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R. Wilson - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of adherence of Mycobacterium avium complex and Mycobacterium tuberculosis to fibronectin on the Respiratory Mucosa.
Respiratory medicine, 2004Co-Authors: A.m. Middleton, M. V. Chadwick, A. G. Nicholson, A. Dewar, Richard K. Groger, Eric J. Brown, Timothy L. Ratliff, R. WilsonAbstract:Abstract Mycobacterium species adhere to the Respiratory Mucosa via mucus and fibronectin of extracellular matrix exposed by damaged epithelium. We have investigated whether inhibiting adherence to fibronectin influences subsequent infection of human Respiratory tissue by Mycobacterium avium complex and Mycobacterium tuberculosis. Human Respiratory tissue was pretreated with mycobacterial fibronectin attachment proteins prior to infection with M. avium complex and M. tuberculosis and the number of recoverable bacteria over time was compared to untreated controls. Inhibition significantly reduced recovery of M. avium complex at 15min ( P =0.02), 7days ( P =0.04), and 14days ( P =0.03); whereas recovery of M. tuberculosis was only reduced at 15min ( P =0.01) and not at later timepoints. We conclude that M. avium complex and M. tuberculosis infection of the Mucosa proceeds by different mechanisms, since M. tuberculosis infection is independent of fibronectin adherence.
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Haemophilus parainfluenzae infection of Respiratory Mucosa.
Respiratory medicine, 2003Co-Authors: A.m. Middleton, Andrew Rutman, R B Dowling, J. L. Mitchell, S. Watanabe, K. Pritchard, G. Tillotson, Susan L. Hill, R. WilsonAbstract:Abstract The pathogenicity of Haemophilus parainfluenzae ( Hpi ) in the Respiratory tract is unclear, in contrast to the accepted pathogenicity of its close relative non-typable H. influenzae . We have investigated the interaction of two Hpi isolates with the Mucosa of adenoid and bronchial tissue organ cultures. The adherence of bacteria to the Mucosa of organ cultures, the effect of broth culture filtrates on human nasal epithelium, and interleukin (IL)-8 production by A549 cell cultures was investigated. Hpi 4846 adhered infrequently in clusters of pleomorphic cocco-bacilli to areas of epithelial damage, mucus and unciliated cells in adenoid organ culture experiments at 24 h, but not bronchial Mucosa. Hpi 3698 was seen in only one adenoid and no bronchial organ cultures at 24 h. In separate experiments, Hpi 3698 was cleared more rapidly from the centre of the adenoid organ culture and was not cultured at 24 h. Although not adhering to the Mucosa at 24 h, Hpi 3698, but not Hpi 4846, caused an increase in the amount of epithelial damage in both types of organ culture. Broth culture filtrates of both strains caused immediate slowing of ciliary beat frequency that progressed, and disrupted epithelial integrity. Dialysed culture filtrates of both strains stimulated IL-8 production by A549 cells, with the culture filtrate of Hpi 3698 being most potent. We conclude that two strains of Hpi varied in their adherence to adenoid tissue, and neither adhered to bronchial tissue. These results lead us to speculate that Hpi is only likely to be a pathogen in the lower Respiratory tract when impaired airway defences delay bacterial clearance.
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Interaction of Mycobacterium Tuberculosis With Human Respiratory Mucosa
Tuberculosis, 2002Co-Authors: A.m. Middleton, M. V. Chadwick, A. G. Nicholson, A. Dewar, Richard K. Groger, Eric J. Brown, Timothy L. Ratliff, R. WilsonAbstract:Objective Endobronchial infection is associated with pulmonary tuberculosis in the majority of cases. We have investigated the adherence of Mycobacterium tuberculosis to the human Respiratory Mucosa. Design Organ cultures constructed with human tissue were infected with M. tuberculosis in the presence or absence of mycobacterial fibronectin attachment cell surface proteins and examined by scanning electron microscopy. Results M. tuberculosis adhered mainly to extracellular matrix (ECM) in areas of Mucosal damage, but not to ciliated Mucosa, intact extruded cells, basement membrane or collagen fibres. Bacteria also adhered to fibrous but not globular mucus and occasionally to healthy unciliated Mucosa, open tight junctions and to extruded cells that had degenerated, exposing their contents. There was a significant reduction (p Conclusion We conclude that M. tuberculosis adheres to ECM in areas of Mucosal damage at least in part via FAP and antigen 85B protein.
