Cetirizine counter‐regulates interleukin‐8 release from human epithelial cells (A549)

Arnold, R.; Rihoux, J P; König, Wolfgang

doi:10.1046/j.1365-2222.1999.00630.x

Cited by 56 publications

(29 citation statements)

References 57 publications

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“…Antihistamines down-regulate activation of NF-ĸB to inhibit inflammatory cell accumulation and activation [43]. Cetirizine and azelastine have been shown to down-regulate NF-ĸB expression in parallel with inhibition of generation of the cytokines, IL-1β, IL-6, IL-8, TNF-α and GM-CSF [44, 45]. Antihistamine-induced NF-ĸB down-regulation may also lead to inhibition of expression of adhesion molecules such as ICAM-1 [46].…”

Section: Discussionmentioning

confidence: 99%

Characterization of Anti-Inflammatory Properties and Evidence for No Sedation Liability for the Novel Antihistamine SUN-1334H

Mandhane

Shah

Bahekar

et al. 2009

Int Arch Allergy Immunol

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Background: The anti-inflammatory potential of antihistamines has significant clinical utility. Long-term pharmacotherapy of so-called ‘safe’ antihistamines may be hampered by side effects in the central nervous system. In the present study, the new potential antihistamine SUN-1334H was compared with different antihistamines for anti-inflammatory effects, sedation potential and interaction with alcohol. Method: Nasal and skin allergy were induced in guinea pig and mice by ovalbumin sensitization and challenge. Neurogenic nasal inflammation was induced by capsaicin. Sedation potential and interaction with alcohol were assessed by i.v. and intracerebroventricular pentobarbital-induced sedation and alcohol-induced ataxia models. Results: Ovalbumin sensitization and challenge caused rhinitis pathology including inflammatory cell infiltration, IL-4, and protein leakage in the nasal lavage fluid (NLF) and presence of inflammatory cells in nasal epithelium. A 5-day treatment of antihistamines reduced these markers of inflammation. SUN-1334H, cetirizine and hydroxyzine caused comparable inhibition of NLF leukocytes, IL-4 and total protein concentrations. Fexofenadine and desloratadine showed moderate inhibition of NLF leukocytes and had no significant effect on IL-4 concentration. While fexofenadine had no effect on total protein concentration, the effect of desloratadine was comparable with the other antihistamines. In neurogenic nasal inflammation induced by capsaicin, SUN-1334H and fexofenadine caused better inhibition at lower and middle dose levels than the other antihistamines. In skin allergy models, SUN-1334H showed potent reduction of passive and active cutaneous anaphylactic reactions. In central nervous system side effects models, SUN-1334H, desloratadine and fexofenadine were devoid of any significant effects. Conclusions: The results are suggestive of a high anti-inflammatory to sedation index of SUN-1334H among leading antihistamines.

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Section: Discussionmentioning

confidence: 99%

Characterization of Anti-Inflammatory Properties and Evidence for No Sedation Liability for the Novel Antihistamine SUN-1334H

Mandhane

Shah

Bahekar

et al. 2009

Int Arch Allergy Immunol

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“…With higher LPS concentrations or longer contact times LPS may bind to receptors with lower affinity and may induce a different cytokine response pattern, e.g. an increase in TNF-α and consequently in IL-8 [3]. Miadonna and colleagues [14] demonstrated enhanced histamine release from human basophils after stimulation with IL-6.…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide-induced nasal cytokine response: a dose–response evaluation

Danuser¹,

Rebsamen²,

Weber³

et al. 2000

European Archives of Oto-Rhino-Laryngology

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Information on the dose-response relationship is a prerequisite to defining the non-response threshold of exposure. We investigated whether nasal lipopolysaccharide (LPS) challenges induce an inflammatory response in a dose-dependent way. In three settings nasal lavage was performed before, and 20 min, 1, 6, 23, and 29 h after instillation of 0 microg, 10 microg, and 40 microg LPS for 10 s, in seven healthy subjects. Lavage fluids were analysed for concentrations of interleukin-6 (IL-6), IL-8, tumour necrosis factor-alpha (TNF-alpha), histamine, and albumin. Symptoms were recorded by questionnaire and spirometric lung function was assessed after each lavage. The instillation of 40 microg LPS caused a small increase in nasal symptoms. TNF-alpha was below the detection limit (0.5 pg/ml) in most subjects and, like IL-8 and albumin, showed no relation to the LPS challenge. IL-6 increased over twofold with 10 microg LPS and over 13-fold with 40 microg LPS, with a peak at 6 h after LPS provocation, and the repeated design ANOVA was significant for dose and for time. Six hours after the 40 microg LPS challenge the histamine level significantly increased compared to the saline treatment. We conclude that short-lasting instillation of LPS causes a dose-dependent IL-6 release in the upper airways and minor nasal symptoms.

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“…Anti-inflammatory effects of such a drug in endothelial or epithelial cells [6]might be mediated by a modulating effect on the recruitment of transcription factors like NFĸB and AP-1, since both proteins are involved in the TNFα-induced CAM and cytokine expression [7]. Nevertheless, cetirizine also modulates the IL-4- and IFNγ-induced cellular response.…”

Section: Discussionmentioning

confidence: 99%

Effect of the H<sub>1</sub>-Receptor Antagonist Cetirizine on the Stimulated Expression of Adhesion Molecules and the Activation of NFκB in Human Endothelial Cells

Ambrosch

Borgmann

Rihoux

et al. 2001

Int Arch Allergy Immunol

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Background: In the present work, we studied the effect of cetirizine on the cytokine-stimulated immune response of human umbilical vein endothelial cells (HUVECs). Methods: Our research was directed to analyze the effect of preincubation of HUVECs with cetirizine (1 µg/ml) on (1) the TNFα-, IL-4- and IFNγ-induced surface expression of ICAM-1 and VCAM-1, (2) the secretion of IL-6 and IL-8, (3) the recruitment of NFĸB and AP-1 and (4) the adhesion of histiocytic monocytes (U937) to activated endothelial monolayers. Results and Conclusion: Cetirizine exerts a stimulus-dependent pattern of regulatory action on various parameters of endothelial cell activation. In detail, cetirizine significantly reduces the expression of ICAM-1 and VCAM-1 paralleled by a reduced monocytic adhesion in particular to TNFα-activated HUVECs. With regard to the cytokine release, dual effects are obtained by cetirizine: IL-6 and IL-8 secretion is suppressed by cetirizine in TNFα and IL-4-activated cells, whereas the IFNγ-induced suppression of IL-8 is nearly abrogated. In this context, the TNFα-induced signal transduction with regard to NFĸB and AP-1 was also suppressed by cetirizine.

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Cetirizine counter‐regulates interleukin‐8 release from human epithelial cells (A549)

Cited by 56 publications

References 57 publications

Characterization of Anti-Inflammatory Properties and Evidence for No Sedation Liability for the Novel Antihistamine SUN-1334H

Characterization of Anti-Inflammatory Properties and Evidence for No Sedation Liability for the Novel Antihistamine SUN-1334H

Lipopolysaccharide-induced nasal cytokine response: a dose–response evaluation

Effect of the H<sub>1</sub>-Receptor Antagonist Cetirizine on the Stimulated Expression of Adhesion Molecules and the Activation of NFκB in Human Endothelial Cells

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