2022.101419.

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Mullol, J., J. N. Baraniuk, C. Logun, M. Merida, J. Hausfeld, J. H. Shelhamer, and M. A. Kaliner. "M1 and M3 muscarinic antagonists inhibit human nasal glandular secretion in vitro." Journal of Applied Physiology 73, no. 5 (November 1, 1992): 2069–73. http://dx.doi.org/10.1152/jappl.1992.73.5.2069.

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Mucus glycoproteins (MGP) are high-molecular-weight glycoconjugates that are released from submucosal glands and epithelial goblet cells in the respiratory tract. Muscarinic receptors have an important role in the regulation of human nasal glandular secretion and mucus production, but it is not known which of the five muscarinic receptor subtypes are involved. The effect of nonselective and M1-, M2-, and M3-selective muscarinic antagonists on methacholine (MCh)-induced MGP secretion from human nasal mucosal explants was tested in vitro. MGP was assayed by enzyme-linked immunosorbent assay using a specific anti-MGP monoclonal antibody (7F10). MCh (100 microM) induced MGP secretion up to 127% compared with controls. MCh-induced MGP release was significantly inhibited by atropine (100 microM), the M, receptor antagonist pirenzepine (10–100 microM), and the M3 receptor antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP; 1–100 microM). 4-DAMP significantly inhibited MCh-induced MGP release at a lower concentration (1 microM) than pirenzepine (10 microM). The M2 receptor antagonists AF-DX 116 and gallamine (both at 100 microM) had no effect. No antagonist alone had a significant effect on MGP release. These results indicate that the M1 and M3 muscarinic receptor subtypes regulate MGP secretion from human nasal mucosa and suggest that the M3 receptor has the predominant effect.

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Gallego, Carolina, Andrew M. Middleton, Nhora Martínez, Stefany Romero, and Carlos Iregui. "Interaction ofBordetella bronchisepticaand Its Lipopolysaccharide withIn VitroCulture of Respiratory Nasal Epithelium." Veterinary Medicine International 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/347086.

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The nasal septa of fetal rabbits at 26 days of gestation were harvested by cesarean section of the does while under anesthesia and then exposed toBordetella bronchisepticaor its lipopolysaccharide (LPS) for periods of 2 and 4 hours. A total of 240 explants were used. The tissues were examined using the Hematoxylin & Eosin technique. Then, semithin sections (0.5 μm) were stained with toluidine blue and examined with indirect immunoperoxidase (IPI) and lectin histochemistry. The most frequent and statistically significant findings were as follows: (1) cell death and increased goblet cell activity when exposed to bacteria and (2) cell death, cytoplasmic vacuolation and infiltration of polymorphonuclear leukocytes when exposed to LPS. The lesions induced by the bacterium were more severe than with LPS alone, except for the cytoplasmic vacuolation in epithelial cells. IPI stained the ciliated border of the epithelium with the bacterium more intensely, while LPS lectin histochemistry preferentially labeled the cytoplasm of goblet cell. These data indicate thatB. bronchisepticaand its LPS may have an affinity for specific glycoproteins that would act as adhesion receptors in both locations.

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Walter, J., S. Henke-Fahle, and F. Bonhoeffer. "Avoidance of posterior tectal membranes by temporal retinal axons." Development 101, no. 4 (December 1, 1987): 909–13. http://dx.doi.org/10.1242/dev.101.4.909.

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Membrane carpets consisting of alternating membrane stripes were prepared from plasma membranes of anterior and posterior chick optic tectum. Axons from retinal explants extend neurites on these carpets. Axons of the nasal retina do not distinguish between the stripes. Axons of the temporal retina prefer to extend neurites on anterior tectal membranes. Treatment of the membrane fragments with high temperature interferes with the pattern of neurite outgrowth from temporal axons. When growing on carpets consisting of treated anterior and posterior tectal membranes, temporal retinal axons no longer distinguish between the stripes. Treatment of posterior membranes alone is sufficient to abolish the preference of temporal axons to extend neurites on anterior tectal membranes. Treatment of the anterior membranes alone has no effect. This result is best explained by a repulsive component in the posterior tectal membranes. Temporal, but not nasal, axons specifically recognize and avoid that component, with the result that they do not extend neurites on posterior tectal membrane stripes. Once the repulsive component is destroyed, temporal axons are able to extend neurites on posterior tectal membranes.

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Cheung, A. W. S., J. S. Y. Lam, and S. O. Chan. "Selective inhibition of ventral temporal but not dorsal nasal neurites from mouse retinal explants during contact with chondroitin sulphate." Cell and Tissue Research 321, no. 1 (May 18, 2005): 9–19. http://dx.doi.org/10.1007/s00441-005-1104-x.

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Raphael, J. H., J. Strupish, D. A. Selwyn, H. C. Hann, and J. A. Langton. "Recovery of respiratory ciliary function after depression by inhalation anaesthetic agents: an in vitro study using nasal turbinate explants." British Journal of Anaesthesia 76, no. 6 (June 1996): 854–59. http://dx.doi.org/10.1093/bja/76.6.854.

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Constantin, Stephanie, and Susan Wray. "Gonadotropin-Releasing Hormone-1 Neuronal Activity Is Independent of Hyperpolarization-Activated Cyclic Nucleotide-Modulated Channels but Is Sensitive to Protein Kinase A-Dependent Phosphorylation." Endocrinology 149, no. 7 (March 27, 2008): 3500–3511. http://dx.doi.org/10.1210/en.2007-1508.

