Document Detail


Oxytetracycline attenuates allergic airway inflammation in mice via inhibition of the NF-κB pathway.
MedLine Citation:
PMID:  21136283     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oxytetracycline has been used in the treatment of acute and chronic bronchial inflammation and infectious asthma. However, its potential use for non-infectious asthma has not yet been studied. The objective of this study was to investigate the anti-inflammatory properties of oxytetracycline using a mouse asthma model. Female BALB/c mice, sensitized and challenged with ovalbumin. Naive CD4+ T cells from spleen were stimulated for 72 h with anti-CD3 (5 μg/ml) plus anti-CD28 (2.5 μg/ml) and differentiated into Th2 cells. IL-4, IL-5, IL-9, IL-13, and ovalbumin (OVA)-specific IgE production were measured by ELISA in BALF and cell supernatants. Histopathological evaluation was used to study the alterations in lung tissue. The mRNA levels of CCL5, CCL11, CCR1, and CCR3 were detected by real-time PCR. In addition, the protein levels of p-Akt, Akt, nuclear factor kappa B (NF-κB), IκBα and p-IκBα in lung tissue and cells were measured by western blot or immunofluorescence analysis. Oxytetracycline treatment caused a marked reduction in IL-4, IL-5, IL-13, immune cells, and the level of ovalbumin-specific IgE. Real-time PCR studies demonstrated that oxytetracycline can significantly reduce CCL5, CCL11 and their specific receptor CCR1 and CCR3. Histological studies demonstrated that oxytetracycline substantially inhibited ovalbumin-induced inflammatory cell infiltration in lung tissue and goblet cell hyperplasia in airway. Oxytetracycline inhibited the NF-κB activation via phosphorylation and degradation of IκBα both in vivo and in vitro. Furthermore, the increased phosphorylated Akt but not Akt protein levels in lung tissues after OVA inhalation were significantly reduced by the oral administration of oxytetracycline. These findings demonstrate an anti-inflammatory effect of oxytetracycline that might be mediated via reduction of inflammatory mediators and activation of transcription factors.
Authors:
Xinxin Ci; Xiao Chu; Chi Chen; Xiangchao Li; Shuhan Yan; Xinrui Wang; Yongjun Yang; Xuming Deng
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-12-07
Journal Detail:
Title:  Journal of clinical immunology     Volume:  31     ISSN:  1573-2592     ISO Abbreviation:  J. Clin. Immunol.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-06-01     Completed Date:  2011-09-28     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  8102137     Medline TA:  J Clin Immunol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  216-27     Citation Subset:  IM    
Affiliation:
Institute of Zoonoses, College of Animal Science and Veterinary Medicine, Jilin University, Changchun, Jilin 130062, People's Republic of China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anti-Asthmatic Agents / pharmacology*
Asthma / immunology*
Cytokines / immunology
Disease Models, Animal
Enzyme Activation / drug effects
Female
Gene Expression Regulation / drug effects,  immunology
I-kappa B Proteins / immunology
Immunoglobulin E / blood
Inflammation / immunology
Mice
Mice, Inbred BALB C
NF-kappa B / immunology*
Ovalbumin / immunology
Oxytetracycline / pharmacology*
Phosphorylation / drug effects
Protein-Serine-Threonine Kinases / immunology*
Proto-Oncogene Proteins c-akt / immunology
Respiratory System / drug effects*,  pathology
Signal Transduction / drug effects*
Chemical
Reg. No./Substance:
0/Anti-Asthmatic Agents; 0/Cytokines; 0/I-kappa B Proteins; 0/NF-kappa B; 37341-29-0/Immunoglobulin E; 79-57-2/Oxytetracycline; 9006-59-1/Ovalbumin; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.25/NF-kappa B kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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