No involvement of interleukin-5 or eosinophils in experimental allergic rhinitis in guinea pigs

Yamasaki, Masashi; Mizutani, Nobuaki; Sasaki, K; Nabe, Takeshi; Kohno, Shigekatsu

doi:10.1016/s0014-2999(02)01372-9

Cited by 31 publications

(36 citation statements)

References 40 publications

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“…15 TXA 2 is reported to increase endothelial permeability and mediate intestinal reperfusion-induced pneumonia 16 and allergic nasal inflammation. 17 However, the mechanism by which PGD 2 modulates vascular permeability and inflammation remained unclear. We have previously shown that various types of endothelial cells express DP receptor and that PGD 2 -DP signaling reduces vascular permeability in growing tumors.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin D ₂ -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway

Kobayashi

Tsubosaka

Hori

et al. 2013

ATVB

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Objective-Prostaglandin D 2 (PGD 2 ) is one of the prostanoids produced during inflammation. Although PGD 2 is known to decrease endothelial permeability through D prostanoid (DP) receptor stimulation, the detailed mechanism is unknown. Methods and Results-Treatment with PGD 2 (0.1-3 μmol/L) or the DP receptor agonist, BW245C (0.1-3 μmol/L), dosedependently increased transendothelial electrical resistance and decreased the FITC-dextran permeability of human umbilical vein endothelial cells. Both indicated decreased endothelial permeability. These phenomena were accompanied by Tiam1/Rac1-dependent cytoskeletal rearrangement. BW245C (0.3 μmol/L) increased the intracellular cAMP level and subsequent protein kinase A (PKA) activity. Pretreatment with PKA inhibitory peptide, but not gene depletion of exchange protein directly activated by cAMP 1 (Epac1), attenuated BW245C-induced Rac1 activation and transendothelial electric resistance increase. In vivo, application of 2.5% croton oil or histamine (100 μg) caused vascular leakage indexed by dye extravasation. Pretreatment with BW245C (1 mg/kg) attenuated the dye extravasation. Gene deficiency of DP abolished, or inhibition of PKA significantly reduced, the DP-mediated barrier enhancement. Conclusion-PGD

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Section: Discussionmentioning

confidence: 99%

Prostaglandin D ₂ -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway

Kobayashi

Tsubosaka

Hori

et al. 2013

ATVB

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“…Regarding involvement of inflammatory cells in the induction of nasal hyperresponsiveness, because eosinophils markedly increased in the nasal cavity lavage fluid after challenges in our model (30), we previously evaluated whether eosinophils recruited are true pathogenic component of the nasal hyperresponsiveness (26). Unexpectedly, when the eosinophilia in the nasal cavity was completely suppressed by a treatment of an anti-IL-5 mAb (TRFK-5), the magnitude of the nasal hyperresponsiveness was not affected (26).…”

Section: Discussionmentioning

confidence: 99%

“…Unexpectedly, when the eosinophilia in the nasal cavity was completely suppressed by a treatment of an anti-IL-5 mAb (TRFK-5), the magnitude of the nasal hyperresponsiveness was not affected (26). Thus, it is strongly suggested that eosinophils are not required for the development of the induction.…”

Section: Discussionmentioning

confidence: 99%

Acquired Nasal Hyperresponsiveness Aggravates Antigen-Induced Rhinitis in the Guinea Pig

et al. 2003

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Abstract. Whether a state of nasal hyperresponsiveness influences antigen-induced biphasic nasal blockage and sneezing were examined using a guinea pig model of allergic rhinitis. Sensitized animals were challenged with an antigen, Japanese cedar pollen, once every week. Before the 13th challenge, the animals were randomly divided into 2 groups, and then the 13th challenge was performed (Groups A-0 and B-0). The 14th challenge was done on day 2 (Group A-2) and on day 7 (Group B-7) after the 13th challenge, on which nasal hyperresponsiveness was present and absent, respectively. Biphasic nasal blockage and sneezing after the challenge in Group A-2 were more severe than those in Group A-0, while those of Group B-7 were almost the same as those of Group B-0. An anti-histaminic, mepyramine, inhibited sneezing but not the biphasic nasal blockage in Group B-7. A cysteinyl leukotriene (CysLT) antagonist, pranlukast, suppressed the late nasal blockage but not the early blockage and sneezing in Group B-7. In contrast, in Group A-2, mepyramine significantly attenuated not only sneezing but also the early nasal blockage. Pranlukast significantly inhibited both nasal blockage and sneezing in Group A-2. In conclusion, nasal hyperresponsiveness aggravated the antigen-induced nasal responses, to which histamine and CysLTs considerably contributed.

