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Granulomatous Inflammation
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Granulomatous Inflammation

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: closed (20 February 2021) | Viewed by 8282

Special Issue Editors

Dr. Sergio Arce

E-Mail Website
Guest Editor
Department of Biomedical Sciences, School of Medicine Greenville, University of South Carolina, Greenville, SC 29605, USA
Interests: autoimmunity; immune biomarkers; sarcoidosis; granulomatous inflammation; cytokine networks; signal transduction; lipid rafts; plasma cell biology; B cells; T cells; immunoglobulins; multiple myeloma; bone marrow microenvironment; vaccines; adjuvants; bacterial enterotoxins; lymphocyte subpopulations; anergy and clonal exhaustion
Dr. Steven E. Fiester

E-Mail Website
Co-Guest Editor
1. Department of Chemistry, Furman University, Greenville, SC 29613, USA
2. Department of Pathology, Prisma Health, School of Health Science Research, Clemson University, Clemson, SC 29634, USA
3. Dorn Research Institute, Wm. Jennings Bryan Dorn VA Medical Center, Columbia, SC 29209, USA
Interests: Acinetobacter; Klebsiella; drug discovery; antimicrobial stewardship; virulence factors; infectious diseases; bacteriology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Advancements within the field of immunology have led to a greater understanding of the human immune response.  These advances have answered many questions about the immune system while still leaving many unanswered.  Specifically, an in-depth understanding of granulomatous inflammation, especially as it pertains to sarcoidosis, Crohn’s disease and common variable immunodeficiency remains wanting.  The lack of understanding of these processes has resulted in treatment options with limited efficacy that target inflammation not underlying fibrosis.   This open-access special issue will bring together original research and review articles related to etiologies of granulomatous inflammation whether, infectious, genetic, environmental, autoimmune or dysbiotic in nature.  This issue will additionally serve as a resource highlighting the latest in novel molecular diagnostics as well as innovative therapeutics particularly those that target macrophages, B cells and/or B and T cell interactions for the treatment of granulomatous inflammation.       

Topics of this special issue include, but are not limited to:

  • Infections leading to granulomatous inflammation especially those in which granulomatous inflammation is poorly described
  • Infectious, genetic, autoimmune, environmental or dysbiotic etiology of sarcoidosis, Crohn’s disease and/or CVID
  • Innovative diagnostics for sarcoidosis, Crohn’s and/or common variable immunodeficiency
  • Therapeutics for the treatment of granulomatous inflammation
  • Therapeutics for the treatment of sarcoidosis, Crohn’s and common variable immunodeficiency specifically those modulating macrophage and lymphocyte responses

Dr. Sergio Arce
Guest Editors
Dr. Steven E. Fiester
Co-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. 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

  • antigen
  • macrophages
  • Th1 cells
  • B cells
  • cytokines
  • granuloma
  • sarcoidal
  • mycobacterial
  • inflammation

Published Papers (2 papers)