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Interaction of Bordetella pertussis with human Respiratory Mucosa in vitro.
Respiratory medicine, 2000Co-Authors: M.c Soane, A. Dewar, A Jackson, Duncan J. Maskell, Andrew G. Allen, P Keig, Gordon Dougan, R. WilsonAbstract:Abstract The human Respiratory tract pathogen Bordetella pertussis is the major cause of whooping cough in infants and young children, and also causes chronic cough in adults. B. pertussis infection damages ciliated epithelium in the Respiratory tract. However, the interaction of the bacterium with the Respiratory Mucosa is poorly understood, and previous studies have either utilized animal tissue which may not be appropriate, or isolated cell systems which lack the complexity of the Respiratory Mucosa. We have studied the interaction of B. pertussis strain BP536 with human nasal turbinate tissue in an air-interface organ culture over 5 days. We have also compared infection by BP536 with two other strains, Tohama I and CN2992, to determine whether the interactions observed with BP536 are consistent, and, in both nasal turbinate and adenoid organ cultures at 24 h, to determine whether there were differences between tissue from different parts of the Respiratory tract. BP536 adhered to cilia, most commonly at their base, and disorganized their spatial arrangement; they also adhered to damaged tissue and muscus, but very rarely to unciliated cells. Within the first 24 h there was a five-fold increase in bacterial density on ciliated cells, and the total number of adherent bacteria increased up to 96 h. Infection caused increased mucus at 24 h and an increase in damaged epithelium from 72 h which involved both ciliated and unciliated cells. The number of residual ciliated cells did not decrease after 72 h. The three different strains of B. pertussis exhibited similar interactions with the Mucosa, and there was no tissue specificity for adenoid or turbinate tissue. We conclude that B. pertussis adhered to multiple sites on the Mucosa and caused hypersecretion and epithelial damage which are the pathological changes described in vivo .
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Effect of fluticasone propionate and salmeterol on Pseudomonas aeruginosa infection of the Respiratory Mucosa in vitro.
The European respiratory journal, 1999Co-Authors: R B Dowling, M. Johnson, P. J. Cole, R. WilsonAbstract:The purpose of this study was to investigate the effect of the corticosteroid, fluticasone propionate (FP), on Pseudomonas aeruginosa infection of the Respiratory Mucosa of an organ culture model in vitro. Organ cultures infected with P. aeruginosa had significantly (p< or =0.05) elevated levels of Mucosal damage and significantly (p< or =0.05) less ciliated cells compared to controls. Preincubation of tissue with FP (10(-6) or 10(-5) but not 10(-7) M) prior to P. aeruginosa infection significantly (p< or =0.05) reduced the bacterially induced Mucosal damage in a concentration-dependent manner. FP (10(-5) M) also significantly (p< or =0.05) prevented loss of ciliated cells. FP did not alter the density of bacteria adherent to the different Mucosal features of the organ cultures, but did reduce total bacterial numbers due to the reduced amount of damaged tissue, which is a preferred site of P. aeruginosa adherence. It has previously been shown that the long-acting beta2-agonist salmeterol (4 x 10(-7)M) also reduces the Mucosal damage caused by P. aeruginosa infection, probably via elevation of intracellular cyclic adenosine monophosphate concentrations. Preincubation of tissue with both 10(-7)M FP and 10(-7)M salmeterol, concentrations at which they did not by themselves influence the effect of P. aeruginosa infection, significantly (p< or =0.05) reduced P. aeruginosa-induced loss of cilia. However, there was no additional benefit from adding 4 x 10(-7)M salmeterol to 10(-6)M FP. In conclusion fluticasone propionate reduced Mucosal damage caused by P. aeruginosa infection in vitro and preserved ciliated cells. There was a synergistic action with salmeterol in the preservation of ciliated cells.
