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8.3
5.5
Journals
Biomolecules
Special Issues
The Role of Chemokines in Inflammatory Pathologies
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The Role of Chemokines in Inflammatory Pathologies

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (1 April 2018) | Viewed by 3912

Special Issue Editors

Dr. Christina Bursill

E-Mail Website
Guest Editor
South Australian Health and Medical Research Institute, and Department of Health and Medical Sciences—The University of Adelaide, Adelaide, SA, Australia
Interests: chemokine biology; atherosclerosis; angiogenesis; lipoproteins
Dr. Joanne Tan

E-Mail Website
Guest Editor
Sydney Medical School, The University of Sydney, Sydney, NSW, Australia
Interests: virology; molecular biology; immunology; blood transfusion

Special Issue Information

Dear Colleagues, 

Chemokines play diverse and complex roles in a host of different inflammatory diseases, including wound repair, cancer, retinopathy, atherosclerosis, multiple sclerosis, inflammatory bowel disease, and allergy. The primary role of chemokines is to direct the migration of cells to sites of inflammation or injury in order to clear pathogens or unwanted modified lipids or proteins. Dysregulation of this process can, however, exacerbate disease. This has led to a host of different strategies designed to block chemokine activity. There are approximately 50 chemokines to date and whilst it was initially thought that there was a large amount of redundancy in chemokine signalling, more recent evidence points to more specific roles for each chemokine and chemokine receptor interaction. This therefore highlights the importance of understanding the function of each individual chemokine in more detail so the chemokine-directed therapies can be designed to target disease with great specificity and not incur unwanted off target effects.

We invite scientists focussing on chemokine regulation in inflammatory pathologies to submit their original work or reviews. Both translational and basic research papers are welcome.

Dr. Christina Bursill
Dr. Joanne Tan
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • chemokines
  • inflammatory disease
  • chemokine inhibitors

Published Papers (1 paper)

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Research

13 pages, 394 KiB  
Article
The Role of Specific Chemokines in the Amelioration of Colitis by Appendicitis and Appendectomy
by Rajkumar Cheluvappa, Dennis G. Thomas and Selwyn Selvendran
Biomolecules 2018, 8(3), 59; https://doi.org/10.3390/biom8030059 - 20 Jul 2018
Cited by 8 | Viewed by 3620
Abstract
The appendix contains abundant lymphoid tissue and is constantly exposed to gut flora. When completed at a young age, appendicitis followed by appendectomy (AA) prevents or significantly ameliorates Inflammatory Bowel Diseases (IBDs) in later life. Inflammatory bowel disease comprises Crohn’s disease and ulcerative [...] Read more.
The appendix contains abundant lymphoid tissue and is constantly exposed to gut flora. When completed at a young age, appendicitis followed by appendectomy (AA) prevents or significantly ameliorates Inflammatory Bowel Diseases (IBDs) in later life. Inflammatory bowel disease comprises Crohn’s disease and ulcerative colitis. Our murine AA model is the only existing experimental model of AA. In our unique model, AA performed in the most proximal colon limits colitis pathology in the most distal colon by curbing T-helper 17 cell activity, diminishing autophagy, modulating interferon activity-associated molecules, and suppressing endothelin vaso-activity-mediated immunopathology. In the research presented in this paper, we have examined the role of chemokines in colitis pathology with our murine AA model. Chemokines are a family of small cytokines with four conserved cysteine residues. Chemokines induce chemotaxis in adjacent cells with corresponding receptors. All 40 known chemokine genes and 24 chemokine receptor genes were examined for gene expression levels in distal colons three days post-AA and 28 days post-AA. At 28 days post-AA, the chemokine gene CCL5 was significantly upregulated. Furthermore, Gene Set Enrichment Analysis (GSEA) showed upregulation of seven CCL5-associated gene-sets 28 days post-AA in contrast to just one gene-set downregulated at the same time-point. The chemokine gene CXCL11 was significantly upregulated three days post-AA and 28 days post-AA. Evaluation using GSEA showed upregulation of six CXCL11-associated gene sets but no downregulation of any gene set. At 28 days post-AA, CCL17 gene expression was significantly downregulated. There was no expression of any chemokine receptor gene three days post-AA, but CCR10 was the only chemokine receptor gene that displayed differential gene expression (upregulation) 28 days post-AA. No CCR10-associated gene set was upregulated in GSEA in contrast to one downregulated gene set. Our analysis resulted in identifying three new therapeutic targets towards ameliorating colitis: CCL5, CXCL11, and CCL17. While CCL5 and CXCL11 are good therapeutic chemokine candidates to be exogenously administered, CCL17 is a good candidate chemokine to competitively inhibit or limit colitis pathology. Full article
(This article belongs to the Special Issue The Role of Chemokines in Inflammatory Pathologies)
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