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“…Nasal obstruction is caused by the nasal mucosal swelling, which is induced either by mucosal edema, resulting from increased vascular permeability, or by dilation of capacitance vessels, leading to engorgement of blood in the nasal mucosa (23). The presence of intraluminal secretions also contributes to nasal obstruction (29).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Neuropeptides in the Allergic Nasal Obstruction in Guinea Pigs

Kaise

Akamatsu

Ikemura

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-The purposes of the present study were i) to determine whether neuropeptides induce the nasal obstruction in guinea pigs, and ii) to examine the possible involvement of neuropeptides in allergic nasal obstruction. The decrease in nasal cavity volume was determined by acoustic rhinometry as an index of nasal obstruction. In non-sensitized guinea pigs, substance P (SP), neurokinin A (NKA) and calcitonin gene-related peptide (CGRP) caused the nasal obstruction 10 to 30 min after their intranasal application. LY303870 (1 mg/kg), a tachykinin NK 1-receptor antagonist; SR48968 (1 mg/kg), a tackykinin NK2-receptor antagonist; and CGRP(8 -37) (50 nmol / kg), a CGRP1-receptor antagonist, administered intravenously before the intranasal application of the neuropeptides, inhibited the responses induced by SP, NKA and CGRP, respectively. In the guinea pigs sensitized with dinitrophenyl-coupled Ascaris suum allergenic extract, the intranasal antigen challenge caused nasal obstruction. The response was biphasic and consisted of the early phase response (EPR) and the late phase response (LPR), which developed 30 min and 6 h, respectively, after the antigen challenge. Intravenous administration of LY303870 (1 mg / kg) before the antigen challenge inhibited the EPR, while those of SR48968 (1 mg /kg) and CGRP(8 -37) (50 nmol/ kg) inhibited the LPR. The present results suggest that neuropeptides are involved in the allergic nasal obstruction.Keywords: Nasal obstruction, Substance P, Neurokinin A, Calcitonin gene-related peptide Nasal obstruction is one of the major symptoms of allergic rhinitis. The previous studies in allergic rhinitis patients demonstrated that classical histamine H1-receptor antagonists such as chlorpheniramine, hydroxyzine and clemastine were not effective in the treatment of nasal obstruction (1, 2), suggesting an involvement of mediators other than histamine in the pathogenesis of the nasal obstruction. The involvement of peptide leukotrienes (p-LTs) and thromboxane A2 has been suggested as pranlukast (3), a p-LTs receptor antagonist, and ramatroban (4), a thromboxane A2-receptor antagonist, showed clinical efficacy in the treatment of nasal obstruction.There are some results suggesting the involvement of neuropeptides in the pathogenesis of nasal obstruction, although the effectiveness of an antagonist against neuropeptide receptor has not been elucidated in humans. Nerve fibers containing neuropeptides such as substance P (SP), neurokinin A (NKA) and calcitonin gene-related peptide (CGRP) have been found in the human nasal mucosa (5, 6).Their receptors, that is, tachykinin NK 1, tachykinin NK2 and CGRP1 receptors, respectively, have also been shown to exist in human nasal mucosa (5, 6). Moreover, the intranasal administration of SP, NKA or CGRP has been reported to cause nasal obstruction in humans (7 -9).The purposes of the present study were i) to determine the effects of SP, NKA and CGRP on the nasal cavity volume in guinea pigs and ii) to examine the possible involvement of the neuropeptides i...

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No involvement of interleukin-5 or eosinophils in experimental allergic rhinitis in guinea pigs

Cited by 31 publications

References 40 publications

Prostaglandin D ₂ -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway

Prostaglandin D ₂ -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway

Acquired Nasal Hyperresponsiveness Aggravates Antigen-Induced Rhinitis in the Guinea Pig

Involvement of Neuropeptides in the Allergic Nasal Obstruction in Guinea Pigs

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No involvement of interleukin-5 or eosinophils in experimental allergic rhinitis in guinea pigs

Cited by 31 publications

References 40 publications

Prostaglandin D 2 -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway

Prostaglandin D 2 -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway

Acquired Nasal Hyperresponsiveness Aggravates Antigen-Induced Rhinitis in the Guinea Pig

Involvement of Neuropeptides in the Allergic Nasal Obstruction in Guinea Pigs

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Prostaglandin D ₂ -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway

Prostaglandin D ₂ -DP Signaling Promotes Endothelial Barrier Function via the cAMP/PKA/Tiam1/Rac1 Pathway