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Pulsatile release of GnRH-1 stimulates the anterior pituitary and induces secretion of gonadotropin hormones. GnRH-1 release is modulated by many neurotransmitters that act via G protein-coupled membrane receptors. cAMP is the most ubiquitous effector for these receptors. GnRH-1 neurons express hyperpolarization-activated cyclic nucleotide-modulated (HCN) channel protein in vivo. HCN channels are involved in neuronal pacemaking and can integrate cAMP signals. cAMP-dependent protein kinase (PKA) is also activated by cAMP signals, and PKA-dependent phosphorylation modulates voltage-activated channels. In this report, these two pathways were examined in GnRH-1 neurons as integrators of forskolin (FSK)-induced stimulation. The HCN3 isoform was detected in GnRH-1 neurons obtained from mouse nasal explants. ZD7288, a HCN channel blocker, significantly reduced the efficiency of FSK to stimulate GnRH-1 neurons, whereas blockade of PKA with Rp-adenosine-3′,5′-cyclic monophosphorothioate triethylammonium did not attenuate the FSK-induced stimulation. To ensure that disruption of HCN channels on GnRH-1 neurons was responsible for reduction of FSK stimulation, experiments were performed removing γ-aminobutyric acid (GABA), the major excitatory input to GnRH-1 neurons in nasal explants. Under these conditions, Rp-adenosine-3′,5′-cyclic monophosphorothioate triethylammonium, but not ZD7288, altered the FSK-induced response of GnRH-1 neurons. These studies indicate that PKA-dependent phosphorylation is involved in the FSK-induced stimulation of GnRH-1 neurons rather than HCN channels, and HCN channels integrate the FSK-induced stimulation on GABAergic neurons. In addition, blockade of HCN channels did not modify basal GnRH-1 neuronal activity when GABAergic input was intact or removed, negating a role for these channels in basal GABAergic or GnRH-1 neuronal activity.

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Carey, Ryan M., Jenna R. Freund, Benjamin M. Hariri, Nithin D. Adappa, James N. Palmer, and Robert J. Lee. "Polarization of protease-activated receptor 2 (PAR-2) signaling is altered during airway epithelial remodeling and deciliation." Journal of Biological Chemistry 295, no. 19 (April 2, 2020): 6721–40. http://dx.doi.org/10.1074/jbc.ra120.012710.

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Protease-activated receptor 2 (PAR-2) is activated by secreted proteases from immune cells or fungi. PAR-2 is normally expressed basolaterally in differentiated nasal ciliated cells. We hypothesized that epithelial remodeling during diseases characterized by cilial loss and squamous metaplasia may alter PAR-2 polarization. Here, using a fluorescent arrestin assay, we confirmed that the common fungal airway pathogen Aspergillus fumigatus activates heterologously-expressed PAR-2. Endogenous PAR-2 activation in submerged airway RPMI 2650 or NCI–H520 squamous cells increased intracellular calcium levels and granulocyte macrophage–colony-stimulating factor, tumor necrosis factor α, and interleukin (IL)-6 secretion. RPMI 2650 cells cultured at an air–liquid interface (ALI) responded to apically or basolaterally applied PAR-2 agonists. However, well-differentiated primary nasal epithelial ALIs responded only to basolateral PAR-2 stimulation, indicated by calcium elevation, increased cilia beat frequency, and increased fluid and cytokine secretion. We exposed primary cells to disease-related modifiers that alter epithelial morphology, including IL-13, cigarette smoke condensate, and retinoic acid deficiency, at concentrations and times that altered epithelial morphology without causing breakdown of the epithelial barrier to model early disease states. These altered primary cultures responded to both apical and basolateral PAR-2 stimulation. Imaging nasal polyps and control middle turbinate explants, we found that nasal polyps, but not turbinates, exhibit apical calcium responses to PAR-2 stimulation. However, isolated ciliated cells from both polyps and turbinates maintained basolateral PAR-2 polarization, suggesting that the calcium responses originated from nonciliated cells. Altered PAR-2 polarization in disease-remodeled epithelia may enhance apical responses and increase sensitivity to inhaled proteases.

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Baraniuk, J. N., P. B. Silver, J. D. Lundgren, P. Cole, M. A. Kaliner, and P. J. Barnes. "Bombesin stimulates human nasal mucous and serous cell secretion in vivo." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 1 (January 1, 1992): L48—L52. http://dx.doi.org/10.1152/ajplung.1992.262.1.l48.

