Increases in airway responsiveness to histamine precede allergen-induced late asthmatic responses

Durham, Stephen R.; Craddock, Charles; Cookson, W. O. C. M.; Benson, MK

doi:10.1016/0091-6749(88)90077-2

Cited by 124 publications

(60 citation statements)

References 34 publications

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“…The in vivo response to an inhaled agonist may be assessed in mice. While this is the most widely used method of assessing airway responsiveness in man (32) and larger animal models (8), it has seen limited use in our murine studies due to the difficulty of delivering an aerosol to the airways while continually assessing airway function (33). The responsiveness of airway smooth muscle from mice may also be assessed in tissue baths (34).…”

Section: Resultsmentioning

confidence: 99%

Airway response to electrical field stimulation in sensitized inbred mice. Passive transfer of increased responsiveness with peribronchial lymph nodes.

Larsen¹,

Renz²,

Loader³

et al. 1992

J. Clin. Invest.

102

107

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We have examined the effects of repeated exposure to antigen on airway responses to cholinergic stimulation in two inbred strains of mice that are similar in underlying cholinergic airway responsiveness, yet differ in their ability to produce IgE. Both BALB/c and SJL/J mice were repeatedly exposed to ovalbumin by inhalation for a 10-d period. While the BALB/c mice developed IgE antibody to this allergen, the SJL/J strain failed to mount an appreciable IgE response. In vitro assessments of the response of tracheal smooth muscle from saline exposed mice (controls) of both strains demonstrated responses to both methacholine and electrical field stimulation that were not significantly different between the strains. Following exposure to ovalbumin, the BALB/c strain developed a significant increase in their response to electrical field stimulation, while their response to methacholine was unaltered. In contrast, the in vitro responsiveness to these stimuli did not increase in SJL/J mice following similar exposure to inhaled nebulized ovalbumin. The passive transfer of cells from the peribronchial lymph nodes of ovalbumin-sensitized BALB/c mice into syngeneic nonimmune mice also led to increases in responsiveness of tracheal smooth muscle to electrical field stimulation. In contrast, transfer of cells from nonsensitized mice did not alter responsiveness. These results suggest that murine species capable of developing an IgE response to allergen also develop alterations in the neural control of their airways. Further, this alteration appears to be lymphocyte dependent, in that cells found within peribronchial lymph nodes following allergen exposure are capable of transferring this increase in responsiveness to nonimmune mice. (J. Clin. Invest. 1992. 89:747-752.)

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Section: Resultsmentioning

confidence: 99%

Airway response to electrical field stimulation in sensitized inbred mice. Passive transfer of increased responsiveness with peribronchial lymph nodes.

Larsen¹,

Renz²,

Loader³

et al. 1992

J. Clin. Invest.

102

107

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“…[45,46] and LMW occupational agents [47,48] are associated with an increase in NSBHR that occurs 6-8 h after exposure, and returns to baseline level within a period of 24 h to 4 weeks [47,48]. This increase in NSBHR may precede the development of the late component of DAR, since it has been recorded 1-3 h after resolution of the immediate response [49][50][51]. Recently, significant increases in NSBHRs have been documented within 12 h after isolated EARs to various occupational agents [52].…”

Section: Research Purposesmentioning

confidence: 99%

“…A number of studies have documented that asthmatic reactions induced by sensitizing agents can be associated with an increase in NSBHR that may persist for several hours to several weeks [45][46][47][48][49][50][51][52]. This increase in NSBHR may help to distinguish asthmatic reactions due to specific hyperresponsiveness mechanisms from nonspecific bronchoconstriction triggered by irritants.…”

Section: Assessment Of Bronchial Responsementioning

confidence: 99%

Inhalation challenges with agents causing occupational asthma

Vandenplas¹,

Jl²

1997

Eur Respir J

124

103

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Occupational asthma (OA) is steadily emerging as the principal cause of respiratory disease due to the workplace environment. One of the key means to ascertain diagnosis of OA is specific inhalation challenge (SIC) with occupational agents. This review: 1) describes the methodology of SIC, with a special emphasis on procedures aimed at increasing the safety and validity of these tests; and 2) outlines the roles of SIC in the diagnosis of OA in clinical and medicolegal assessment, epidemiological studies, surveillance programmes and the investigation of the pathophysiological mechanisms of asthma and OA. We discuss areas of future development, including the development of apparatus which allows exposure of subjects to low and stable concentrations of the occupational agent and the assessment of preventive procedures.

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“…The current paradigm explaining the EPR in asthmatic subjects involves mechanisms in which allergen binds to, and cross-links, IgE receptors on mast cells (7,8). This event subsequently leads to activation and the release of histamine and leukotrienes, triggering an immediate bronchoconstrictive response (9,10). In contrast, the LPR begins ϳ3 h following allergen provocation, peaks between 6 -12 h, and generally resolves within 24 h (3,5).…”

mentioning

confidence: 99%

Early Phase Bronchoconstriction in the Mouse Requires Allergen-Specific IgG

Crosby

Cieslewicz

Borchers

et al. 2002

The Journal of Immunology

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Allergen provocation of allergic asthma patients is often characterized by an initial period of bronchoconstriction, or early phase reaction (EPR), that leads to maximal airway narrowing within 15–30 min, followed by a recovery period returning airway function to baseline within 1–2 h. In this study, we used a defined OVA provocation model and mice deficient for specific leukocyte populations to investigate the cellular/molecular origins of the EPR. OVA-sensitized/challenged wild-type (C57BL/6J) mice displayed an EPR following OVA provocation. However, this response was absent in gene knockout animals deficient of either B or T cells. Moreover, transfer of OVA-specific IgG, but not IgE, before the OVA provocation, was capable of inducing the EPR in both strains of lymphocyte-deficient mice. Interestingly, an EPR was also observed in sensitized/challenged mast cell-deficient mice following an OVA provocation. These data show that the EPR in the mouse is an immunologically based pathophysiological response that requires allergen-specific IgG but occurs independent of mast cell activities. Thus, in the mouse the initial period of bronchoconstriction following allergen exposure may involve neither mast cells nor IgE-mediated events.

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Increases in airway responsiveness to histamine precede allergen-induced late asthmatic responses

Cited by 124 publications

References 34 publications

Airway response to electrical field stimulation in sensitized inbred mice. Passive transfer of increased responsiveness with peribronchial lymph nodes.

Airway response to electrical field stimulation in sensitized inbred mice. Passive transfer of increased responsiveness with peribronchial lymph nodes.

Inhalation challenges with agents causing occupational asthma

Early Phase Bronchoconstriction in the Mouse Requires Allergen-Specific IgG

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