A murine model of latex allergy-induced airway hyperreactivity

J. C. Thakker, J. Q. Xia, D. A. Rickaby, G. S. Krenz, K. J. Kelly, V. P. Kurup, C. A. Dawson

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Sensitization to latex proteins can cause immediate IgE mast cell-mediated reactions. Health care workers have been found to be particularly at risk because of high exposure. Latex allergy can be produced in mice as demonstrated by IgE and eosinophil responses. Thus the mouse is a potential animal model for studying this disease, but the airway response to latex sensitization in mice has not been evaluated previously. In the present study, we immunized BALB/c mice intranasally with nonammoniated latex proteins. Animals were anesthetized, and lung mechanics were evaluated plethysmographically. Changes in pulmonary conductance (GL) and compliance (Cdyn) were measured in response to a nonspecific challenge with methacholine or to a direct challenge with intravenous latex antigen. Latex sensitization resulted in elevated levels of IgE and latex-specific IgG1 as well as interstitial infiltrates consistent with an allergic response. The methacholine dose-response ED50 for GL was 116.4 μg for the control mice and fell significantly to 20.9 μg for latex-sensitized mice. The ED50 calculated for Cdyn was also significantly lower after latex sensitization. The GL in latex-sensitized mice challenged with latex antigen fell significantly from a prechallenge value of 1.87 ± 0.41 (S.E.) to 0.198 ± 0.03 ml · s-1 · cmH2O after latex antigen challenge. The results indicate that latex-sensitized mice did exhibit increased airway reactivity in the methacholine challenge test. The latex allergic response in mice is unique in that direct challenge with latex antigen itself also resulted in a significant airway response.

Original languageEnglish (US)
Pages (from-to)89-100
Number of pages12
JournalLung
Volume177
Issue number2
DOIs
StatePublished - Jan 1 1999

Fingerprint

Latex Hypersensitivity
Latex
Methacholine Chloride
Immunoglobulin E
Antigens
Animal Disease Models
Lung
Mechanics
Eosinophils

Keywords

  • 11-4 knockout
  • IgE
  • Latex allergy
  • Lung compliance
  • Pulmonary resistance

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Thakker, J. C., Xia, J. Q., Rickaby, D. A., Krenz, G. S., Kelly, K. J., Kurup, V. P., & Dawson, C. A. (1999). A murine model of latex allergy-induced airway hyperreactivity. Lung, 177(2), 89-100. https://doi.org/10.1007/PL00007633

A murine model of latex allergy-induced airway hyperreactivity. / Thakker, J. C.; Xia, J. Q.; Rickaby, D. A.; Krenz, G. S.; Kelly, K. J.; Kurup, V. P.; Dawson, C. A.

In: Lung, Vol. 177, No. 2, 01.01.1999, p. 89-100.

Research output: Contribution to journalArticle

Thakker, JC, Xia, JQ, Rickaby, DA, Krenz, GS, Kelly, KJ, Kurup, VP & Dawson, CA 1999, 'A murine model of latex allergy-induced airway hyperreactivity', Lung, vol. 177, no. 2, pp. 89-100. https://doi.org/10.1007/PL00007633
Thakker JC, Xia JQ, Rickaby DA, Krenz GS, Kelly KJ, Kurup VP et al. A murine model of latex allergy-induced airway hyperreactivity. Lung. 1999 Jan 1;177(2):89-100. https://doi.org/10.1007/PL00007633
Thakker, J. C. ; Xia, J. Q. ; Rickaby, D. A. ; Krenz, G. S. ; Kelly, K. J. ; Kurup, V. P. ; Dawson, C. A. / A murine model of latex allergy-induced airway hyperreactivity. In: Lung. 1999 ; Vol. 177, No. 2. pp. 89-100.
@article{61437afe06f84e8ca4464552e331e2e6,
title = "A murine model of latex allergy-induced airway hyperreactivity",
abstract = "Sensitization to latex proteins can cause immediate IgE mast cell-mediated reactions. Health care workers have been found to be particularly at risk because of high exposure. Latex allergy can be produced in mice as demonstrated by IgE and eosinophil responses. Thus the mouse is a potential animal model for studying this disease, but the airway response to latex sensitization in mice has not been evaluated previously. In the present study, we immunized BALB/c mice intranasally with nonammoniated latex proteins. Animals were anesthetized, and lung mechanics were evaluated plethysmographically. Changes in pulmonary conductance (GL) and compliance (Cdyn) were measured in response to a nonspecific challenge with methacholine or to a direct challenge with intravenous latex antigen. Latex sensitization resulted in elevated levels of IgE and latex-specific IgG1 as well as interstitial infiltrates consistent with an allergic response. The methacholine dose-response ED50 for GL was 116.4 μg for the control mice and fell significantly to 20.9 μg for latex-sensitized mice. The ED50 calculated for Cdyn was also significantly lower after latex sensitization. The GL in latex-sensitized mice challenged with latex antigen fell significantly from a prechallenge value of 1.87 ± 0.41 (S.E.) to 0.198 ± 0.03 ml · s-1 · cmH2O after latex antigen challenge. The results indicate that latex-sensitized mice did exhibit increased airway reactivity in the methacholine challenge test. The latex allergic response in mice is unique in that direct challenge with latex antigen itself also resulted in a significant airway response.",
keywords = "11-4 knockout, IgE, Latex allergy, Lung compliance, Pulmonary resistance",
author = "Thakker, {J. C.} and Xia, {J. Q.} and Rickaby, {D. A.} and Krenz, {G. S.} and Kelly, {K. J.} and Kurup, {V. P.} and Dawson, {C. A.}",
year = "1999",
month = "1",
day = "1",
doi = "10.1007/PL00007633",
language = "English (US)",
volume = "177",
pages = "89--100",
journal = "Lung",
issn = "0341-2040",
publisher = "Springer New York",
number = "2",