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Bombesin, gastrin-related peptide (GRP), and related peptides sharing the common carboxyterminal sequence stimulate lactoferrin (serous cell marker) and glycoconjugate (mucous cell and goblet cell marker) release from human nasal mucosal explants in vitro. In vivo, GRP released from trigeminal sensory nerves may act upon GRP-bombesin binding sites on respiratory epithelial cells and submucosal glands. To determine whether GRP-bombesin can stimulate nasal secretion in vivo, bombesin was administered to eight normal subjects by unilateral, topical administration. Secretions from both nostrils were collected for measurement of total protein, lysozyme, hexose-containing glycoconjugates, and albumin (marker of vascular permeability). Baseline secretions contained 72.0 +/- 17.3 micrograms/ml of total protein, 14 +/- 2 micrograms/ml of lysozyme, 113 +/- 44 micrograms/ml of hexose-containing glycoconjugates, and 7.8 +/- 3.4 micrograms/ml of albumin. Hexose-containing glycoconjugate secretion was significantly increased after 1 nmol (385 +/- 63 micrograms/ml, P less than 0.001 by analysis of variance), 10, 100, and 1,000 nmol of bombesin, but the secretion was not dose dependent. Significant lysozyme (24 +/- 3 micrograms/ml, P less than 0.05) and total protein (155 +/- 23 micrograms/ml, P less than 0.01) secretion occurred after 1,000 nmol. No statistically significant changes in albumin secretion occurred at any dose. Saline had no significant effects on secretion. Therefore, bombesin stimulated secretion from submucosal glands and possibly epithelial cells in the human nose without affecting vascular permeability.

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Glorieux, Sarah, W. Van den Broeck, K. M. van der Meulen, K. Van Reeth, H. W. Favoreel, and H. J. Nauwynck. "In vitro culture of porcine respiratory nasal mucosa explants for studying the interaction of porcine viruses with the respiratory tract." Journal of Virological Methods 142, no. 1-2 (June 2007): 105–12. http://dx.doi.org/10.1016/j.jviromet.2007.01.018.

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Lam, Emily, Harsha H. Kariyawasam, Stephen R. Durham, Joanne Rimmer, Valerie J. Lund, David Cousins, and Stephen Till. "CD4+ T Cells From Nasal Polyp Explants Contain Abundant Th2 Cells Expressing Functional Interleukin-25 Receptors Together With Th17 Cells." Journal of Allergy and Clinical Immunology 133, no. 2 (February 2014): AB87. http://dx.doi.org/10.1016/j.jaci.2013.12.327.

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Tulic, Meri K., Pota Christodoulopoulos, Pierre Olivier Fiset, Patrice Vaillancourt, Francois Lavigne, Jason D. Marshall, Gary Van Nest, Joseph J. Eiden, and Qutayba Hamid. "Local Induction of a Specific Th1 Immune Response by Allergen Linked Immunostimulatory DNA in the Nasal Explants of Ragweed- Allergic Subjects." Allergology International 58, no. 4 (2009): 565–72. http://dx.doi.org/10.2332/allergolint.09-oa-0108.

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Fueshko, S. M., S. Key, and S. Wray. "Luteinizing Hormone Releasing Hormone (LHRH) Neurons Maintained in Nasal Explants Decrease LHRH Messenger Ribonucleic Acid Levels after Activation of GABAA Receptors." Endocrinology 139, no. 6 (June 1, 1998): 2734–40. http://dx.doi.org/10.1210/endo.139.6.6034.

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Lowings, K. M., S. J. Wilson, and J. A. Warner. "Comparison of Anti-IgE-Induced Cytokine Release from Human Skin, Lung and Nasal Tissue Explants and the Effect of a Corticosteroid." Journal of Allergy and Clinical Immunology 125, no. 2 (February 2010): AB182. http://dx.doi.org/10.1016/j.jaci.2009.12.711.

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Morse, Diane M., Jennifer L. Smullen, and C. William Davis. "Differential effects of UTP, ATP, and adenosine on ciliary activity of human nasal epithelial cells." American Journal of Physiology-Cell Physiology 280, no. 6 (June 1, 2001): C1485—C1497. http://dx.doi.org/10.1152/ajpcell.2001.280.6.c1485.

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The purinergic regulation of ciliary activity was studied using small, continuously superfused explants of human nasal epithelium. The P2Y2 purinoceptor (P2Y2-R) was identified as the major purinoceptor regulating ciliary beat frequency (CBF); UTP (EC50 = 4.7 μM), ATP, and adenosine-5′- O-(3-thiotriphosphate) elicited similar maximal responses, approximately twofold over baseline. ATP, however, elicited a post-peak sustained plateau in CBF (1.83 ± 0.1-fold), whereas the post-peak CBF response to UTP declined over 15 min to a low-level plateau (1.36 ± 0.16-fold). UDP also stimulated ciliary beating, probably via P2Y6-R, with a maximal effect approximately one-half that elicited by P2Y2-R stimulation. Not indicated were P2Y1-R-, P2Y4-R-, or P2Y11-R-mediated effects. A2B-receptor agonists elicited sustained responses in CBF approximately equal to those from UTP/ATP [5′-( N-ethylcarboxamido)adenosine, EC50 = 0.09 μM; adenosine, EC50 = 0.7 μM]. Surprisingly, ADP elicited a sustained stimulation in CBF. The ADP effect and the post-peak sustained portion of the ATP response in CBF were inhibited by the A2-R antagonist 8-( p-sulfophenyl)theophylline. Hence, ATP affects ciliary activity through P2Y2-R and, after an apparent ectohydrolysis to adenosine, through A2BAR.

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Dolberg, Anne M., and Stephan Reichl. "Activity of Multidrug Resistance-Associated Proteins 1–5 (MRP1–5) in the RPMI 2650 Cell Line and Explants of Human Nasal Turbinate." Molecular Pharmaceutics 14, no. 5 (March 30, 2017): 1577–90. http://dx.doi.org/10.1021/acs.molpharmaceut.6b00838.

