Formyl peptide-induced contraction of human airways in vitro

Armour, C. L.; Black, J. L.; Johnson, Peter R.; Vincenc, K. S.; Berend, Norbert

doi:10.1152/jappl.1986.60.1.141

Cited by 20 publications

(14 citation statements)

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“…Fpr1 is expressed in leukocytes (30), and is thought to modulate bronchoconstriction indirectly through the action of metabolites of arachidonic acid in guinea pigs and humans (31,32). Previous reports documented the expression of Fpr1 in human bronchial ASM and in numerous other tissues (33), but we did not detect it in murine ASM using immunohistochemistry, arguing for an indirect role in the contraction of ASM.…”

Section: Discussioncontrasting

confidence: 72%

Strain-Dependent Genomic Factors Affect Allergen-Induced Airway Hyperresponsiveness in Mice

Kelada

Wilson

Tavarez

et al. 2011

Am J Respir Cell Mol Biol

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Asthma is etiologically and clinically heterogeneous, making the genomic basis of asthma difficult to identify. We exploited the straindependence of a murine model of allergic airway disease to identify different genomic responses in the lung. BALB/cJ and C57BL/6J mice were sensitized with the immunodominant allergen from the Dermatophagoides pteronyssinus species of house dust mite (Der p 1), without exogenous adjuvant, and the mice then underwent a single challenge with Der p 1. Allergic inflammation, serum antibody titers, mucous metaplasia, and airway hyperresponsiveness were evaluated 72 hours after airway challenge. Whole-lung gene expression analyses were conducted to identify genomic responses to allergen challenge. Der p 1-challenged BALB/cJ mice produced all the key features of allergic airway disease. In comparison, C57BL/6J mice produced exaggerated Th2-biased responses and inflammation, but exhibited an unexpected decrease in airway hyperresponsiveness compared with control mice. Lung gene expression analysis revealed genes that were shared by both strains and a set of down-regulated genes unique to C57BL/6J mice, including several G-protein-coupled receptors involved in airway smooth muscle contraction, most notably the M2 muscarinic receptor, which we show is expressed in airway smooth muscle and was decreased at the protein level after challenge with Der p 1. Murine strain-dependent genomic responses in the lung offer insights into the different biological pathways that develop after allergen challenge. This study of two different murine strains demonstrates that inflammation and airway hyperresponsiveness can be decoupled, and suggests that the downmodulation of expression of G-protein-coupled receptors involved in regulating airway smooth muscle contraction may contribute to this dissociation.

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Section: Discussioncontrasting

confidence: 72%

Strain-Dependent Genomic Factors Affect Allergen-Induced Airway Hyperresponsiveness in Mice

Kelada

Wilson

Tavarez

et al. 2011

Am J Respir Cell Mol Biol

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“…An alternate mechanism for the bronchoconstriction effect of FMLP is a direct effect on a smooth muscle receptor. The previous reports on the effects of FMLP on guinea pig smooth muscle in vitro [13] and a recent report in which human airway smooth muscle contracted in response to FMLP [15] are in keeping with this notion. However, the fact that FMLP failed to elicit contraction of rabbit airway smooth muscle in vitro in the present study suggests that the bronchoconstriction is not mediated by a smooth muscle receptor.…”

Section: Discussionsupporting

confidence: 63%

“…Recent reports [13,14] suggest that FMLP causes contraction of guinea pig and human [15] airway smooth muscle. It has been shown that neutrophil infiltration into the airway wall, whether induced by exposure to ozone or chemotactic complement components, is associated with increased airway responsiveness to acetylcholine [18,19] and histamine [20].…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that FMLP is not only chemotactic for these cells but also causes cell aggregation [7], granule enzyme secretion [8,9], stimulation of the respiratory burst with generation of free radicals [10], liberation of products of the lipoxygenase pathway [11], and increased Fc receptor activity [12]. More recently, FMLP has been shown to contract guinea pig and human airway smooth muscle [13,14,15]. Because of our interest in inflammation and airway reactivity this study was undertaken to see if FMLP causes bronchoconstriction in the rabbit in vivo and whether it contracts the airway smooth muscle in vitro.…”

Section: Introductionmentioning

confidence: 99%

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Formyl-methionyl-leucyl-phenylalanine causes bronchoconstriction in rabbits

1986

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Formyl-methionyl-leucyl-phenylalanine (FMLP) is a synthetic acylated oligopeptide related to chemotactic peptides released by bacteria. In order to determine whether FMLP causes bronchoconstriction in vivo, we studied the effects of nebulized FMLP on lung resistance (RL) in the rabbit. In fourteen rabbits baseline RL was measured and than dimethylsulfoxide (DMSO) alone and 0.3, 1, 3 and 10 mg/ml FMLP in DMSO was nebulized and inhaled by the rabbits over periods of 2 min each. After each concentration the RL was re-measured and the results expressed as a % of the RL following DMSO alone. In 6 rabbits the response to serial nebulization of DMSO alone was 5.5 +/- 10.4% (mean +/- 2 SD). In 8 rabbits receiving FMLP there was a dose dependent increase in RL of 20% or greater whereas 6 rabbits failed to respond. Since there are known receptors for FMLP on neutrophils, 10 further rabbits were rendered neutropenic using nitrogen mustard and then studied as above. Eight of these rabbits failed to respond significantly to FMLP whereas 2 had a 20% or greater increase in RL. In each bronchial specimen from 6 additional rabbits FMLP failed to induce airway contraction in vitro. We conclude that FMLP causes a variable degree of bronchoconstriction in rabbits, that this response may, in part, be mediated via the neutrophil and is unlikely to be due to direct smooth muscle contraction.

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“…The synthetie baeterial chemotaetie factor formyl-methionyl-leucylphenylalanine (FMLP) also aetivates neutrophils [7]. In addition it has been shown to cause bronchoconstriction in vitro [8] and in vivo [9]. Human neutrophils primed with GM-CSF and then stimulated with FMLP produee detectable amounts of the leucocyte chemotactic factor leukotriene B4 [10].…”

Section: Introductionmentioning

confidence: 99%

Neutrophil–induced human bronchial hyper responsiveness in vitro—pharmacological modulation

Hughes

McKay

Johnson

et al. 1993

Clin Experimental Allergy

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Although it has been postulated that inflammatory cells cause the bronchial hyperresponsiveness which is diagnostic of asthma, until recently there has been little direct evidence of such a link. We have recently shown that calcium ionophore-activated human neutrophils and eosinophils can induce a state of human airway hyperresponsiveness in vitro. In this study we have shown that the anti-inflammatory agent nedocromil sodium, 10(-7) M, inhibited the hyperresponsiveness induced by products released from ionophore activated neutrophils but did not inhibit the release of leukotriene B4 from the same cells. Neutrophil-induced bronchial hyperresponsiveness was also inhibited by pre-treatment of the bronchial tissues with a thromboxane A2 and prostaglandin receptor antagonist, GR32191, 10(-7) M. These findings indicate that cyclooxygenase products are involved in bronchial hyperresponsiveness induced by inflammatory cell products in vitro and that their release can be inhibited by nedocromil sodium.

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Formyl peptide-induced contraction of human airways in vitro

Cited by 20 publications

References 0 publications

Strain-Dependent Genomic Factors Affect Allergen-Induced Airway Hyperresponsiveness in Mice

Strain-Dependent Genomic Factors Affect Allergen-Induced Airway Hyperresponsiveness in Mice

Formyl-methionyl-leucyl-phenylalanine causes bronchoconstriction in rabbits

Neutrophil–induced human bronchial hyper responsiveness in vitro—pharmacological modulation

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