}

TY - JOUR

T1 - A murine model of latex allergy-induced airway hyperreactivity

AU - Thakker, J. C.

AU - Xia, J. Q.

AU - Rickaby, D. A.

AU - Krenz, G. S.

AU - Kelly, K. J.

AU - Kurup, V. P.

AU - Dawson, C. A.

PY - 1999/1/1

Y1 - 1999/1/1

N2 - Sensitization to latex proteins can cause immediate IgE mast cell-mediated reactions. Health care workers have been found to be particularly at risk because of high exposure. Latex allergy can be produced in mice as demonstrated by IgE and eosinophil responses. Thus the mouse is a potential animal model for studying this disease, but the airway response to latex sensitization in mice has not been evaluated previously. In the present study, we immunized BALB/c mice intranasally with nonammoniated latex proteins. Animals were anesthetized, and lung mechanics were evaluated plethysmographically. Changes in pulmonary conductance (GL) and compliance (Cdyn) were measured in response to a nonspecific challenge with methacholine or to a direct challenge with intravenous latex antigen. Latex sensitization resulted in elevated levels of IgE and latex-specific IgG1 as well as interstitial infiltrates consistent with an allergic response. The methacholine dose-response ED50 for GL was 116.4 μg for the control mice and fell significantly to 20.9 μg for latex-sensitized mice. The ED50 calculated for Cdyn was also significantly lower after latex sensitization. The GL in latex-sensitized mice challenged with latex antigen fell significantly from a prechallenge value of 1.87 ± 0.41 (S.E.) to 0.198 ± 0.03 ml · s-1 · cmH2O after latex antigen challenge. The results indicate that latex-sensitized mice did exhibit increased airway reactivity in the methacholine challenge test. The latex allergic response in mice is unique in that direct challenge with latex antigen itself also resulted in a significant airway response.

AB - Sensitization to latex proteins can cause immediate IgE mast cell-mediated reactions. Health care workers have been found to be particularly at risk because of high exposure. Latex allergy can be produced in mice as demonstrated by IgE and eosinophil responses. Thus the mouse is a potential animal model for studying this disease, but the airway response to latex sensitization in mice has not been evaluated previously. In the present study, we immunized BALB/c mice intranasally with nonammoniated latex proteins. Animals were anesthetized, and lung mechanics were evaluated plethysmographically. Changes in pulmonary conductance (GL) and compliance (Cdyn) were measured in response to a nonspecific challenge with methacholine or to a direct challenge with intravenous latex antigen. Latex sensitization resulted in elevated levels of IgE and latex-specific IgG1 as well as interstitial infiltrates consistent with an allergic response. The methacholine dose-response ED50 for GL was 116.4 μg for the control mice and fell significantly to 20.9 μg for latex-sensitized mice. The ED50 calculated for Cdyn was also significantly lower after latex sensitization. The GL in latex-sensitized mice challenged with latex antigen fell significantly from a prechallenge value of 1.87 ± 0.41 (S.E.) to 0.198 ± 0.03 ml · s-1 · cmH2O after latex antigen challenge. The results indicate that latex-sensitized mice did exhibit increased airway reactivity in the methacholine challenge test. The latex allergic response in mice is unique in that direct challenge with latex antigen itself also resulted in a significant airway response.

KW - 11-4 knockout

KW - IgE

KW - Latex allergy

KW - Lung compliance

KW - Pulmonary resistance

UR - http://www.scopus.com/inward/record.url?scp=0032608788&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032608788&partnerID=8YFLogxK

U2 - 10.1007/PL00007633

DO - 10.1007/PL00007633

M3 - Article

C2 - 9929406

AN - SCOPUS:0032608788

VL - 177

SP - 89

EP - 100

JO - Lung

JF - Lung

SN - 0341-2040

IS - 2

ER -