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Mackenzie, A., G. L. Leeming, A. K. Jowett, M. W. Ferguson, and P. T. Sharpe. "The homeobox gene Hox 7.1 has specific regional and temporal expression patterns during early murine craniofacial embryogenesis, especially tooth development in vivo and in vitro." Development 111, no. 2 (February 1, 1991): 269–85. http://dx.doi.org/10.1242/dev.111.2.269.

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Hox 7.1 is a murine homeobox-containing gene expressed in a range of neural-crest-derived tissues and areas of putative epithelial-mesenchymal interactions during embryogenesis. We have examined the expression of Hox 7.1 during craniofacial development in the mouse embryo between days 8 and 16 of development. Whereas facial expression at day 10 of gestation is broadly localised in the neural-crest-derived mesenchyme of the medial nasal, lateral nasal, maxillary and mandibular processes, by day 12 expression is restricted to the mesenchyme immediately surrounding the developing tooth germs in the maxillary and mandibular processes. Hox 7.1 expression in the mesenchyme of the dental papilla and follicle is maximal at the cap stage of development and progressively declines in the bell stage prior to differentiation of odontoblasts and ameloblasts. Hox 7.1 expression in tooth germs is independent of overall embryonic stage of development but is dependent on stage of development of the individual tooth. Similar patterns of transient Hox 7.1 expression can also be detected in tooth germs in vitro in organ cultures of day 11 first branchial arch explants cultured for up to 7 days. Hox 7.1 is also expressed early in development (days 10/11) in the epithelium of the developing anterior pituitary (Rathke's pouch), the connective tissue capsule and meninges of the developing brain, and specific regions of neuroepithelium in the developing brain.

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Quesnel-Hellmann, Anne, Daniel Fiole, Jacques Mathieu, and Jean-Nicolas Tournier. "Two-photon imaging kinetic analysis of Bacillus anthracis spore uptake in the respiratory tract. (45.17)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 45.17. http://dx.doi.org/10.4049/jimmunol.184.supp.45.17.

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Abstract Inhalational anthrax is a life-threatening infectious disease of considerable concern, especially because anthrax is an emerging bioterrorism agent. The exact mechanisms leading to a severe clinical form through the inhalational route are still unclear, particularly how immobile spores are captured in the upper respiratory tract and transported to the lymph nodes in the early steps of infection. To investigate the role of dendritic cells (DCs) in spore uptake and transport, we infected intranasally CX3CR1 +/gfp mice with Alexa 647-labeled spores. Nasal mucosa, nasal-associated lymphoid tissue (NALT), trachea, lungs and the draining lymph nodes explants were analyzed at different time-points after infection by confocal and/or two photon (2P)-microscopy. We demonstrated that DCs present along the respiratory tract are involved in spore uptake. However, differences in the kinetics of spore phagocytosis between the organs were observed. As soon as 2 hours after infection, DCs bearing spores were found in the thoracic lymph nodes whereas no uptake was observed in the NALT. The role of the NALT in inhalational anthrax will be discussed, as well as some results on lung tissue capture in vivo. Our results demonstrate that DCs play a critical role in spore transport rapidly after infection. The rapid kinetics of pathogen transport may contribute to the clinical features of inhalational anthrax.

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Harris, William Thomas, and Farruk Kabir. "2058 miRNA manipulation to improve CFTR correction in cystic fibrosis." Journal of Clinical and Translational Science 2, S1 (June 2018): 20. http://dx.doi.org/10.1017/cts.2018.96.

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OBJECTIVES/SPECIFIC AIMS: CFTR is the mutant protein that causes cystic fibrosis (CF), a fatal respiratory diseases affecting 1 in 3500 children. CFTR modulators are small molecules that directly address mutant CFTR function. Improving correction of the F508del CFTR mutation (affecting 90% of CF patients) is one of the most pressing unmet needs in CF. Currently available F508del therapeutics only marginally improve CF, In vitro, we have identified a miRNA that impairs utility of CFTR directed therapies. miR-145 is upregulated by TGF-β (a genetic modifier of CF lung disease) with a direct binding site on the 3’-untranslated region of CFTR mRNA. Binding of miR-145 to CFTR destabilizes mRNA transcript and impedes protein translation. Overexpression of miR-145 abolishes benefit of F508del CFTR correction. Antagonists to miR-145 block TGF-β suppression of CFTR function and augment response to CFTR correction. This project evaluate in vivo impact of TGF-beta and miRNA manipulation on CFTR functional readouts including nasal potential difference (NPD) and short circuit current (Isc) across tracheal explants in addition to standard biochemical measures. METHODS/STUDY POPULATION: Wild-type Sprague-Dawley rats were inoculated with an adenoviral vector containing bioactive TGF-beta or sham at 1×109 pfu/animal placed in the left nares. Seven days post-inoculation, functional, and biochemical measures were conducted. NPD was measured with a microelectrode placed in the left nare and grounded the tail. The nare was sequentially perfused with standard Ringer’s solution, amiloride (to block the ENaC sodium channel), low chloride Ringer’s (to stimulate chloride efflux), forskolin (to open the CFTR channel) and CFTRinh-172 (to block the CFTR channel. Tracheal explants were harvested, microdissected, and placed on modified Ussing chambers. RESULTS/ANTICIPATED RESULTS: We have inoculated WT rats with bioactive TGF-β Versus sham delivered by intranasal inoculation of an adenoviral vector. Functional readout of CFTR function is by Isc across tracheal epithelia and NPD. Lung homogenates are analyzed for TGF-β signaling, miRNA expression, and CFTR transcripts. Both tracheal explants and NPD indicate TGF-β stimulation diminishes CFTR function in vivo. In tracheal explants, TGF-β exposure diminishes CFTR response to forskolin-stimulation by 75%. Loss of current after CFTR inhibition (CFTRinh-172) is halved. By nasal PD, TGF-β inoculation similarly halves the bioelectric response to low chloride and forskolin stimulation. Evaluation by qPCR reveals a strong increase in TGF-β signaling demarcated by PAI-1, prompting a reduction in CFTR mRNA. miR-145 is expressed highly in rat pulmonary tissue, but no change in overall miR-145 levels was detected between TGF-β and sham exposed rats. This finding reflects what we have observed in human lungs, with a localized increased miR-145 expression in CF epithelia, but similarly high levels of miR-145 in both CF and non-CF whole lung homogenates. Although expressed at lower levels than miR-145, we did find increased expression in TGF-β relevant miR-101, miR-494, and miR-144 that have a predicted binding site on rat 3’-UTR in TGF-β exposed Versus sham lungs. DISCUSSION/SIGNIFICANCE OF IMPACT: Our data indicate the relevance of TGF-β stimulation to suppress CFTR synthesis and function in vivo. Future work will evaluate whether these additional miRNA with CFTR binding sites may mediate TGF-β suppression of CFTR in the rat model, and the utility of miRNA manipulation to augment F508del CFTR correction.