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Review

21 pages, 1927 KiB  
Review
Granulomatous Inflammation in ANCA-Associated Vasculitis
by Antje Müller, Bettina Krause, Anja Kerstein-Stähle, Sara Comdühr, Sebastian Klapa, Sebastian Ullrich, Konstanze Holl-Ulrich and Peter Lamprecht
Int. J. Mol. Sci. 2021, 22(12), 6474; https://doi.org/10.3390/ijms22126474 - 17 Jun 2021
Cited by 25 | Viewed by 4839
Abstract
ANCA-associated vasculitis (AAV) comprises granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA). While systemic vasculitis is a hallmark of all AAV, GPA is characterized by extravascular granulomatous inflammation, preferentially affecting the respiratory tract. The mechanisms underlying the emergence [...] Read more.
ANCA-associated vasculitis (AAV) comprises granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA). While systemic vasculitis is a hallmark of all AAV, GPA is characterized by extravascular granulomatous inflammation, preferentially affecting the respiratory tract. The mechanisms underlying the emergence of neutrophilic microabscesses; the appearance of multinucleated giant cells; and subsequent granuloma formation, finally leading to scarred or destroyed tissue in GPA, are still incompletely understood. This review summarizes findings describing the presence and function of molecules and cells contributing to granulomatous inflammation in the respiratory tract and to renal inflammation observed in GPA. In addition, factors affecting or promoting the development of granulomatous inflammation such as microbial infections, the nasal microbiome, and the release of damage-associated molecular patterns (DAMP) are discussed. Further, on the basis of numerous results, we argue that, in situ, various ways of exposure linked with a high number of infiltrating proteinase 3 (PR3)- and myeloperoxidase (MPO)-expressing leukocytes lower the threshold for the presentation of an altered PR3 and possibly also of MPO, provoking the local development of ANCA autoimmune responses, aided by the formation of ectopic lymphoid structures. Although extravascular granulomatous inflammation is unique to GPA, similar molecular and cellular patterns can be found in both the respiratory tract and kidney tissue of GPA and MPA patients; for example, the antimicrobial peptide LL37, CD163+ macrophages, or regulatory T cells. Therefore, we postulate that granulomatous inflammation in GPA or PR3-AAV is intertwined with autoimmune and destructive mechanisms also seen at other sites. Full article
(This article belongs to the Special Issue Granulomatous Inflammation)
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11 pages, 1059 KiB  
Review
Studies in a Murine Granuloma Model of Instilled Carbon Nanotubes: Relevance to Sarcoidosis
by Barbara P. Barna, Anagha Malur and Mary Jane Thomassen
Int. J. Mol. Sci. 2021, 22(7), 3705; https://doi.org/10.3390/ijms22073705 - 02 Apr 2021
Cited by 4 | Viewed by 2673
Abstract
Poorly soluble environmental antigens, including carbon pollutants, are thought to play a role in the incidence of human sarcoidosis, a chronic inflammatory granulomatous disease of unknown causation. Currently, engineered carbon products such as multiwall carbon nanotubes (MWCNT) are manufactured commercially and have been [...] Read more.
Poorly soluble environmental antigens, including carbon pollutants, are thought to play a role in the incidence of human sarcoidosis, a chronic inflammatory granulomatous disease of unknown causation. Currently, engineered carbon products such as multiwall carbon nanotubes (MWCNT) are manufactured commercially and have been shown to elicit acute and chronic inflammatory responses in experimental animals, including the production of granulomas or fibrosis. Several years ago, we hypothesized that constructing an experimental model of chronic granulomatosis resembling that associated with sarcoidosis might be achieved by oropharyngeal instillation of MWCNT into mice. This review summarizes the results of our efforts to define mechanisms of granuloma formation and identify potential therapeutic targets for sarcoidosis. Evidence is presented linking findings from the murine MWCNT granuloma model to sarcoidosis pathophysiology. As our goal was to determine what pulmonary inflammatory pathways might be involved, we utilized mice of knock-out (KO) backgrounds which corresponded to deficiencies noted in sarcoidosis patients. A primary example of this approach was to study mice with a myeloid-specific knock-out of the lipid-regulated transcription factor, peroxisome proliferator-activated receptor gamma (PPARγ) which is strikingly depressed in sarcoidosis. Among the major findings associated with PPARγ KO mice compared to wild-type were: (1) exacerbation of granulomatous and fibrotic histopathology in response to MWCNT; (2) elevation of inflammatory mediators; and (3) pulmonary retention of a potentially antigenic ESAT-6 peptide co-instilled with MWCNT. In line with these data, we also observed that activation of PPARγ in wild-type mice by the PPARγ-specific ligand, rosiglitazone, significantly reduced both pulmonary granuloma and inflammatory mediator production. Similarly, recognition of a deficiency of ATP-binding cassette (ABC) lipid transporter ABCG1 in sarcoidosis led us to study MWCNT instillation in myeloid-specific ABCG1 KO mice. As anticipated, ABCG1 deficiency was associated with larger granulomas and increased levels of inflammatory mediators. Finally, a transcriptional survey of alveolar macrophages from MWCNT-instilled wild-type mice and human sarcoidosis patients revealed several common themes. One of the most prominent mediators identified in both human and mouse transcriptomic analyses was MMP12. Studies with MMP12 KO mice revealed similar acute reactions to those in wild-type but at chronic time points where wild-type maintained granulomatous disease, resolution occurred with MMP12 KO mice suggesting MMP12 is necessary for granuloma progression. In conclusion, these studies suggest that the MWCNT granuloma model has relevance to human sarcoidosis study, particularly with respect to immune-specific pathways. Full article
(This article belongs to the Special Issue Granulomatous Inflammation)
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