ijms-logo

Journal Browser

Journal Browser

Special Issue "Mechanisms Involved in Granuloma and Fibrosis Resolution: Spontaneous or Mediated"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 30 November 2021.

Special Issue Editor

Dr. Anagha Malur
E-Mail Website
Guest Editor
The Brody School of Medicine, Department of Internal Medicine, Div. of Pulmonary, Critical Care and Sleep Medicine, Greenville, SC, USA
Interests: sarcoid; asthma and pulmonary; hypertension

Special Issue Information

Dear Colleagues,

The recent literature on granuloma formation and fibrosis has evolved and indicated they can be mediated by environmental factors and triggers. The long-term analysis of mediators involving their resolution of granuloma and fibrosis represents a poorly addressed area. Multiple immune cells are shown to be involved in regulating the development of granuloma formation and fibrosis, such as macrophages, lymphocytes, neutrophils, and some subtypes of these cells. The actual role of these cells in granulomas are not clear. In addition, a large number of cytokines and chemokines play an important role in the progression from recurrent inflammation to fibrosis. However, the network of those immune cells and cytokines is remains underinvestigated.

For this Special Issue, we welcome submissions on mechanisms that could possibly be involved in resolution, including the molecular basis of the interaction of the innate and adaptive immune responses. Animal studies, in vitro studies, and clinical studies addressing this resolution will help in delineating pathways which could lead to potential studies toward clinical trials.

Dr. Anagha Malur
Guest Editor

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 papers will be 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • granuloma
  • fibrosis
  • inflammation
  • immune regulation

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Article
The M2a Macrophage Phenotype Accompanies Pulmonary Granuloma Resolution in Mmp12 Knock-Out Mice Instilled with Multiwall Carbon Nanotubes
Int. J. Mol. Sci. 2021, 22(20), 11019; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222011019 - 13 Oct 2021
Viewed by 191
Abstract
Sarcoidosis is a chronic disease with unknown etiology and pathophysiology, characterized by granuloma formation. Matrix Metalloproteinase-12 (MMP12) is an elastase implicated in active granulomatous sarcoidosis. Previously, we reported that oropharyngeal instillation of multiwall carbon nanotubes (MWCNT) into C57Bl/6 mice induced sarcoid-like granulomas and [...] Read more.
Sarcoidosis is a chronic disease with unknown etiology and pathophysiology, characterized by granuloma formation. Matrix Metalloproteinase-12 (MMP12) is an elastase implicated in active granulomatous sarcoidosis. Previously, we reported that oropharyngeal instillation of multiwall carbon nanotubes (MWCNT) into C57Bl/6 mice induced sarcoid-like granulomas and upregulation of MMP12. When Mmp12 knock-out (KO) mice were instilled with MWCNT, granuloma formation occurred 10 days post-instillation but subsequently resolved at 60 days. Thus, we concluded that MMP12 was essential to granuloma persistence. The aim of the current study was to identify potential mechanisms of granuloma resolution in Mmp12KO mice. Strikingly, an M2 macrophage phenotype was present in Mmp12KO but not in C57Bl/6 mice. Between 10 and 60 days, macrophage populations in MWCNT-instilled Mmp12KO mice demonstrated an M2c to M2a phenotypic shift, with elevations in levels of IL-13, an M2 subtype-regulating factor. Furthermore, the M2 inducer, Apolipoprotein E (ApoE), and Matrix Metalloproteinase-14 (MMP14), a promoter of collagen degradation, were upregulated in 60-day MWCNT-instilled Mmp12KO mice. In conclusion, alveolar macrophages express two M2 phenotypes in Mmp12KO mice: M2c at 10 days when granulomas form, and M2a at 60 days when granulomas are resolving. Findings suggest that granuloma resolution in 60-day Mmp12KO mice requires an M2a macrophage phenotype. Full article
Show Figures

Figure 1

Article
Tauroursodeoxycholic Acid Decreases Keloid Formation by Reducing Endoplasmic Reticulum Stress as Implicated in the Pathogenesis of Keloid
Int. J. Mol. Sci. 2021, 22(19), 10765; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910765 - 05 Oct 2021
Viewed by 283
Abstract
Keloids are a common form of pathologic wound healing and are characterized by an excessive production of extracellular matrix. This study examined the major contributing mechanism of human keloid pathogenesis using transcriptomic analysis. We identified the upregulation of mitochondrial oxidative stress response, protein [...] Read more.
Keloids are a common form of pathologic wound healing and are characterized by an excessive production of extracellular matrix. This study examined the major contributing mechanism of human keloid pathogenesis using transcriptomic analysis. We identified the upregulation of mitochondrial oxidative stress response, protein processing in the endoplasmic reticulum, and TGF-β signaling in human keloid tissue samples compared to controls, based on ingenuity pathway and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Electron microscopic examinations revealed an increased number of dysmorphic mitochondria and expanded endoplasmic reticulum (ER) in human keloid tissue samples than that in controls. Western blot analysis performed using human tissues suggested noticeably higher ER stress signaling in keloids than in normal tissues. Treatment with tauroursodeoxycholic acid (TUDCA), an ER stress inhibitor, significantly decreased scar formation in rabbit models, compared to normal saline and steroid injections. In summary, our findings demonstrate the contributions of mitochondrial dysfunction and dysregulated ER stress signaling in human keloid formation and the potential of TUDCA in the treatment of keloids. Full article
Show Figures

Figure 1

Back to TopTop