Skip header and navigation

Refine By

   MORE

4 records – page 1 of 1.

Contribution of intercellular-adhesion molecule-1 in allergen-induced airway hyperresponsiveness and inflammation in sensitised brown-Norway rats.

https://arctichealth.org/en/permalink/ahliterature15953
Source
Int Arch Allergy Immunol. 1994 Jul;104(3):291-5
Publication Type
Article
Date
Jul-1994
Author
J. Sun
W. Elwood
A. Haczku
P J Barnes
P G Hellewell
K F Chung
Author Affiliation
Department of Thoracic Medicine, National Heart and Lung Institute, London, UK.
Source
Int Arch Allergy Immunol. 1994 Jul;104(3):291-5
Date
Jul-1994
Language
English
Publication Type
Article
Keywords
Allergens - immunology
Animals
Asthma - immunology - prevention & control
Bronchial Hyperreactivity - immunology - prevention & control
Bronchial Provocation Tests
Bronchoalveolar Lavage Fluid - cytology
Cell Adhesion Molecules - immunology
Eosinophils - immunology
Female
Inflammation - pathology
Intercellular Adhesion Molecule-1
Leukocyte Count
Lymphocytes - immunology
Ovalbumin
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Abstract
We investigated the potential role of intercellular-adhesion molecule-1 (ICAM-1) in allergen-induced bronchial hyperresponsiveness (BHR) and inflammation in sensitised Brown-Norway rats. Rats were sensitised with ovalbumin (OA) intraperitoneally and 21 days later they were either exposed to 0.9% NaCl or 1% OA aerosol for 15 min. Rats exposed to OA aerosol were pretreated either with ICAM-1 antibody (3 mg/kg i.p. and i.v., 45 min prior to OA exposure) or with the diluent for the antibody. Eighteen to twenty-four hours after OA or 0.9% NaCl exposure, rats were anaesthetised, tracheostomised and mechanically ventilated, and airway responsiveness to acetylcholine (ACh) aerosol was measured as the provocative concentration of ACh needed to increase pulmorary resistance by 100% (PC100). Mean -log PC100 was increased in rats exposed to OA but pretreated with diluent (2.75 +/- 0.06) compared to rats treated with ICAM-1 antibody (2.51 +/- 0.08;
PubMed ID
7913357 View in PubMed
Less detail

Involvement of alpha-4 integrins in allergic airway responses and mast cell degranulation in vivo.

https://arctichealth.org/en/permalink/ahliterature57560
Source
Am J Respir Crit Care Med. 1998 Oct;158(4):1127-33
Publication Type
Article
Date
Oct-1998
Author
M. Hojo
K. Maghni
T B Issekutz
J G Martin
Author Affiliation
Meakins-Christie Laboratories, McGill University, Montreal, Quebec; and the Izaak Walton Killam Children's Hospital, Grace Centre, Dalhousie University, Halifax, Nova Scotia, Canada.
Source
Am J Respir Crit Care Med. 1998 Oct;158(4):1127-33
Date
Oct-1998
Language
English
Publication Type
Article
Keywords
Adjuvants, Immunologic - administration & dosage
Airway Resistance - immunology
Allergens - administration & dosage - immunology
Animals
Anti-Allergic Agents - immunology
Antibodies, Monoclonal - therapeutic use
Antigens, CD - immunology
Antigens, CD29 - immunology
Bile - chemistry
Bronchoalveolar Lavage Fluid - chemistry
Cell Adhesion Molecules - immunology
Cell Degranulation - immunology
Histamine - analysis
Immunization
Integrin alpha4
Integrin alpha4beta1
Integrins - immunology
Leukotriene E4 - analogs & derivatives - analysis
Male
Mast Cells - immunology
Ovalbumin - administration & dosage - immunology
Rats
Rats, Inbred BN
Receptors, Lymphocyte Homing - immunology
Receptors, Very Late Antigen - immunology
Research Support, Non-U.S. Gov't
Respiratory Hypersensitivity - immunology
Serine Endopeptidases - analysis
Virulence Factors, Bordetella - administration & dosage
Abstract
Antibodies against integrins have been shown to inhibit allergic airway responses. The purpose of this study was to test the hypothesis that the beta1 integrin, very late antigen-4 (VLA-4), is involved in mast cell activation triggered by allergen exposure in sensitized animals. To do this we studied Brown Norway rats that were sensitized to ovalbumin (OA; 1 mg subcutaneously) using Bordetella pertussis as an adjuvant. Two weeks later rats were challenged with OA, pulmonary resistance (RL) was determined, and the concentrations of histamine and tryptase in bronchoalveolar lavage fluid and N-acetyl-leukotriene (LT)E4 in bile were measured. Pretreatment with a monoclonal antibody against VLA-4 (TA-2) attenuated the early response after OA challenge (342.9 +/- 24.4% baseline RL versus 153.3 +/- 19.4%; p
PubMed ID
9769271 View in PubMed
Less detail

