Research Topic

Macrophage Plasticity in Sterile and Pathogen-Induced Inflammation

About this Research Topic

Macrophages form a heterogeneous group of immune cells that play an instrumental role in the maintenance of homeostasis, body surveillance, and host defense. Owing to remarkable plasticity, macrophages are involved in the initiation, amplification, and termination of immune responses. The localization of macrophages in a variety of tissues and their capacity to respond timely to a plethora of stimuli including danger signals (Pathogen-associated molecular patterns or PAMPs and danger-associated molecular patterns or DAMPs) underscores their importance in the modulation of inflammatory responses.

Several types of pathogens including bacteria, fungi, viruses, protozoa, and helminths can activate macrophages that, based on their polarization status, either boost or dampen inflammation. Additionally, macrophages closely interact with other immune and non-immune cells to orchestrate immune responses, resolve inflammation, and promote tissue repair. Interestingly, some pathogens can bias macrophage polarization to their own benefit, increasing their fitness and spreading. Besides PAMPs, DAMPs released by injured or stressed cells during sterile inflammatory processes contribute to the shaping of macrophage phenotype. Macrophages are major determinants in disease models that are linked to sterile inflammation. Actually, there is particular evidence that the pathogenesis of sterile inflammatory diseases including metabolic and oncologic diseases is affected by macrophage activity. All these observations have generated great interest in deciphering the mechanisms underlying macrophage plasticity, with the aim to identify novel therapeutic targets to curb macrophage polarization towards beneficial effects in a range of pathologies.

This Research Topic aims to focus on processes and mechanisms that orchestrate the versatile function of macrophages and their interaction with other immune or non-immune cell types in response to pathogens and sterile inflammatory insults. We welcome the submission of Original Research, Method, Review, and Perspective articles that cover but are not limited to the following research subtopics:

1. Pathogen-dependent macrophage responses (including microbes, parasites, and viruses)
2. Macrophage reprogramming as a result of sterile inflammatory signals including trauma and metabolic disturbances


Keywords: macrophage plasticity, resolution of inflammation, reprograming, memory, sterile inflammation


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

Macrophages form a heterogeneous group of immune cells that play an instrumental role in the maintenance of homeostasis, body surveillance, and host defense. Owing to remarkable plasticity, macrophages are involved in the initiation, amplification, and termination of immune responses. The localization of macrophages in a variety of tissues and their capacity to respond timely to a plethora of stimuli including danger signals (Pathogen-associated molecular patterns or PAMPs and danger-associated molecular patterns or DAMPs) underscores their importance in the modulation of inflammatory responses.

Several types of pathogens including bacteria, fungi, viruses, protozoa, and helminths can activate macrophages that, based on their polarization status, either boost or dampen inflammation. Additionally, macrophages closely interact with other immune and non-immune cells to orchestrate immune responses, resolve inflammation, and promote tissue repair. Interestingly, some pathogens can bias macrophage polarization to their own benefit, increasing their fitness and spreading. Besides PAMPs, DAMPs released by injured or stressed cells during sterile inflammatory processes contribute to the shaping of macrophage phenotype. Macrophages are major determinants in disease models that are linked to sterile inflammation. Actually, there is particular evidence that the pathogenesis of sterile inflammatory diseases including metabolic and oncologic diseases is affected by macrophage activity. All these observations have generated great interest in deciphering the mechanisms underlying macrophage plasticity, with the aim to identify novel therapeutic targets to curb macrophage polarization towards beneficial effects in a range of pathologies.

This Research Topic aims to focus on processes and mechanisms that orchestrate the versatile function of macrophages and their interaction with other immune or non-immune cell types in response to pathogens and sterile inflammatory insults. We welcome the submission of Original Research, Method, Review, and Perspective articles that cover but are not limited to the following research subtopics:

1. Pathogen-dependent macrophage responses (including microbes, parasites, and viruses)
2. Macrophage reprogramming as a result of sterile inflammatory signals including trauma and metabolic disturbances


Keywords: macrophage plasticity, resolution of inflammation, reprograming, memory, sterile inflammation


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

30 September 2020 Abstract
31 January 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

30 September 2020 Abstract
31 January 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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