L -Selectin is required for the development of airway hyperresponsiveness but not airway inflammation in a murine model of asthma

Fiscus, Lynne C.; Herpen, Jenny Van; Steeber, Douglas A.; Tedder, Thomas F.; Tang, Mimi L.K.

doi:10.1067/mai.2001.114703

Cited by 54 publications

(29 citation statements)

References 33 publications

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“…Both humoral and cellular immune responses are generally normal in these adhesion molecule-deficient mice (5,34,35). In addition, loss of L-selectin or ICAM-1 does not affect total or Ag-specific IgE production in a murine model of asthma (12,36). Therefore, it is unlikely that the observed reduction in IgE production is due to a defective immune response in the adhesion molecule-deficient mice.…”

Section: Figurementioning

confidence: 94%

“…Importantly, atopic dermatitis (AD) is usually caused by repeated epicutaneous exposure to various environmental Ags. Although L-selectin deficiency reduces airway hyper-responsiveness in a murine asthma model induced by repeated Ag exposure through the respiratory mucosa (12), the contribution of adhesion molecules to the development of chronic cutaneous inflammation remains unknown. However, Kitagaki et al (9) have established a murine model of chronic CH responses that provides an appropriate animal model for chronic skin inflammation.…”

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confidence: 99%

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L-Selectin or ICAM-1 Deficiency Reduces an Immediate-Type Hypersensitivity Response by Preventing Mast Cell Recruitment in Repeated Elicitation of Contact Hypersensitivity

Shimada

Hasegawa

Kaburagi

et al. 2003

The Journal of Immunology

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Repeated Ag exposure results in a shift in the time course of contact hypersensitivity (CH) from a typical delayed-type to an immediate-type response followed by a late phase reaction. Chronic CH responses are clinically relevant to human skin allergic diseases, such as atopic dermatitis, that are usually caused by repeated stimulation with environmental Ags. Chronic inflammatory responses result in part from infiltrating leukocytes. To determine the role of leukocyte adhesion molecules in chronic inflammation, chronic CH responses were assessed in mice lacking L-selectin, ICAM-1, or both adhesion molecules. Following repeated hapten sensitization for 24 days at 2-day intervals, wild-type littermates developed an immediate-type response at 30 min after elicitation, followed by a late phase reaction. By contrast, loss of ICAM-1, L-selectin, or both, eliminated the immediate-type response and inhibited the late phase reaction. Similar results were obtained when wild-type littermates repeatedly exposed to hapten for 22 days were treated with mAbs to L-selectin and/or ICAM-1 before the elicitation on day 24. The lack of an immediate-type response on day 24 paralleled a lack of mast cell accumulation after 30 min of elicitation and decreased serum IgE production. Repeated Ag exposure in wild-type littermates resulted in increased levels of serum L-selectin, a finding also observed in atopic dermatitis patients. The current study demonstrates that L-selectin and ICAM-1 cooperatively regulate the induction of the immediate-type response by mediating mast cell accumulation into inflammatory sites and suggests that L-selectin and ICAM-1 are potential therapeutic targets for regulating human allergic reactions.

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Section: Figurementioning

confidence: 94%

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confidence: 99%

L-Selectin or ICAM-1 Deficiency Reduces an Immediate-Type Hypersensitivity Response by Preventing Mast Cell Recruitment in Repeated Elicitation of Contact Hypersensitivity

Shimada

Hasegawa

Kaburagi

et al. 2003

The Journal of Immunology

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“…Following measurement of airway reactivity, BAL was performed by three washes of 0.5 ml saline containing 5% (v/v) fetal calf serum and total and differential cell counts of inflammatory cells determined. 15,40 Total viable cell counts were determined using a hemocytometer with trypan blue exclusion. Differential counts of eosinophils, neutrophils, lymphocytes and monocytes were determined on cytospin smears of BAL samples (4 x 10 5 cells) from individual mice stained with DiffQuick (Life Technologies, Auckland, New Zealand) and identified by standard morphological criteria after counting 300 cells.…”

Section: Methodsmentioning

confidence: 99%

Protective effects of valproic acid against airway hyperresponsiveness and airway remodeling in a mouse model of allergic airways disease

et al. 2011

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“…23 By contrast, L-selectin is required for the development of airway hyperresponsiveness and lymphocyte migration into the inflamed lung during an allergic inflammatory response. 24,25 Radiation-induced, endotoxin-induced, or antigen-dependent allergic pulmonary inflammation is attenuated in ICAM-1 Ϫ/Ϫ mice. [25][26][27][28] By contrast, ICAM-1 loss increases mortality in Escherichia coli or Klebsiella pneumonia.…”

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confidence: 99%

Intercellular Adhesion Molecule-1 and L-Selectin Regulate Bleomycin-Induced Lung Fibrosis

Hamaguchi

Nishizawa

Yasui

et al. 2002

The American Journal of Pathology

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L -Selectin is required for the development of airway hyperresponsiveness but not airway inflammation in a murine model of asthma

Cited by 54 publications

References 33 publications

L-Selectin or ICAM-1 Deficiency Reduces an Immediate-Type Hypersensitivity Response by Preventing Mast Cell Recruitment in Repeated Elicitation of Contact Hypersensitivity

L-Selectin or ICAM-1 Deficiency Reduces an Immediate-Type Hypersensitivity Response by Preventing Mast Cell Recruitment in Repeated Elicitation of Contact Hypersensitivity

Protective effects of valproic acid against airway hyperresponsiveness and airway remodeling in a mouse model of allergic airways disease

Intercellular Adhesion Molecule-1 and L-Selectin Regulate Bleomycin-Induced Lung Fibrosis

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