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Biomedical subjects

Lars Olaf Cardell

Publications and source records attributed to Lars Olaf Cardell.

7 recordsLinked to original sources
PubMed2002

Increased expression of Vascular Endothelial Growth Factor-A in seasonal allergic rhinitis.

Increased vascular dilatation and permeability characterize allergic rhinitis. In this study oligonucleotide microarrays (Affymetrix HuGe95A) were used to identify differentially expressed vasoactive genes in nasal biopsies from 23 patients with symptomatic seasonal allergic rhinitis (SAR) and 12 healthy controls. RNA was extracted from the biopsies and pooled in three patient and three control pools. Out of 12,626 analysed transcripts, 39 were higher and 81 lower in the patients. Of these transcripts two have vasoactive effects: Vascular Endothelial Growth Factor-A (VEGF-A) and the Beta-1-Adrenergic Receptor. Both were higher in patients than in controls. The mean +/- SEM expression levels in arbitrary units of VEGF-A were 130 +/- 123 in the patients and 59 +/- 53 in the controls. The fold ratio in expression levels between patients/controls was 2.2. The corresponding values for the beta-1-adrenergic receptor were 129 +/- 123 in the patients and 40 +/- 31 in the controls. The fold ratio between patient/controls was 3.2. The role of VEGF-A was assessed by determining VEGF-A concentrations in nasal fluids from another 30 patients with SAR before and after allergen provocation. VEGF-A increased from 124.3 +/- 30.2 to 163.2 +/- 37.8 pg/ml after challenge, P < 0.05. In summary, oligonucleotide microarray analysis of nasal biopsies and protein analyses of nasal fluids indicate that VEGF-A may be an important mediator in SAR.

Betula↗
PubMed2002

PACAP enhances the expression of CD11b, CD66b and CD63 in human neutrophils.

Pituitary adenylate cyclase-activating peptide (PACAP) is a neuropeptide with strong bronchodilator capacity, present in the human airways. There is recent evidence that PACAP decreases the release of proinflammatory cytokines. We have previously shown that PACAP inhibits neutrophil chemotaxis, but altogether little is known about the effects of PACAP on granulocytes. The present study was designed to investigate if PACAP and the closely related peptide vasoactive intestinal peptide (VIP) could affect the cell surface expression of CD11b, CD63 and CD66b in human neutrophils. Neutrophils isolated from 12 healthy blood donors were incubated with either PACAP or VIP, and the expression of neutrophil cell surface markers was assessed using flowcytometry. Neutrophils incubated with PACAP38 exhibited a marked, concentration-dependent increase in their expression of CD11b, CD63 and CD66b. In contrast, neutrophils incubated with VIP showed no increase of the investigated surface markers. This indicates a role for PACAP in granulocyte activation, mediated via a pathway not shared with VIP. Together with the previously presented data on leukocyte migration it suggests that PACAP acts as a regulator of neutrophil inflammation.

Antigens, CD↗
PubMed2002

Increased carbon monoxide levels in the nasal airways of subjects with a history of seasonal allergic rhinitis and in patients with upper respiratory tract infection.

BACKGROUND: Carbon monoxide (CO) has emerged as an endogenously produced gaseous mediator known to be involved in bronchial smooth muscle regulation. Increased amounts of CO have been found in exhaled air during asthma and lower airway inflammation. Recently CO has been shown to be produced in the nasal airways, but there are no reports of altered CO levels in nasal airways during inflammation. OBJECTIVE: This study was designed to investigate if CO levels increase in the human nasal airways during inflammatory conditions, such as allergy and upper airway respiratory tract infection (URTI). METHODS: CO was sampled separately from the upper and lower airways of 13 healthy control subjects, six patients with a history of allergic rhinitis and six patients with URTI. RESULTS: Nasal CO levels were increased in subjects with allergic rhinitis, compared to healthy controls (2.07 +/- 0.15 ppm, n = 6 and 1.62 +/- 0.08 ppm, n = 13, respectively, P < 0.01). CO levels were also increased in patients with URTI, compared to the same controls (1.92 +/- 0.09 ppm, n = 6, P < 0.05). Normal levels of CO were found in air from the lower airways among subjects with allergic rhinitis, whereas corresponding levels in the URTI patients were increased. CONCLUSION: The present data demonstrates that upper airway CO levels increase in parallel with different inflammatory stimuli, such as allergy and infection, suggesting a role for CO as marker or mediator of nasal inflammation.