Francesco Giannessi - One of the best experts on this subject based on the ideXlab platform.
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Immunohistochemical localization of 3-nitrotyrosine in the nasal Respiratory Mucosa of patients with vasomotor rhinitis.
Acta oto-laryngologica, 2005Co-Authors: Francesco Giannessi, Francesco Ursino, Bruno Fattori, M. Anita Giambelluca, Maria Concetta Scavuzzo, Francesca Ceccarelli, Riccardo RuffoliAbstract:Conclusion This study demonstrates that, in the nasal Respiratory Mucosa of patients with vasomotor rhinitis, oxidative stress following peroxynitrite formation is confined to the Respiratory epithelium. This suggests that the role of peroxynitrite in vasomotor rhinitis differs from its role in other diseases of the Respiratory tract. The results of this study also support the concept that different pathogenetic mechanisms are probably involved in vasomotor rhinitis. Objective Previous studies indicated that nitric oxide (NO) is involved in the pathogenesis of vasomotor rhinitis, strong expression of NO synthase being detected in the smooth muscle cells of the cavernous sinuses and in the Respiratory epithelium. However, most adverse effects of high levels of NO originate from the reaction of NO with superoxide anions to form peroxynitrite. Therefore, in this study we evaluated the involvement of peroxynitrite in the pathogenesis of vasomotor rhinitis. Material and methods Sites of peroxynitrite formation...
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ultracytochemical localization of the nadph d activity in the human nasal Respiratory Mucosa in vasomotor rhinitis
Laryngoscope, 2000Co-Authors: Riccardo Ruffoli, M. Anita Giambelluca, Bruno Fattori, Paola Soldani, Francesco GiannessiAbstract:Objectives Description of the ultrastructural localization of nitric oxide synthase in the blood vessels of the nasal Respiratory Mucosa in patients with vasomotor rhinitis. Study Design This research was conducted on seven patients—men and women, ages 20 to 45 years—suffering from vasomotor rhinitis and who had undergone surgical therapy for reduction of the inferior turbinates. Methods To study the ultrastructural localization of nitric oxide synthase, NADPH-diaphorase cytochemistry was employed. Samples of the nasal Mucosa were obtained from inferior turbinates. Results The endothelial cells of the arterioles, capillaries , venules and cavernous sinuses revealed a distribution of the enzymatic activity similar to that found in unaffected subjects. A strong enzymatic activity was recognized in the smooth muscle cells of the cavernous sinuses. The smooth muscle cells of arterioles and venules were generally found to be negative to enzymatic reaction. Conclusions This study suggests that the vascular disorders of the vasomotor rhinitis depend, at least in part, from nitric oxide synthase induction in the smooth muscle cells of the cavernous sinuses.
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Ultracytochemical Localization of the NADPH‐d Activity in the Human Nasal Respiratory Mucosa in Vasomotor Rhinitis
The Laryngoscope, 2000Co-Authors: Riccardo Ruffoli, M. Anita Giambelluca, Bruno Fattori, Paola Soldani, Francesco GiannessiAbstract:Objectives Description of the ultrastructural localization of nitric oxide synthase in the blood vessels of the nasal Respiratory Mucosa in patients with vasomotor rhinitis. Study Design This research was conducted on seven patients—men and women, ages 20 to 45 years—suffering from vasomotor rhinitis and who had undergone surgical therapy for reduction of the inferior turbinates. Methods To study the ultrastructural localization of nitric oxide synthase, NADPH-diaphorase cytochemistry was employed. Samples of the nasal Mucosa were obtained from inferior turbinates. Results The endothelial cells of the arterioles, capillaries , venules and cavernous sinuses revealed a distribution of the enzymatic activity similar to that found in unaffected subjects. A strong enzymatic activity was recognized in the smooth muscle cells of the cavernous sinuses. The smooth muscle cells of arterioles and venules were generally found to be negative to enzymatic reaction. Conclusions This study suggests that the vascular disorders of the vasomotor rhinitis depend, at least in part, from nitric oxide synthase induction in the smooth muscle cells of the cavernous sinuses.
