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    Cell-Bound IL-8 Increases in Bronchial Epithelial Cells after Arylsulfatase B Silencing due to Sequestration with Chondroitin-4-Sulfate

    Author
    Bhattacharyya, Sumit; Solakyildirim, Kemal; Zhang, Zhenqing; Chen, Mei Ling; Linhardt, Robert J.; Tobacman, Joanne K.
    ORCID
    https://orcid.org/0000-0003-2219-5833
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    Other Contributors
    Date Issued
    2010-01-01
    Subject
    Biology; Chemistry and chemical biology; Chemical and biological engineering; Biomedical engineering
    Degree
    Terms of Use
    In Copyright : this Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s). https://rightsstatements.org/page/InC/1.0/;
    Full Citation
    Cell-Bound IL-8 Increases in Bronchial Epithelial Cells after Arylsulfatase B Silencing due to Sequestration with Chondroitin-4-Sulfate, S. Bhattacharyya, K. Solakyildirim Z. Zhang, R. J. Linhardt, J. K. Tobacman, American Journal of Respiratory Cell and Molecular Biology, 42, 51-61, 2010.
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    URI
    https://doi.org/10.1165/rcmb.2008-0482OC; https://hdl.handle.net/20.500.13015/5744
    Abstract
    The chemokine IL-8 is critically important in inflammatory processes in human tissues, and IL-8 interactions with sulfated glycosaminoglycans have been implicated in modification of inflammatory responses in bronchial epithelium. To determine the role of chondroitin-4-sulfate (C4S) in mediating effects of IL-8, we silenced the enzyme N-acetylgalactosamine-4-sulfatase (arylsulfatase B [ASB]) that removes the 4-sulfate group from C4S, in the IB3-1 and C38 bronchial epithelial cell lines and in normal primary bronchial epithelial cells. When ASB was silenced and IL-8 production stimulated by exposure to TNF-alpha, ASB activity declined by roughly 75%, cellular C4S content increased by over 7.5 microg/mg protein, cell-bound IL-8 increased by over 530 pg/mg protein, and secreted IL-8 declined by over 520 pg/mg protein in all cell lines (P < 0.001). When cell lysates were immunoprecipitated with C4S antibody after ASB silencing and TNF-alpha, the IL-8 content of the immunoprecipitate was approximately 500 pg/mg protein, indicating that most of the cell-bound IL-8 was associated with C4S. Cell fractionation demonstrated that the IL-8 content associated with the cell membranes was about twice that of the cytosolic fraction. Also, ASB appeared to localize in the cell membrane, as well as in lysosomes. Neutrophil attraction to the cell lysates increased after ASB silencing, consistent with increased attraction to the cell-bound IL-8. These findings provide evidence for the influential role of ASB and C4S in the regulation of IL-8 secretion, and suggest that changes in ASB activity and C4S content may have a significant impact on IL-8-mediated inflammatory responses.;
    Description
    American Journal of Respiratory Cell and Molecular Biology, 42, 51-61; Note : if this item contains full text it may be a preprint, author manuscript, or a Gold OA copy that permits redistribution with a license such as CC BY. The final version is available through the publisher’s platform.
    Department
    The Linhardt Research Labs.; The Shirley Ann Jackson, Ph.D. Center for Biotechnology and Interdisciplinary Studies (CBIS);
    Relationships
    The Linhardt Research Labs Online Collection; Rensselaer Polytechnic Institute, Troy, NY; American Journal of Respiratory Cell and Molecular Biology; https://harc.rpi.edu/;
    Access
    https://login.libproxy.rpi.edu/login?url=https://doi.org/10.1165/rcmb.2008-0482OC;
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