Macrophages and Antimicrobial Immune Response

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: 31 January 2025 | Viewed by 2124

Special Issue Editor


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Guest Editor
Department of Biological and Biomedical Sciences, College of Arts and Science, North Carolina Central University, Durham, NC 27707, USA
Interests: macrophages; inflammation; immunity

Special Issue Information

Dear Colleagues,

Macrophage cells play a vital role in the surveillance and detection of potential infectious agents within the innate immune system and provide important links to the adaptive immune response. Indeed, these cells play important sentinel roles within organs as diverse as the skin, gut, lung and brain. Interestingly, macrophage responses to microbial pathogens are tempered depending on the tissue they reside in and the type of insult that is incurred, and they can range from highly pro-inflammatory to distinctly anti-inflammatory. Due to their importance in regulating and coordinating all immunity, a special interest is being taken in current and novel discoveries regarding macrophages and immunity. For this Special Issue, we invite researchers to contribute with either original research (both in vivo and in vitro studies) or review articles focusing on the complex and myriad ways that macrophages provide antimicrobial effects within the body and their relevance for therapeutic intervention.

Dr. Vijay Sivaraman
Guest Editor

Manuscript Submission Information

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Keywords

  • macrophage
  • inflammation
  • inflammasome
  • innate immunity
  • anti-microbial
  • microbicidal
  • polarization
  • MDSC

Published Papers (2 papers)

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Research

14 pages, 2607 KiB  
Article
Lysophosphatidylcholine Acetyltransferase 2 (LPCAT2) Influences the Gene Expression of the Lipopolysaccharide Receptor Complex in Infected RAW264.7 Macrophages, Depending on the E. coli Lipopolysaccharide Serotype
by Victory Ibigo Poloamina, Hanaa Alrammah, Wondwossen Abate, Neil D. Avent, Gyorgy Fejer and Simon K. Jackson
Biology 2024, 13(5), 314; https://doi.org/10.3390/biology13050314 - 1 May 2024
Viewed by 632
Abstract
Escherichia coli (E. coli) is a frequent gram-negative bacterium that causes nosocomial infections, affecting more than 100 million patients annually worldwide. Bacterial lipopolysaccharide (LPS) from E. coli binds to toll-like receptor 4 (TLR4) and its co-receptor’s cluster of differentiation protein 14 [...] Read more.
Escherichia coli (E. coli) is a frequent gram-negative bacterium that causes nosocomial infections, affecting more than 100 million patients annually worldwide. Bacterial lipopolysaccharide (LPS) from E. coli binds to toll-like receptor 4 (TLR4) and its co-receptor’s cluster of differentiation protein 14 (CD14) and myeloid differentiation factor 2 (MD2), collectively known as the LPS receptor complex. LPCAT2 participates in lipid-raft assembly by phospholipid remodelling. Previous research has proven that LPCAT2 co-localises in lipid rafts with TLR4 and regulates macrophage inflammatory response. However, no published evidence exists of the influence of LPCAT2 on the gene expression of the LPS receptor complex induced by smooth or rough bacterial serotypes. We used RAW264.7—a commonly used experimental murine macrophage model—to study the effects of LPCAT2 on the LPS receptor complex by transiently silencing the LPCAT2 gene, infecting the macrophages with either smooth or rough LPS, and quantifying gene expression. LPCAT2 only significantly affected the gene expression of the LPS receptor complex in macrophages infected with smooth LPS. This study provides novel evidence that the influence of LPCAT2 on macrophage inflammatory response to bacterial infection depends on the LPS serotype, and it supports previous evidence that LPCAT2 regulates inflammatory response by modulating protein translocation to lipid rafts. Full article
(This article belongs to the Special Issue Macrophages and Antimicrobial Immune Response)
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11 pages, 1463 KiB  
Article
Prostaglandin E2 Boosts the Hyaluronan-Mediated Increase in Inflammatory Response to Lipopolysaccharide by Enhancing Lyve1 Expression
by Pauline Hog, Silvia Kuntschar, Peter Rappl, Arnaud Huard, Andreas Weigert, Bernhard Brüne and Tobias Schmid
Biology 2023, 12(11), 1441; https://doi.org/10.3390/biology12111441 - 16 Nov 2023
Viewed by 1189
Abstract
Macrophages are a highly versatile and heterogenic group of immune cells, known for their involvement in inflammatory reactions. However, our knowledge about distinct subpopulations of macrophages and their specific contribution to the resolution of inflammation remains incomplete. We have previously shown, in an [...] Read more.
Macrophages are a highly versatile and heterogenic group of immune cells, known for their involvement in inflammatory reactions. However, our knowledge about distinct subpopulations of macrophages and their specific contribution to the resolution of inflammation remains incomplete. We have previously shown, in an in vivo peritonitis model, that inhibition of the synthesis of the pro-inflammatory lipid mediator prostaglandin E2 (PGE2) attenuates efficient resolution of inflammation. PGE2 levels during later stages of the inflammatory process further correlate with expression of the hyaluronan (HA) receptor Lyve1 in peritoneal macrophages. In the present study, we therefore aimed to understand if PGE2 might contribute to the regulation of Lyve1 and how this might impact inflammatory responses. In line with our in vivo findings, PGE2 synergized with dexamethasone to enhance Lyve1 expression in bone marrow-derived macrophages, while expression of the predominant hyaluronan receptor CD44 remained unaltered. PGE2-mediated Lyve1 upregulation was strictly dependent on PGE2 receptor EP2 signaling. While PGE2/dexamethasone-treated macrophages, despite their enhanced Lyve1 expression, did not show inflammatory responses upon stimulation with low (LMW) or high-molecular-weight hyaluronan (HMW)-HA, they were sensitized towards LMW-HA-dependent augmentation of lipopolysaccharide (LPS)-induced inflammatory responses. Thus, Lyve1-expressing macrophages emerged as a subpopulation of macrophages integrating inflammatory stimuli with extracellular matrix-derived signals. Full article
(This article belongs to the Special Issue Macrophages and Antimicrobial Immune Response)
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