Adult↗
PubMed2002

Epithelial cells in nasal fluids from patients with allergic rhinitis: how do they relate to epidermal growth factor, eosinophils and eosinophil cationic protein?

The nasal epithelium protects the underlying tissue from damage. Epithelial cell growth is controlled by epidermal growth factor (EGF) and is possibly affected by toxic proteins, e.g. eosinophil cationic protein (ECP). The aims of this study were to examine nasal fluid epithelial cell counts and their relations to EGF, eosinophils and ECP in 23 patients with seasonal allergic rhinitis and 20 healthy controls. Nasal fluid epithelial cell counts were lower in patients than in controls. EGF levels did not differ between patients and controls, and correlated with epithelial cell counts in controls but not in patients. Eosinophils and ECP were higher in patients than in controls, but did not correlate with epithelial cell counts. The role of growth factors, such as EGF, in regulating epithelial cells merits further study.

Adolescent↗
PubMed2002

A decrease in maxillary sinus pressure, as seen in upper airway allergy or infection, results in an increase in upper airway nitric oxide levels.

The paranasal sinuses are connected to the nasal cavity via small osties. Ostial occlusion, caused by mucosal swelling, will result in a slowly increasing negative pressure inside the sinus cavity. In parallel, the oxygen content in the sinus will decrease, resulting in the development of relative hypoxia. Hypoxia is a powerful inducer of nitric oxide (NO) synthase, and inducible NO synthase has been shown to be present in considerable amounts in the upper airways, including the sinuses. The present study was designed to investigate whether a reduction in sinus pressure would affect upper airway NO production. Thirteen healthy volunteers were investigated. A pressure chamber was used to lower the ambient pressure to -4.9 kPa. NO was sampled from one nostril or via a drainage tube inserted into the maxillary sinus before, during and after the hypobaric exposure. When the pressure was decreased, NO levels increased from 256 +/- 15 to 316 +/- 19 ppb (n = 13, p < 0.001). The NO levels remained elevated (282 +/- 21 ppb; p < 0.05) when measurements were repeated 20 min after leaving the chamber. The nasal airway resistance (V2tot) also increased as a result of the chamber session (from 16 +/- 2 degrees before to 21 +/- 3 degrees after; p < 0.05). An increase in NO levels was also found when the experiments were repeated with NO sampled directly from the maxillary sinus (225 +/- 6 before and 265 +/- 9 ppb after; n = 6, p < 0.001). For control purposes the nasal analyses were repeated again, this time under hyperbaric conditions (+ 4.9 kPa). This resulted in a slight decrease in the NO levels (from 273 +/- 22 to 241 +/- 17 ppb; n = 10, p < 0.001), but there was no change in the nasal airway resistance. We conclude that a reduction in sinus pressure, as seen in upper airway allergy or infection, may result in an increase in upper airway NO production.

Adult↗
PubMed2002

The paranasal sinuses as reservoirs for nitric oxide.

OBJECTIVE: Nitric oxide (NO) is an important mediator and inflammatory marker in human upper airways. Enzymes responsible for NO production have been demonstrated both in the nose and in the paranasal sinuses, but NO levels in the sinuses are reported to be several times higher than those in the nose. It has been postulated that the paranasal sinuses may be the primary sites for NO production in the upper respiratory tract. The present study was designed to compare the NO levels sampled from the nose with those found in the paranasal sinuses. MATERIAL AND METHODS: NO levels in the maxillary sinus and nose were determined using a continuous chemiluminescence measuring technique in seven healthy volunteers. RESULTS: When NO was sampled, via a drainage tube inserted into the maxillary sinus, a transient peak in NO level was recorded. The maximal NO level (5,761 +/- 1,513 ppb; n = 7) was reached within 10 s and was followed by the establishment of a lower steady-state level (304 +/- 51 ppb). When NO was continuously sampled from the nose a steady-state level, similar to that found in the sinus, was immediately established (313 +/- 52 ppb). CONCLUSION: The data presented confirm previous findings of extremely high NO levels in the paranasal sinuses and suggest that these cavities may also function as reservoirs for NO.

Adult↗