A deficient TLR2 signaling promotes airway mucin production in Mycoplasma pneumoniae-infected allergic mice.

A deficient TLR2 signaling promotes airway mucin production in Mycoplasma pneumoniae-infected allergic mice. Research Abstract Details 

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A deficient TLR2 signaling promotes airway mucin production in Mycoplasma pneumoniae-infected allergic mice. Abstract Text:

Qun Wu,Richard J Martin,John G Rino,Samithamby Jeyaseelan,Rachel Breed,Hong Wei Chu,

The original hygiene hypothesis suggests that early childhood respiratory infections preceding allergen exposure may decrease the prevalence of allergic diseases. We have recently demonstrated that Mycoplasma pneumoniae infection preceding allergen exposure reduced allergic responses in mice. However, the molecular mechanisms underlying the protective role of M. pneumoniae in allergic responses, particularly airway mucin production, remain unclear. Wild-type and Toll-like receptor 2 (TLR2)-deficient mice with a respiratory M. pneumoniae infection preceding allergen (ovalbumin) challenge were utilized to determine the regulatory role of TLR2-IFN-gamma signaling pathway in airway mucin expression. Furthermore, air-liquid interface cultures of mouse primary tracheal epithelial cells were performed to examine the effects of IFN-gamma on mucin expression. In wild-type mice, M. pneumoniae infection preceding allergen challenge significantly reduced airway mucins but increased IFN-gamma. In sharp contrast, in TLR2-deficient mice, M. pneumoniae preceding allergen challenge resulted in increased mucin protein without a noticeable change of IFN-gamma. In cultured mouse primary tracheal epithelial cells, IFN-gamma was shown to directly inhibit mucin expression in a dose-dependent manner. Our study demonstrates for the first time that a respiratory M. pneumoniae infection preceding allergen challenge reduces airway epithelial mucin expression in part through TLR2-IFN-gamma signaling pathway. A bacterial infection in asthmatic subjects with weakened TLR2-IFN-gamma signaling may result in an exaggerated airway mucin production.

A deficient TLR2 signaling promotes airway mucin production in Mycoplasma pneumoniae-infected allergic mice. Publishing Authors By Initials

Q Wu,RJ Martin,JG Rino,S Jeyaseelan,R Breed,HW Chu,

For similar respiratory system: trachea research abstracts see: respiratory system: trachea research

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A deficient TLR2 signaling promotes airway mucin production in Mycoplasma pneumoniae-infected allergic mice. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Lung cellular and

VOLUME: 292

Page Numbers: L1064-72

Journal Abbreviation: Am. J. Physiol. Lung Cell Mol.

ISSN: 1040-0605

DAY: 28

MONTH: 12

YEAR: 2006

A deficient TLR2 signaling promotes airway mucin production in Mycoplasma pneumoniae-infected allergic mice. Information

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LANGUAGE: eng

NlmUniqueID: 100901229

A deficient TLR2 signaling promotes airway mucin production in Mycoplasma pneumoniae-infected allergic mice. Keywords Mesh Terms:

KEYWORDS: Trachea

MESH TERMS: physiology

Chemical & Substance for Abstract: A deficient TLR2 signaling promotes airway mucin production in Mycoplasma pneumoniae-infected allergic mice. Information

Substance Name: Interferon Type II

Registry Number: 82115-62-6

Grant and Affiliation Information for A deficient TLR2 signaling promotes airway mucin production in Mycoplasma pneumoniae-infected allergic mice.

AFFILIATION: Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado 80206, USA.

Country: United States

AGENCY: United States CSR

GRANT: RG-22442-N

ACRONYM: RG

MEDLINETA: Am J Physiol Lung Cell Mol Phy

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