Bradykinin Induced Bronchoconstriction in Man

Fuller, Richard W.; Dixon, C. M. S.; Dollery, C. T.; Barnes, P. J.

doi:10.1042/cs068035p

Cited by 107 publications

(163 citation statements)

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“…Furthermore, the presented data suggest TLR stimulation as a link between microbial invasion and kinin-induced airway hyperreactivity. Bradykinin can be obtained in bronchoalveolar lavage fluid derived from asthmatic patients [41] and it induces bronchoconstriction in patients with asthma but not in healthy subjects [42]. The currently presented TLR-mediated hyper-responsiveness to bradykinin offers a pathway for microbe-induced asthma exacerbations.…”

Section: Discussionmentioning

confidence: 99%

Toll‐like receptor stimulation induces airway hyper‐responsiveness to bradykinin, an effect mediated by JNK and NF‐κB signaling pathways

et al. 2004

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Airway infections induce hyper-responsiveness in asthmatic patients. Toll-like receptors (TLR) mediate inflammatory responses to microbes. Occurrence and effects of TLR2, TLR3 and TLR4 were examined in a mouse organ culture model of asthma focusing on the smooth muscle responses to bradykinin. TLR2, TLR3 and TLR4 mRNA, and TLR2 and TLR4 immunoreactivity were detected in the tracheal muscle layer. Tracheal organ culture for 1 or 4 days with lipopolysaccharide (LPS; TLR2/4 agonist) or polyinosinic polycytidylic acid (poly-I-C; TLR3 agonist) enhanced bradykinin-and [des-Arg 9 ]-bradykinin-induced contractions. Simultaneous LPS and poly-I-C treatment resulted in synergistic enhancement of bradykinin-induced contraction. In carbachol-pre-contracted segments TLR stimulation induced less potent relaxations to bradykinin and [des-Arg 9 ]-bradykinin. The LPS and poly-I-C enhancement of bradykinin-induced contraction was inhibited by the transcriptional inhibitor actinomycin-D, dexamethasone, the proteasome inhibitor MG-132 and the c-Jun Nterminal kinase (JNK) inhibitor SP600125. LPS and poly-I-C induced translocation of NF-‹ B p65 to the nucleus and up-regulation of kinin B 1 and B 2 receptor mRNA. In summary, TLR2, TLR3 and TLR4 are expressed in the mouse tracheal smooth muscle. Costimulation of these receptors results in NF-‹ B-and JNK-mediated transcription of B 1 and B 2 receptor, inducing hyper-responsiveness to bradykinin.

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Section: Discussionmentioning

confidence: 99%

Toll‐like receptor stimulation induces airway hyper‐responsiveness to bradykinin, an effect mediated by JNK and NF‐κB signaling pathways

et al. 2004

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“…25 BK is generated from kininogens by the actions of plasma and tissue kallikreins (kininogenases). 24,25 Although its action includes vasodilation, vascular leakage, and contraction of smooth muscles, 24,25,34 BK stimulated alveolar macrophages and bronchial epithelial cells to release NCA and MCA. 26,27 In the present study, BK induced the release of chemokines from A549 cells, suggesting that BK has the potential to stimulate ATII cells resulting in the release of NCA and MCA and contribute to lung inflammation besides its direct effects on lung cells.…”

Section: Discussionmentioning

confidence: 99%

Bradykinin Stimulates Type II Alveolar Cells to Release Neutrophil and Monocyte Chemotactic Activity and Inflammatory Cytokines

Koyama

Sato

Nomura

et al. 1998

The American Journal of Pathology

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In the present study , we evaluated the potential of bradykinin (BK) to induce the release of neutrophil and monocyte chemotactic activity (NCA and MCA) and cytokines from an alveolar type II epithelial cell line , A549 cells. BK stimulated A549 cells to release NCA and MCA in a dose-and time-dependent manner (P < 0.001). Checkerboard analysis revealed that both NCA and MCA involved chemotactic and chemokinetic activity. Molecular sieve column chromatography showed three molecular weight masses ( Sequestration of peripheral blood neutrophils and monocytes within the lung is characteristic of a number of acute and chronic pulmonary diseases.

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“…This has led to speculation that analogies may be drawn between asthma-associated airway hyperresponsiveness and hyperalgesia (heightened sensitivity to painful stimuli) that often accompanies inflammation in the somatosensory system (23). Most stimuli administered to assess airway hyperresponsiveness, including histamine (24,25), capsaicin (26), bradykinin (27), distilled water (28), and sulfur dioxide (29), cause bronchoconstriction by stimulating primary afferent nerve fibers and initiating central parasympathetic cholinergic reflexes. Experiments in animal models suggest that even the response to a so-called direct smooth muscle spasmogen like methacholine is likely to be mediated in part by a centrally mediated cholinergic reflex (30).…”

Section: Inflammation and The Excitability Of Afferent Neuronsmentioning

confidence: 99%