Polymorphonuclear cell-mediated vascular injury in anergic surgical patients.

https://arctichealth.org/en/permalink/ahliterature222118
Source
Arch Surg. 1993 Jan;128(1):68-71; discussion 72
Publication Type
Article
Date
Jan-1993
Author
S A Stergiopoulos
J. Gordon
N V Christou
Author Affiliation
Department of Surgery, McGill University, Montreal, Quebec, Canada.
Source
Arch Surg. 1993 Jan;128(1):68-71; discussion 72
Date
Jan-1993
Language
English
Publication Type
Article
Keywords
Adult
Cell Adhesion - immunology
Cell Adhesion Molecules - immunology
Cytotoxicity Tests, Immunologic
Endothelium, Vascular - immunology
Evaluation Studies as Topic
Female
Hospitals, University
Humans
Hypersensitivity, Delayed - diagnosis
Immune Tolerance - immunology
Immunity, Cellular - immunology
Infection - blood - epidemiology - immunology
Male
Middle Aged
Neutrophils - immunology
Postoperative Complications - blood - epidemiology - immunology
Quebec - epidemiology
Respiratory Burst
Skin Tests
Abstract
We examined the responses of primed polymorphonuclear neutrophils (PMNs) adhered to vascular endothelium, which can lead to endothelial cell damage as a mechanism of the capillary leak syndrome, the main cause of death in anergic patients. We tested PMNs from (1) preoperative reactive patients, (2) preoperative anergic patients, (3) anergic patients in the surgical intensive care unit, and (4) healthy controls for in vitro adherence and cytotoxicity on cultured human vein endothelial cells. Adherence of PMNs was 12.9% +/- 3.9% in preoperative anergic patients and 13.1% +/- 3.2% in anergic patients in the surgical intensive care unit compared with 9.0% +/- 2.1% in preoperative reactive patients (P
PubMed ID
8418783 View in PubMed
Less detail

Role of eosinophils and cell adhesion molecules in the allergen-induced asthmatic response of rats.

https://arctichealth.org/en/permalink/ahliterature15898
Source
Res Commun Mol Pathol Pharmacol. 1995 Oct;90(1):3-15
Publication Type
Article
Date
Oct-1995
Author
O. Uyama
D. Ihaku
O. Kitada
M. Miyasaka
M. Sugita
Author Affiliation
Division of Pathobiology, College of Nursing Art and Science Hyogo, Akashi, Japan.
Source
Res Commun Mol Pathol Pharmacol. 1995 Oct;90(1):3-15
Date
Oct-1995
Language
English
Publication Type
Article
Keywords
Aerosols
Airway Resistance - drug effects - physiology
Allergens - immunology
Animals
Antibodies, Monoclonal - diagnostic use
Antigens, CD18 - immunology
Asthma - chemically induced - immunology
Cell Adhesion Molecules - immunology - physiology
Eosinophils - immunology
Immunohistochemistry
Male
Ovalbumin - administration & dosage - immunology
Rats
Rats, Inbred BN
Up-Regulation
Abstract
To evaluate the airway infiltration of eosinophils in the asthmatic responses of Brown-Norway rats, which were sensitized with ovalbumin, the time course of eosinophil infiltration and respiratory resistance (Rrs) after ovalbumin challenge was measured. The effect of treatment with monoclonal antibody against ICAM-1 and CD18 was studied. Finally, the expression of ICAM-1 and CD18 in the airway was investigated. All rats showed Rrs increase 6-7 hours after ovalbumin challenge, indicating a late asthmatic response (LAR). Animals with LAR had higher eosinophil counts than those with an immediate asthmatic response (IAR) and in the sensitized but nonchallenged animals. Rats treated with the antibodies showed significantly smaller increases in Rrs and lower eosinophil counts than the control animals. Immunohistochemical staining in airway was performed. ICAM-1 immunoreactivity was positive on both the epithelium and the vascular endothelium of a trachea section, and on the pulmonary vascular endothelium. ICAM-1 expression was upregulated after challenge. The number of CD18-positive cells in sections of trachea and lung increased after challenge. Our results show that eosinophil infiltration is important in LAR development and the treatment with antagonists of ICAM-1 and CD18 may provide a therapeutic approach to reducing asthmatic symptoms.
PubMed ID
8581346 View in PubMed
Less detail