Gil Nam Jeong - One of the best experts on this subject based on the ideXlab platform.
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Changes of glycoconjugate expression in nasal Respiratory Mucosa of rats exposed to welding fumes.
Inhalation toxicology, 2007Co-Authors: Gil Nam JeongAbstract:To investigate the effects of welding fumes on the glycoconjugates in nasal Respiratory Mucosa, male Sprague-Dawley rats were exposed to manual metal arc stainless steel (MMA-SS) welding fumes at a concentration of 56-76 mg/m(3) total suspended particulate for 2 h/day in an inhalation chamber for 90 days. During the exposure period, the experimental animals were sacrificed after 2 h and 15, 30, 60, and 90 days of exposure; then sections were examined using lectin histochemistry. Some remarkable changes, such as destroyed cilia, desquamation and mucification of epithelial cells, and destruction of nasal septal glands, were seen in the welding fume-exposed groups. Specific changes in the lectin binding patterns were also observed in the welding fume-exposed rats. The Ricinus communis agglutinin-I (RCA-I) staining of the cilia and columnar cells increased slightly when compared with the unexposed rats. The RCA-I and Ulex europaeus agglutinin-I (UEA-I) staining of the goblet cells also increased as the exposure continued. The mucigenous epithelial cells reacted with Bandeiraea simplicifolia lectin-I (BSL-I), RCA-I, and succinylated wheat germ agglutinin A (sWGA) after 15 days of exposure, which was not visible in the control group. The dorsal septal glands exhibited an affinity with peanut agglutinin (PNA), BSL-I, and RCA-I, which was also not visible in the control group. The affinity for Dolichos biflorus agglutinin (DBA), soybean agglutinin (SBA), PNA, sWGA, BSL-I, and UEA-I in the ventral septal glands of the welding fume-exposed groups tended to increase, whereas the concanavalin A (Con A) reactivity in the dorsal septal glands decreased slightly. In conclusion, it was assumed that the changes in the glycoconjugate residues in the nasal Respiratory Mucosa of the welding fume-exposed rats represented important components of defense mechanisms against the toxicants in the welding fumes.
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Effects of repeated welding fumes exposure on the histological structure and mucins of nasal Respiratory Mucosa in rats.
Toxicology letters, 2006Co-Authors: Gil Nam JeongAbstract:Abstract To investigate the effects of welding fumes on the histological structure and properties of mucins of the nasal Respiratory Mucosa, Sprague–Dawley rats were exposed to manual metal arc-stainless steel (MMA-SS) welding fumes at a concentration of 56–76 mg/m3 total suspended particulates for 2 h per day in an inhalation chamber for 90 days. Experimental animals were sacrificed at 2 h, 15, 30, 60 and 90 days after exposure. Loss of cilia, desquamation of epithelial cells, mucigenous epithelial cells and destruction of nasal septal glands were observed frequently in the welding fumes-exposed groups. These changes became more severe as the exposure continued. The amount of neutral mucins in goblet cells in the welding fumes-exposed group had a tendency to increase, the amount of sulfomucins decreased, while the sialomucins increased as the exposure continued. Mucinogenic epithelial cells, not visible in the control group, contained minimal to small amounts of neutral mucins. In the dorsal septal glands, neutral mucins not visible in the control group appeared, and neutral mucins in the ventral septal glands increased slightly. These results indicate that the observed changes in the properties of mucins due to inhalation of welding fumes may play roles in protection against toxicants.
