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IL-13 is a potent stimulator of inflammation and tissue remodeling that plays a key role in the pathogenesis of a wide variety of human disorders. To further understand these responses, studies were undertaken to define the role(s) of the chemokine C10/CCL6 in the pathogenesis of IL-13-induced alterations in the murine lung. IL-13 was a very potent stimulator of C10/CCL6 mRNA and protein, and IL-13-induced inflammation, alveolar remodeling, and compliance alterations were markedly ameliorated after C10/CCL6 neutralization. Treatment with anti-C10/CCL6 decreased the levels of mRNA encoding matrix metalloproteinase-2 (MMP-2), MMP-9, and tissue inhibitor of metalloproteinase-4 (TIMP-4) in lungs from wild-type mice. C10/CCL6 neutralization also decreased the ability of IL-13 to stimulate the production of monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha, MMP-2, MMP-9, and cathepsins-K, -L, and -S and the ability of IL-13 to inhibit alpha1-antitrypsin. In accord with these findings, a targeted null mutation of CCR1, a putative C10/CCL6 receptor, also decreased IL-13-induced inflammation and alveolar remodeling and caused alterations in chemokines, proteases, and antiproteases comparable to those seen after C10/CCL6 neutralization. These C10/CCL6 and CCR1 manipulations did not alter the production of transgenic IL-13. These studies demonstrate that IL-13 is a potent stimulator of C10/CCL6 and highlight the importance of C10/CCL6 and signaling via CCR1 in the pathogenesis of the IL-13-induced pulmonary phenotype. They also describe a C10/CCL6 target gene cascade in which C10/CCL6 induction is required for optimal IL-13 stimulation of selected chemokines (monocyte chemoattractant protein-1 and MIP-1alpha) and proteases (MMP-2, MMP-9, and cathepsins-K, -L, and -S) and the inhibition of alpha1-antitrypsin.
Zhu Z, et al.
J Immunol. 2002 Mar 15;168(6):2953-62. doi: 10.4049/jimmunol.168.6.2953.
J Immunol. 2002.
PMID:
11884467
Chen Q, et al.
J Immunol. 2005 Feb 15;174(4):2305-13. doi: 10.4049/jimmunol.174.4.2305.
J Immunol. 2005.
PMID:
15699166
Ma B, et al.
J Immunol. 2006 Apr 15;176(8):4968-78. doi: 10.4049/jimmunol.176.8.4968.
J Immunol. 2006.
PMID:
16585593
Lee CG, et al.
Proc Am Thorac Soc. 2006 Jul;3(5):418-23. doi: 10.1513/pats.200602-017AW.
Proc Am Thorac Soc. 2006.
PMID:
16799085
Free PMC article.
Review.
Saeki T, et al.
Curr Pharm Des. 2003;9(15):1201-8. doi: 10.2174/1381612033454937.
Curr Pharm Des. 2003.
PMID:
12769747
Review.
Muthumalage T, et al.
FASEB Bioadv. 2024 Jan 15;6(2):53-71. doi: 10.1096/fba.2023-00115. eCollection 2024 Feb.
FASEB Bioadv. 2024.
PMID:
38344410
Free PMC article.
Alavi M, et al.
Cancers (Basel). 2023 Nov 15;15(22):5427. doi: 10.3390/cancers15225427.
Cancers (Basel). 2023.
PMID:
38001687
Free PMC article.
Lee H, et al.
J Microbiol. 2023 May;61(5):579-587. doi: 10.1007/s12275-023-00047-3. Epub 2023 May 26.
J Microbiol. 2023.
PMID:
37233907
Free PMC article.
Dragan P, et al.
Pharmaceutics. 2023 Feb 3;15(2):516. doi: 10.3390/pharmaceutics15020516.
Pharmaceutics. 2023.
PMID:
36839838
Free PMC article.
Klein Y, et al.
Front Immunol. 2022 Oct 7;13:928132. doi: 10.3389/fimmu.2022.928132. eCollection 2022.
Front Immunol. 2022.
PMID:
36275768
Free PMC article.
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