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Starbæk, Sofie M. R., Malene Rask Andersen, Louise Brogaard, Anna Spinelli, Victoria Rapson, Helena Aagaard Glud, Lars E. Larsen, Peter M. H. Heegaard, Hans Nauwynck, and Kerstin Skovgaard. "Innate antiviral responses in porcine nasal mucosal explants inoculated with influenza A virus are comparable with responses in respiratory tissues after viral infection." Immunobiology 227, no. 3 (May 2022): 152192. http://dx.doi.org/10.1016/j.imbio.2022.152192.

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Krüger, Nadine, Cheila Rocha, Sandra Runft, Johannes Krüger, Iris Färber, Federico Armando, Eva Leitzen, et al. "The Upper Respiratory Tract of Felids Is Highly Susceptible to SARS-CoV-2 Infection." International Journal of Molecular Sciences 22, no. 19 (September 30, 2021): 10636. http://dx.doi.org/10.3390/ijms221910636.

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Natural or experimental infection of domestic cats and virus transmission from humans to captive predatory cats suggest that felids are highly susceptible to SARS-CoV-2 infection. However, it is unclear which cells and compartments of the respiratory tract are infected. To address this question, primary cell cultures derived from the nose, trachea, and lungs of cat and lion were inoculated with SARS-CoV-2. Strong viral replication was observed for nasal mucosa explants and tracheal air–liquid interface cultures, whereas replication in lung slices was less efficient. Infection was mainly restricted to epithelial cells and did not cause major pathological changes. Detection of high ACE2 levels in the nose and trachea but not lung further suggests that susceptibility of feline tissues to SARS-CoV-2 correlates with ACE2 expression. Collectively, this study demonstrates that SARS-CoV-2 can efficiently replicate in the feline upper respiratory tract ex vivo and thus highlights the risk of SARS-CoV-2 spillover from humans to felids.

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Vandekerckhove, Annelies P., S. Glorieux, A. C. Gryspeerdt, L. Steukers, J. Van Doorsselaere, N. Osterrieder, G. R. Van de Walle, and H. J. Nauwynck. "Equine alphaherpesviruses (EHV-1 and EHV-4) differ in their efficiency to infect mononuclear cells during early steps of infection in nasal mucosal explants." Veterinary Microbiology 152, no. 1-2 (August 2011): 21–28. http://dx.doi.org/10.1016/j.vetmic.2011.03.038.

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Frydas, Ilias S., and Hans J. Nauwynck. "Replication characteristics of eight virulent and two attenuated genotype 1 and 2 porcine reproductive and respiratory syndrome virus (PRRSV) strains in nasal mucosa explants." Veterinary Microbiology 182 (January 2016): 156–62. http://dx.doi.org/10.1016/j.vetmic.2015.11.016.

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Becker, S., W. Reed, F. W. Henderson, and T. L. Noah. "RSV infection of human airway epithelial cells causes production of the beta-chemokine RANTES." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 3 (March 1, 1997): L512—L520. http://dx.doi.org/10.1152/ajplung.1997.272.3.l512.