Andrew G. Huvos - One of the best experts on this subject based on the ideXlab platform.
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Clinicopathologic Differences in Malignant Melanoma Arising in Oral Squamous and Sinonasal Respiratory Mucosa of the Upper Aerodigestive Tract
Archives of Pathology & Laboratory Medicine, 2003Co-Authors: Manju L. Prasad, Klaus J. Busam, Snehal G. Patel, Stacy Hoshaw-woodard, Jatin P. Shah, Andrew G. HuvosAbstract:Abstract Objective.—Primary Mucosal melanomas are rare tumors. We compare melanomas arising in 2 histologically different Mucosa, the stratified oral squamous Mucosa and pseudostratified sinonasal Respiratory Mucosa, to investigate the clinicopathologic influence of native Mucosal histology on the tumor. Methods.—Clinicopathologic features of 36 melanomas arising in the squamous Mucosa of the oral cavity were compared with 59 melanomas arising in the sinonasal Respiratory Mucosa. Results.—The median age of patients was 61 and 63 years for oral and sinonasal melanomas, respectively, with the squamous and Respiratory Mucosa covering the maxilla being most frequently involved (68.7% and 66%, respectively). The former had a remarkable male predilection (28 men, 8 women), while the latter affected both sexes equally (29 men, 30 women). The oral melanomas were more likely to be detected in the early in situ or microinvasive stage (4 cases vs none, P = .008) and were more frequently amelanotic (14 vs 12, P = .049) than sinonasal melanomas. The sinonasal melanomas were frequently thicker (median thickness, 9 vs 2.6 mm), polypoid (29 vs none), ulcerated (57 vs 20), and necrotic (57 vs 14) than oral melanoma (P < .001). Pseudopapillary architecture was more frequent in sinonasal melanomas (16 tumors vs none, P < .001), and desmoplastic melanomas were more frequent in the oral Mucosa (6 vs 1, P = .005). Sinonasal melanoma showed vascular and deep tissue invasion more frequently than oral melanoma; however, no significant difference in disease-specific survival was noted (median survival, 2.8 years vs 3.0 years; 5-year survival, 37% vs 35%, respectively). Conclusion.—Sinonasal melanomas demonstrated aggressive morphologic features significantly more frequently than oral melanomas; however, prognosis remained similar in both groups.
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Clinicopathologic differences in malignant melanoma arising in oral squamous and sinonasal Respiratory Mucosa of the upper aerodigestive tract.
Archives of pathology & laboratory medicine, 2003Co-Authors: Manju L. Prasad, Klaus J. Busam, Snehal G. Patel, Stacy Hoshaw-woodard, Jatin P. Shah, Andrew G. HuvosAbstract:Abstract Objective.—Primary Mucosal melanomas are rare tumors. We compare melanomas arising in 2 histologically different Mucosa, the stratified oral squamous Mucosa and pseudostratified sinonasal Respiratory Mucosa, to investigate the clinicopathologic influence of native Mucosal histology on the tumor. Methods.—Clinicopathologic features of 36 melanomas arising in the squamous Mucosa of the oral cavity were compared with 59 melanomas arising in the sinonasal Respiratory Mucosa. Results.—The median age of patients was 61 and 63 years for oral and sinonasal melanomas, respectively, with the squamous and Respiratory Mucosa covering the maxilla being most frequently involved (68.7% and 66%, respectively). The former had a remarkable male predilection (28 men, 8 women), while the latter affected both sexes equally (29 men, 30 women). The oral melanomas were more likely to be detected in the early in situ or microinvasive stage (4 cases vs none, P = .008) and were more frequently amelanotic (14 vs 12, P = .04...
Riccardo Ruffoli - One of the best experts on this subject based on the ideXlab platform.
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Immunohistochemical localization of 3-nitrotyrosine in the nasal Respiratory Mucosa of patients with vasomotor rhinitis.
