Modulation of allergic inflammation in mice deficient in TNF receptors

Autor: Melinda C. Aldrich, Mark W. Moore, Harm HogenEsch, Daniel Tumas, Juergen W. Pfeiffer, Daniel G. Rudmann, Jeffery S. Tepper
Rok vydání: 2000
Předmět:
Pulmonary and Respiratory Medicine
Allergy
Ovalbumin
Physiology
medicine.medical_treatment
Inflammation
Receptors
Tumor Necrosis Factor
Proinflammatory cytokine
Allergic inflammation
Interferon-gamma
Mice
T-Lymphocyte Subsets
Physiology (medical)
Respiratory Hypersensitivity
Animals
Medicine
Receptor
Aerosols
Mice
Knockout
Tumor Necrosis Factor-alpha
business.industry
hemic and immune systems
Pneumonia
Cell Biology
Immunoglobulin E
respiratory system
medicine.disease
Asthma
biological factors
respiratory tract diseases
Mice
Inbred C57BL
Disease Models
Animal
Cytokine
Immunoglobulin G
Immunology
Knockout mouse
Interleukin-2
Tumor necrosis factor alpha
Interleukin-4
Interleukin-5
biological phenomena
cell phenomena
and immunity
medicine.symptom
business
Bronchoalveolar Lavage Fluid
Signal Transduction
Zdroj: American Journal of Physiology-Lung Cellular and Molecular Physiology. 279:L1047-L1057
ISSN: 1522-1504
1040-0605
DOI: 10.1152/ajplung.2000.279.6.l1047
Popis: Tumor necrosis factor-α (TNF) is implicated as an important proinflammatory cytokine in asthma. We evaluated mice deficient in TNF receptor 1 (TNFR1) and TNFR2 [TNFR(−/−) mice] in a murine model of allergic inflammation and found that TNFR(−/−) mice had comparable or accentuated responses compared with wild-type [TNFR(+/+)] mice. The responses were consistent among multiple end points. Airway responsiveness after methacholine challenge and bronchoalveolar lavage (BAL) fluid leukocyte and eosinophil numbers in TNFR(−/−) mice were equivalent or greater than those observed in TNFR(+/+) mice. Likewise, serum and BAL fluid IgE; lung interleukin (IL)-2, IL-4, and IL-5 levels; and lung histological lesion scores were comparable or greater in TNFR(−/−) mice compared with those in TNFR(+/+) mice. TNFR(+/+) mice chronically treated with anti-murine TNF antibody had BAL fluid leukocyte numbers and lung lesion scores comparable to control antibody-treated mice. These results suggest that, by itself, TNF does not have a critical proinflammatory role in the development of allergic inflammation in this mouse model and that the production of other cytokines associated with allergic disease may compensate for the loss of TNF bioactivity in the TNFR(−/−) mouse.
Databáze: OpenAIRE
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