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Infection of airway epithelial cells with respiratory syncytial virus (RSV) results in the production of a restricted number of cytokines, which may modulate the inflammatory response to infection. To get a better understanding of epithelial cell-mediated inflammatory processes in RSV disease, the aim of the present study was to identify the production of mononuclear cell/eosinophil/mast cell inflammatory chemokines [monocyte chemotactic protein (MCP)-1, MCP-3, macrophage inflammatory protein-1beta, and RANTES] during productive RSV infection in airway epithelial cells. Normal human primary bronchial epithelial cell cultures, nasal epithelial cell explants, and the BEAS-2B airway epithelial cell line were inoculated with RSV, and chemokine induction was assessed during the phase of logarithmic increase in infectious virus production. Only RANTES was found to increase in epithelial cell cultures in an infection-dependent manner. Furthermore, RANTES was released only by RSV-producing cells. To determine whether RANTES was induced by RSV infection in vivo, RANTES was measured in nasal lavage fluids (NLF) from children with RSV-positive and RSV-negative upper respiratory infection and children when they were well. RANTES was increased significantly during RSV infection (128 +/- 38 pg/ml NFL) compared with non-RSV infection (42 +/- 12 pg/ml NFL) and with asymptomatic baseline (13 +/- 4 ng/ml NFL) in the same children. Because RANTES is an effective eosinophil and memory T cell chemoattractant and activator and because eosinophil-dominated inflammation is a hallmark of asthmatic airways, RANTES may play a role in the pathogenesis of RSV-induced exacerbations of airway reactivity and wheezing.

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Constantin, Stéphanie, and Susan Wray. "Gonadotropin-Releasing Hormone-1 Neuronal Activity Is Independent of Cyclic Nucleotide-Gated Channels." Endocrinology 149, no. 1 (October 4, 2007): 279–90. http://dx.doi.org/10.1210/en.2007-0955.

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Pulsatile release of GnRH-1 is essential for secretion of gonadotropin hormones. The frequency of GnRH-1 pulses is regulated during the reproductive cycle by numerous neurotransmitters. Cyclic nucleotide-gated (CNG) channels have been proposed as a mechanism to integrate the cAMP signal evoked by many neurotransmitters. This study reports the expression of the CNGA2 subunit in GnRH-1 neurons obtained from mouse nasal explants and shows the ability of GnRH-1 neurons to increase their activity in response to forskolin (activator of adenylyl cyclases), or 3-isobutyl-1-methylxanthine (inhibitor of phosphodiesterases) even after removal of γ-aminobutyric acid (A)-ergic input. Next, the endogenous activity of adenylyl cyclases was evaluated as a component of the oscillatory mechanism of GnRH-1 neurons. Inhibition of endogenous activity of adenylyl cyclases did not alter GnRH-1 activity. The potential involvement of CNGA2 subunit in basal or induced activity was tested on GnRH-1 neurons obtained from CNGA2-deficient mice. Without up-regulation of CNGA1 or CNGA3, the absence of functional CNGA2 did not alter either the endogenous GnRH-1 neuronal activity or the response to forskolin, negating CNG channels from cAMP-sensitive mechanisms leading to changes in GnRH-1 neuronal activity. In addition, the potential role of CNGA2 subunit in the synchronization of calcium oscillations previously described was evaluated in GnRH-1 neurons from CNGA2-deficient explants. Synchronized calcium oscillations persisted in CNGA2-deficient GnRH-1 neurons. Taken together, these results indicate that CNGA2 channels are not necessary for either the response of GnRH-1 neurons to cAMP increases or the basal rhythmic activity of GnRH-1 neurons.

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Schlosser, Rodney J., Judith M. Czaja, and Thomas V. McCaffrey. "Honorable Mention — Student Research Award 1995: Signal Transduction Mechanisms in Substance P-Mediated Ciliostimulation." Otolaryngology–Head and Neck Surgery 113, no. 5 (November 1995): 582–88. http://dx.doi.org/10.1177/019459989511300509.

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Substance P is a neuropeptide released by afferent neurons in the respiratory tract during inflammatory reactions. It produces effects on blood vessels, bronchial smooth muscle, nasal glands, and respiratory cilia. We studied the in vitro effect of substance P on the ciliary beat frequency of human adenoid explants and its mechanism of action. Substance P was added to cultured adenoid at concentrations of 10−10, 10−8, 10−6, and 10−4 mol/L. Ciliary beat frequency was determined with phase-contrast microscopy and microphotometry. Substance P increased ciliary beat frequency a maximum of 11.9% ± 3.8% ( p < 0.01). Diclofenac (10−6 mol/L) significantly blocked the ciliostimulatory effects of SP ( p < 0.022), indicating that prostaglandin synthesis is an intermediate step in the action of substance P on ciliary beat frequency. The L-arginine analogs, NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine, inhibit nitric oxide synthesis from L-arginine. L-Arginine analogs (10−4 to 10−2 mol/L) inhibited the effect of substance P ( p < 0.02 at the higher concentration). This inhibition was reversed by adding L-arginine, demonstrating that nitric oxide production is a required step in substance P-induced ciliostimulation. Substance P stimulates ciliary activity in human nasal mucosa as a result of secondary production and release of endogenous prostaglandins and nitric oxide. It is likely that inflammatory disease processes that stimulate release of substance P and subsequent prostaglandin and nitric oxide production modify mucociliary transport. Pharmacologic modification of substance P and its second messengers may eventually permit regulation of this important defense mechanism and control of neurogenic inflammation.

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Lamote, Jochen A. S., Sarah Glorieux, Hans J. Nauwynck, and Herman W. Favoreel. "The US3 Protein of Pseudorabies Virus Drives Viral Passage across the Basement Membrane in Porcine Respiratory Mucosa Explants." Journal of Virology 90, no. 23 (September 28, 2016): 10945–50. http://dx.doi.org/10.1128/jvi.01577-16.

