The CKLF1-C19 peptide attenuates allergic lung inflammation by inhibiting CCR3- and CCR4-mediated chemotaxis in a mouse model of asthma

Tian, Linjie; Li, W.; Wang, J.; Zhang, Y.; Zheng, Yi; Qi, Hui; Guo, Xiaohuan; Ma, Dalong; Shen, Huahao; Wang, Y.

doi:10.1111/j.1398-9995.2010.02478.x

Cited by 31 publications

(27 citation statements)

References 38 publications

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“…C19 has weaker chemotactic activity and inhibits chemotaxis induced by CKLF1 or thymus and activation-regulated chemokine (CCL17) [29]. C19 can be used to treat asthma as a CKLF1 antagonist [30]. Previously, we have shown that treatment with C19 decreased the infarct size and water content [14].…”

Section: Discussionmentioning

confidence: 99%

Neutralization of chemokine-like factor 1, a novel C-C chemokine, protects against focal cerebral ischemia by inhibiting neutrophil infiltration via MAPK pathways in rats

Kong

Wang²,

Han

et al. 2014

J Neuroinflammation

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BackgroundInflammation plays a key role in the pathophysiology of ischemic stroke. Some proinflammatory mediators, such as cytokines and chemokines, are produced in stroke. Chemokine-like factor 1 (CKLF1), as a novel C-C chemokine, displays chemotactic activities in a wide spectrum of leukocytes and plays an important role in brain development. In previous studies, we have found that the expression of CKLF1 increased in rats after focal cerebral ischemia and treatment with the CKLF1 antagonist C19 peptide decreased the infarct size and water content. However, the role of CKLF1 in stroke is still unclear. The objective of the present study was to ascertain the possible roles and mechanism of CKLF1 in ischemic brain injury by applying anti-CKLF1 antibody.MethodsMale Sprague–Dawley rats were subjected to one-hour middle cerebral artery occlusion. Antibody to CKLF1 was applied to the right cerebral ventricle immediately after reperfusion; infarct volume and neurological score were measured at 24 and 72 hours after cerebral ischemia. RT-PCR, Western blotting and ELISA were utilized to characterize the expression of adhesion molecules, inflammatory factors and MAPK signal pathways. Immunohistochemical staining and myeloperoxidase activity was used to determine the extent of neutrophil infiltration.ResultsTreatment with anti-CKLF1 antibody significantly decreased neurological score and infarct volume in a dose-dependent manner at 24 and 72 hours after cerebral ischemia. Administration with anti-CKLF1 antibody lowered the level of inflammatory factors TNF-α, IL-1β, MIP-2 and IL-8, the expression of adhesion molecules ICAM-1 and VCAM-1 in a dose-dependent manner. The results of immunohistochemical staining and detection of MPO activity indicated that anti-CKLF1 antibody inhibited neutrophil infiltration. Further studies suggested MAPK pathways associated with neutrophil infiltration in cerebral ischemia.ConclusionsSelective inhibition of CKLF1 activity significantly protects against ischemia/reperfusion injury by decreasing production of inflammatory mediators and expression of adhesion molecules, thereby reducing neutrophils recruitment to the ischemic area, possibly via inhibiting MAPK pathways. Therefore, CKLF1 may be a novel target for the treatment of stroke.

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Section: Discussionmentioning

confidence: 99%

Neutralization of chemokine-like factor 1, a novel C-C chemokine, protects against focal cerebral ischemia by inhibiting neutrophil infiltration via MAPK pathways in rats

Kong

Wang²,

Han

et al. 2014

J Neuroinflammation

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show abstract

“…62 CCR8 is a more specific T H 2-associated receptor but is also expressed on regulatory T cells. 63 Tian et al 64 showed in a murine model of asthma that a human chemokine-like factor 1 C-terminal peptide (C19), which blocks the function of the chemokine receptor CCR4, reduced airway eosinophilia and airway hyperresponsiveness. There are no reports of the antagonists of any of these receptors in asthmatic patients.…”

Section: Antagonists Of Adhesion and Chemokine Pathways Controlling Ementioning

confidence: 99%

Immune response modifiers in the treatment of asthma: A PRACTALL document of the American Academy of Allergy, Asthma & Immunology and the European Academy of Allergy and Clinical Immunology

Ballow

Akdiş

Casale

et al. 2012

Journal of Allergy and Clinical Immunology

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“…The number of eosinophils in the nasal mucosa was counted at a magnification of × 400 within five fields [3]. The severity of peribronchial and perivascular inflammation was scored according to a published guideline [11].…”

Section: Histologic Analysismentioning

confidence: 99%

Alleviation of murine allergic rhinitis by C19, a C-terminal peptide of chemokine-like factor 1 (CKLF1)

Zheng

Guo

Zhang

et al. 2011

International Immunopharmacology

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The CKLF1-C19 peptide attenuates allergic lung inflammation by inhibiting CCR3- and CCR4-mediated chemotaxis in a mouse model of asthma

Cited by 31 publications

References 38 publications

Neutralization of chemokine-like factor 1, a novel C-C chemokine, protects against focal cerebral ischemia by inhibiting neutrophil infiltration via MAPK pathways in rats

Neutralization of chemokine-like factor 1, a novel C-C chemokine, protects against focal cerebral ischemia by inhibiting neutrophil infiltration via MAPK pathways in rats

Immune response modifiers in the treatment of asthma: A PRACTALL document of the American Academy of Allergy, Asthma & Immunology and the European Academy of Allergy and Clinical Immunology

Alleviation of murine allergic rhinitis by C19, a C-terminal peptide of chemokine-like factor 1 (CKLF1)

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