Macrophages in Human Diseases: From Pathophysiology to Therapeutic Targets

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 3137

Special Issue Editors

Department of Immuno-Oncology, Beckman Research Institute, City of Hope National Medical Center, Duarte, CA 91010, USA
Interests: cancer immunotherapy; tumor associated macrophages; phagocytosis checkpoint; breast cancer; non-hodgkin lymphoma

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Guest Editor
State Key Laboratory of Natural Medicines, School of traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China
Interests: inflammation; hypertension; diabetes; vascular injury; cardiomyopathy, macrophages

Special Issue Information

Dear Colleagues,

As an essential component of innate immune system, macrophages are recognized as a central player in regulating immune responses. They are professional phagocytes, engulfing and digesting foreign substances, damaged cells, and even tumor cells. They are constructors, responsible for wound healing and tissue remodeling. They are also professional antigen presenting cells, together with their role in initiation of inflammation, bridging innate and adaptive immunity. Therefore, it is not surprising that macrophage dysfunction are involved in a plethora of human diseases. There has been explosive growth in macrophage-targeted therapy worldwide during the past decade, showing the great potential of macrophages as a therapeutic target. However, special attention on limiting any possible adverse effect should also be paid due to their broad presence and regulatory effects in nearly every tissue of human body.

This Special Issue is focused on recent advances in the molecular mechanisms of macrophage dysfunction-related diseases, including but not limited to cancers, tumor cell immune escape, cardiovascular disorders, metabolic diseases, neurological diseases, arthritis, inflammatory bowel disease, transplant rejection, and drug-induced diseases, from pathophysiology to therapeutic targets. We invite authors to submit original research articles or review articles relating to the topic.

Dr. Xu Cao
Dr. Hai-Jian Sun
Guest Editors

Manuscript Submission Information

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Keywords

  • macrophages
  • microglia
  • inflammatory diseases
  • innate immunity
  • cancer
  • metabolic diseases
  • immune disorders

Published Papers (1 paper)

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Research

14 pages, 2899 KiB  
Article
Helixor-M Suppresses Immunostimulatory Activity through TLR4-Dependent NF-κB Pathway in RAW 264.7 Cells
by Doil Park, Hyun Min Ko, Wona Jee, So Mi Park, Ye Rin Park, Ji Hoon Jung, Hyung Suk Kim, Won Seok Chung, Sang Ki Kim, Jong Sup Chung and Hyeung Jin Jang
Life 2023, 13(2), 595; https://doi.org/10.3390/life13020595 - 20 Feb 2023
Viewed by 2579
Abstract
Inflammation causes a protective immune response, which can be observed by examining the inflammatory responses of macrophages. Macrophages release various immunostimulatory factors when destroying external pathogens. We induced lipopolysaccharides (LPS) in RAW 264.7 cells, a macrophage cell line, to determine whether Helixor-M can [...] Read more.
Inflammation causes a protective immune response, which can be observed by examining the inflammatory responses of macrophages. Macrophages release various immunostimulatory factors when destroying external pathogens. We induced lipopolysaccharides (LPS) in RAW 264.7 cells, a macrophage cell line, to determine whether Helixor-M can cause immuno-suppression. Helixor-M is known to have anticancer and immune effects. However, an indicator that regulates immunity has not been clearly confirmed. To this end, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was conducted to confirm Helixor-M was not cytotoxic. Western blotting and real-time polymerase chain reaction (RT-PCR) confirmed the anti-inflammatory effects. Additionally, immunofluorescence assay confirmed the translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65, a representative inflammatory pathway. Helixor-M was found to be non-cytotoxic, induce the NF-κB pathway, and reduce the levels of pro-inflammatory cytokine and mitogen-activated protein kinase (MAPK). We found Helixor-M affected the PI3K/AKT/JNK pathway. Therefore, we confirmed Helixor-M acts as an anti-inflammatory agent through NF-κB, TLR4 and PI3K inhibition and that it could be an effective immunosuppressive drug. Full article
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