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ABSTRACT Passage of the basement membrane (BM), which forms a barrier between the epithelium and the underlying lamina propria, represents an important step in the early pathogenesis of different alphaherpesviruses. Rho GTPase signaling plays an important role in transmigration of cells across the BM during physiological and pathological processes. We reported earlier that the US3 protein kinase of the alphaherpesvirus pseudorabies virus (PRV) interferes with Rho GTPase signaling and causes a reorganization of the host cell cytoskeleton, which as a consequence, enhances viral cell-to-cell spread in epithelial cell cultures. Here, using an ex vivo system of porcine nasal respiratory mucosa explants that allows to study PRV invasion through the BM, we found that a PRV strain that lacks US3 expression (ΔUS3 PRV) showed a reduced spread in mucosal epithelium and was virtually unable to breach the BM, in contrast to isogenic wild-type (WT) or US3 rescue PRV strains. Interestingly, addition of IPA3, an inhibitor of p21-activated kinases that blocks the effects of US3 on the cytoskeleton, suppressed the ability of WT PRV to spread across the BM. In addition, artificial suppression of RhoA signaling using CPC3 (cell-permeable C3 transferase) to mimic the effects of US3 on Rho GTPase signaling, significantly increased passage of ΔUS3 PRV through the BM, whereas it did not significantly affect BM passage of WT or US3 rescue PRV. In conclusion, these data indicate that US3 plays an important role in PRV mucosal invasion across the BM, which involves its interference with Rho GTPase signaling. This is the first report describing an alphaherpesvirus protein that drives viral BM passage. IMPORTANCE Many viruses, including alphaherpesviruses, primarily replicate in epithelial cells of surface mucosae, such as the respiratory mucosa. Some of these viruses breach the basement membrane underlying these epithelial cells to reach underlying connective tissue and blood vessels and invade the host. Hence, epithelial spread and basement membrane passage represent crucial but still poorly understood early steps in (alphaherpes)virus pathogenesis. Here, using ex vivo porcine respiratory mucosa explants, we show that the conserved US3 protein of the porcine alphaherpesvirus pseudorabies virus (PRV) is critical for passage of PRV across the basement membrane and contributes to efficient viral epithelial spread. In addition, we show that US3-mediated viral epithelial spread and passage across the basement membrane depend at least in part on the ability of this viral protein to modulate cellular Rho GTPase signaling. This is the first report that identifies an alphaherpesvirus protein that drives viral basement membrane passage.

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Hajeer, Mohammad Y., Zhili Mao, Declan T. Millett, Ashraf F. Ayoub, and Jan Paul Siebert. "A New Three-Dimensional Method of Assessing Facial Volumetric Changes after Orthognathic Treatment." Cleft Palate-Craniofacial Journal 42, no. 2 (March 2005): 113–20. http://dx.doi.org/10.1597/03-132.1.

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Objective To validate a new method of facial volumetric assessment that is dependent on the use of stereophotogrammetric models and a software-based Facial Analysis Tool. Design The method was validated in vitro with three-dimensional (3D) models of a lifelike plastic female dummy head and in vivo with a male-subject head. Methods Thirty facial silicone explants were added in the nasal and perioral regions of each head, and their volumes were obtained by three different algorithms. These were compared with the actual values obtained by a “water displacement” method. Results The least mean error was found with the “tetrahedron formation” method followed by the “projection” method and the “back-plane construction” method. The error with the tetrahedron formation method was 0.071 cm3 (95% confidence interval [CI]: −0.074 to 0.2161 cm3) with the in vitro models and 0.314 cm3 (95% CI: −0.080 to 0.708 cm3) with the in vivo models. The increased volumetric assessment error observed in vivo was attributed to the registration procedure and possible changes in facial expression. Conclusions These results encourage the use of this method in the 3D assessment of orthognathic surgical outcome, provided a standardized facial expression is used for image acquisition.

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Färber, Iris, Johannes Krüger, Cheila Rocha, Federico Armando, Maren von Köckritz-Blickwede, Stefan Pöhlmann, Armin Braun, Wolfgang Baumgärtner, Sandra Runft, and Nadine Krüger. "Investigations on SARS-CoV-2 Susceptibility of Domestic and Wild Animals Using Primary Cell Culture Models Derived from the Upper and Lower Respiratory Tract." Viruses 14, no. 4 (April 16, 2022): 828. http://dx.doi.org/10.3390/v14040828.

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Several animal species are susceptible to SARS-CoV-2 infection, as documented by case reports and serological and in vivo infection studies. However, the susceptibility of many animal species remains unknown. Furthermore, the expression patterns of SARS-CoV-2 entry factors, such as the receptor angiotensin-converting enzyme 2 (ACE2), as well as transmembrane protease serine subtype 2 (TMPRSS2) and cathepsin L (CTSL), cellular proteases involved in SARS-CoV-2 spike protein activation, are largely unexplored in most species. Here, we generated primary cell cultures from the respiratory tract of domestic and wildlife animals to assess their susceptibility to SARS-CoV-2 infection. Additionally, the presence of ACE2, TMPRSS2 and CTSL within respiratory tract compartments was investigated in a range of animals, some with unknown susceptibility to SARS-CoV-2. Productive viral replication was observed in the nasal mucosa explants and precision-cut lung slices from dogs and hamsters, whereas culture models from ferrets and multiple ungulate species were non-permissive to infection. Overall, whereas TMPRSS2 and CTSL were equally expressed in the respiratory tract, the expression levels of ACE2 were more variable, suggesting that a restricted availability of ACE2 may contribute to reduced susceptibility. Summarized, the experimental infection of primary respiratory tract cell cultures, as well as an analysis of entry-factor distribution, enable screening for SARS-CoV-2 animal reservoirs.