Acta oto-laryngologica, 2005Co-Authors: Francesco Giannessi, Francesco Ursino, Bruno Fattori, M. Anita Giambelluca, Maria Concetta Scavuzzo, Francesca Ceccarelli, Riccardo RuffoliAbstract:Conclusion This study demonstrates that, in the nasal Respiratory Mucosa of patients with vasomotor rhinitis, oxidative stress following peroxynitrite formation is confined to the Respiratory epithelium. This suggests that the role of peroxynitrite in vasomotor rhinitis differs from its role in other diseases of the Respiratory tract. The results of this study also support the concept that different pathogenetic mechanisms are probably involved in vasomotor rhinitis. Objective Previous studies indicated that nitric oxide (NO) is involved in the pathogenesis of vasomotor rhinitis, strong expression of NO synthase being detected in the smooth muscle cells of the cavernous sinuses and in the Respiratory epithelium. However, most adverse effects of high levels of NO originate from the reaction of NO with superoxide anions to form peroxynitrite. Therefore, in this study we evaluated the involvement of peroxynitrite in the pathogenesis of vasomotor rhinitis. Material and methods Sites of peroxynitrite formation...
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ultracytochemical localization of the nadph d activity in the human nasal Respiratory Mucosa in vasomotor rhinitis
Laryngoscope, 2000Co-Authors: Riccardo Ruffoli, M. Anita Giambelluca, Bruno Fattori, Paola Soldani, Francesco GiannessiAbstract:Objectives Description of the ultrastructural localization of nitric oxide synthase in the blood vessels of the nasal Respiratory Mucosa in patients with vasomotor rhinitis. Study Design This research was conducted on seven patients—men and women, ages 20 to 45 years—suffering from vasomotor rhinitis and who had undergone surgical therapy for reduction of the inferior turbinates. Methods To study the ultrastructural localization of nitric oxide synthase, NADPH-diaphorase cytochemistry was employed. Samples of the nasal Mucosa were obtained from inferior turbinates. Results The endothelial cells of the arterioles, capillaries , venules and cavernous sinuses revealed a distribution of the enzymatic activity similar to that found in unaffected subjects. A strong enzymatic activity was recognized in the smooth muscle cells of the cavernous sinuses. The smooth muscle cells of arterioles and venules were generally found to be negative to enzymatic reaction. Conclusions This study suggests that the vascular disorders of the vasomotor rhinitis depend, at least in part, from nitric oxide synthase induction in the smooth muscle cells of the cavernous sinuses.
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Ultracytochemical Localization of the NADPH‐d Activity in the Human Nasal Respiratory Mucosa in Vasomotor Rhinitis
The Laryngoscope, 2000Co-Authors: Riccardo Ruffoli, M. Anita Giambelluca, Bruno Fattori, Paola Soldani, Francesco GiannessiAbstract:Objectives Description of the ultrastructural localization of nitric oxide synthase in the blood vessels of the nasal Respiratory Mucosa in patients with vasomotor rhinitis. Study Design This research was conducted on seven patients—men and women, ages 20 to 45 years—suffering from vasomotor rhinitis and who had undergone surgical therapy for reduction of the inferior turbinates. Methods To study the ultrastructural localization of nitric oxide synthase, NADPH-diaphorase cytochemistry was employed. Samples of the nasal Mucosa were obtained from inferior turbinates. Results The endothelial cells of the arterioles, capillaries , venules and cavernous sinuses revealed a distribution of the enzymatic activity similar to that found in unaffected subjects. A strong enzymatic activity was recognized in the smooth muscle cells of the cavernous sinuses. The smooth muscle cells of arterioles and venules were generally found to be negative to enzymatic reaction. Conclusions This study suggests that the vascular disorders of the vasomotor rhinitis depend, at least in part, from nitric oxide synthase induction in the smooth muscle cells of the cavernous sinuses.
