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Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice.
Acta Pharmacol Sin. 2007 Nov; 28(11):1791-6.AP

Abstract

AIM

To evaluate the effect of C-C chemokine receptor 3 (CCR3) blockade on pulmonary inflammation and mucus production in allergic mice.

METHODS

We used the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigen and generated murine monoclonal antibody against the human CCR3. In addition, the generated antibody was administered to mice sensitized and challenged with ovalbumin. The inflammatory cells in bronchoalveolar lavage, cytokine levels, pulmonary histopathology, and mucus secretion were examined.

RESULTS

The Western blotting analysis indicated that the generated antibody bound to CCR3 specifically. The allergic mice treated with the antihuman CCR3 antibody exhibited a significant reduction of pulmonary inflammation accompanied with the alteration of cytokine.

CONCLUSION

The antibody we generated was specific to CCR3. The inhibition of airway inflammation and mucus overproduction by the antibody suggested that the blockade of CCR3 is an appealing therapeutical target for asthma. The present research may provide an experimental basis for the further study of this agent.

Authors+Show Affiliations

Department of Respiratory Medicine, the Second Affiliated Hospital, Medical School of Zhejiang University, Hangzhou 310009, China. doctorhuxi@163.comNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17959030

Citation

Wang, Kai, et al. "Human C-C Chemokine Receptor 3 Monoclonal Antibody Inhibits Pulmonary Inflammation in Allergic Mice." Acta Pharmacologica Sinica, vol. 28, no. 11, 2007, pp. 1791-6.
Wang K, Shen HH, Li W, et al. Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice. Acta Pharmacol Sin. 2007;28(11):1791-6.
Wang, K., Shen, H. H., Li, W., & Huang, H. Q. (2007). Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice. Acta Pharmacologica Sinica, 28(11), 1791-6.
Wang K, et al. Human C-C Chemokine Receptor 3 Monoclonal Antibody Inhibits Pulmonary Inflammation in Allergic Mice. Acta Pharmacol Sin. 2007;28(11):1791-6. PubMed PMID: 17959030.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Human C-C chemokine receptor 3 monoclonal antibody inhibits pulmonary inflammation in allergic mice. AU - Wang,Kai, AU - Shen,Hua-hao, AU - Li,Wen, AU - Huang,Hua-qiong, PY - 2007/10/26/pubmed PY - 2009/5/13/medline PY - 2007/10/26/entrez SP - 1791 EP - 6 JF - Acta pharmacologica Sinica JO - Acta Pharmacol Sin VL - 28 IS - 11 N2 - AIM: To evaluate the effect of C-C chemokine receptor 3 (CCR3) blockade on pulmonary inflammation and mucus production in allergic mice. METHODS: We used the synthetic peptide of the CCR3 NH2-terminal as the immunizing antigen and generated murine monoclonal antibody against the human CCR3. In addition, the generated antibody was administered to mice sensitized and challenged with ovalbumin. The inflammatory cells in bronchoalveolar lavage, cytokine levels, pulmonary histopathology, and mucus secretion were examined. RESULTS: The Western blotting analysis indicated that the generated antibody bound to CCR3 specifically. The allergic mice treated with the antihuman CCR3 antibody exhibited a significant reduction of pulmonary inflammation accompanied with the alteration of cytokine. CONCLUSION: The antibody we generated was specific to CCR3. The inhibition of airway inflammation and mucus overproduction by the antibody suggested that the blockade of CCR3 is an appealing therapeutical target for asthma. The present research may provide an experimental basis for the further study of this agent. SN - 1671-4083 UR - https://www.unboundmedicine.com/medline/citation/17959030/Human_C_C_chemokine_receptor_3_monoclonal_antibody_inhibits_pulmonary_inflammation_in_allergic_mice_ L2 - https://doi.org/10.1111/j.1745-7254.2007.00635.x DB - PRIME DP - Unbound Medicine ER -