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Buttle, D. J., and J. Saklatvala. "Lysosomal cysteine endopeptidases mediate interleukin 1-stimulated cartilage proteoglycan degradation." Biochemical Journal 287, no. 2 (October 15, 1992): 657–61. http://dx.doi.org/10.1042/bj2870657.

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The peptidyl diazomethane inactivator of cysteine endopeptidases, benzyloxycarbonyl-Tyr-Ala-CHN2, was tested as an inhibitor of interleukin 1 alpha-stimulated release of proteoglycan from bovine nasal septum cartilage explants. Like the previously tested epoxidyl peptide proinhibitor trans-epoxysuccinyl-leucylamido-(3-methyl)butane ethyl ester, it proved to be an effective inhibitor of proteoglycan release from cartilage, with significant inhibition at a concentration of 1 microM. The inhibition did not seem to be due to a general toxic effect. The rates of inactivation of the bovine cysteine endopeptidases by the peptidyl diazomethane, the epoxidyl peptide proinhibitor and its active form were determined. Benzyloxycarbonyl-Tyr-Ala-CHN2 proved to be a rapid inactivator of cathepsins L, S and B, but reacted much more slowly with cathepsin H and calpain. Thus it would appear that the latter two enzymes are not implicated in proteoglycan release in our test system. The peptidyl diazomethane and epoxidyl peptide proinhibitor (above) were also tested for their effects on three other interleukin 1-mediated cellular events, namely epidermal growth factor receptor transmodulation, and interleukin 6 and prostaglandin E2 production. In all cases the inactivators did not interfere with the response to interleukin 1 in human gingival fibroblasts. We conclude that one or more of the lysosomal cysteine endopeptidases cathepsins B, L and S mediate interleukin 1-stimulated cartilage proteoglycan degradation without affecting signal transduction.

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Glorieux, Sarah, Annelies P. Vandekerckhove, Nesya Goris, Xiao-Yun Yang, Lennert Steukers, Gerlinde R. Van de Walle, Siska Croubels, Johan Neyts, and Hans J. Nauwynck. "Evaluation of the antiviral activity of (1′S,2′R)-9-[[1′,2′-bis(hydroxymethyl)cycloprop-1′-yl]methyl]guanine (A-5021) against equine herpesvirus type 1 in cell monolayers and equine nasal mucosal explants." Antiviral Research 93, no. 2 (February 2012): 234–38. http://dx.doi.org/10.1016/j.antiviral.2011.11.016.

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Constantin, Stephanie, Claudia Simone Caligioni, Stanko Stojilkovic, and Susan Wray. "Kisspeptin-10 Facilitates a Plasma Membrane-Driven Calcium Oscillator in Gonadotropin-Releasing Hormone-1 Neurons." Endocrinology 150, no. 3 (October 23, 2008): 1400–1412. http://dx.doi.org/10.1210/en.2008-0979.

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Kisspeptins, the natural ligands of the G-protein-coupled receptor (GPR)-54, are the most potent stimulators of GnRH-1 secretion and as such are critical to reproductive function. However, the mechanism by which kisspeptins enhance calcium-regulated neuropeptide secretion is not clear. In the present study, we used GnRH-1 neurons maintained in mice nasal explants to examine the expression and signaling of GPR54. Under basal conditions, GnRH-1 cells exhibited spontaneous baseline oscillations in intracellular calcium concentration ([Ca2+]i), which were critically dependent on the operation of voltage-gated, tetrodotoxin (TTX)-sensitive sodium channels and were not coupled to calcium release from intracellular pools. Activation of native GPR54 by kisspeptin-10 initiated [Ca2+]i oscillations in quiescent GnRH-1 cells, increased the frequency of calcium spiking in oscillating cells that led to summation of individual spikes into plateau-bursting type of calcium signals in a subset of active cells. These changes predominantly reflected the stimulatory effect of GPR54 activation on the plasma membrane oscillator activity via coupling of this receptor to phospholipase C signaling pathways. Both components of this pathway, inositol 1,3,4-trisphosphate and protein kinase C, contributed to the receptor-mediated modulation of baseline [Ca2+]i oscillations. TTX and 2-aminoethyl diphenylborinate together abolished agonist-induced elevation in [Ca2+]i in almost all cells, whereas flufenamic acid was less effective. Together these results indicate that a plasma membrane calcium oscillator is spontaneously operative in the majority of prenatal GnRH-1 neurons and is facilitated by kisspeptin-10 through phosphatidyl inositol diphosphate hydrolysis and depolarization of neurons by activating TTX-sensitive sodium channels and nonselective cationic channels. GnRH-1 neurons exhibit a spontaneously active calcium oscillator, dependent on tetrodotoxin-sensitive sodium conductance. Kisspeptin-10/GPR54, via phosphatidyl inositol diphosphate 2 hydrolysis, utilizes these channels and non-selective cationic channels.

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Journal articles on the topic 'Nasal explants'

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