About this Research Topic
Background
Cells' activity shapes the inter-cellular milieu and immediate cellular environment. When physiological stress or pathogenic stimuli damage cells, they shift to a new steady state to survive. Cell damage can cause adaptation or death. Regulatory processes like receptor binding, signal transduction, and protein synthesis can trigger or control injury-induced cell changes. Atrophy, hypertrophy, hyperplasia, and metaplasia are the most common visibly evident adaptive modifications. These injured cells may store fat, cholesterol, protein, glycogen, or pigment. When cells die irreversibly, necrosis or apoptosis may occur, causing nuclear modifications like pyknosis, karyorrhexis, and karyolysis. In conclusion, microbial infection induces systemic inflammation, which affects several biological functions. Acute and chronic diseases can result from pathogen-induced systemic inflammation. It can damage the kidneys, liver, heart, lungs, and brain and has high-risk consequences. Microbial-induced cellular damage and systemic inflammation include several cell types. By causing apoptosis, pyroptosis, and necrosis, pro-inflammatory cytokines harm many immune cells.
Goal
The precise mechanism by which microbial infection leads to cellular adaptation or death is still not well understood. The ongoing research will investigate the relationship between the host and pathogen, specifically examining the pharmacological mechanism that limits the growth of microbial pathogens. Cellular homeostasis gaps can still exist even with the use of medications, antibodies, and other therapies. Our objective is to discover host-directed treatments (HDTs) that promote equilibrium between cell death and cellular adaptation in response to cell or tissue injury, with the goal of restoring the body's defense mechanisms. We will utilize state-of-the-art technologies such as advanced sequencing methods, multicolor flow cytometric assays, advanced imaging approaches, and pathological studies to enhance our comprehension of host-directed immunotherapies and the intricacies of cellular homeostasis during microbial infection.
Scope
We encourage the submission of original research, methodologies, reviews, mini-reviews, and graphical commentaries that contribute to our knowledge of microbial infection signals, processes, and their associated pathological consequences, such as cell/tissue injury/death and adaptation. This research theme covers a broad spectrum of subjects.
- The molecular mechanism behind cell damage, death, or adaptation.
- Immunological quincunxes
- The mechanisms that govern the interactions between a host and a pathogen.
- Novel therapeutic techniques
- A computational model for elucidating the inherent mechanisms of cell death, damage, or adaptation.
We strongly invite authors to provide innovative perspectives in these various fields, promoting a thorough comprehension of cell damage and death and cellular responses to microbial infection.
Cells' activity shapes the inter-cellular milieu and immediate cellular environment. When physiological stress or pathogenic stimuli damage cells, they shift to a new steady state to survive. Cell damage can cause adaptation or death. Regulatory processes like receptor binding, signal transduction, and protein synthesis can trigger or control injury-induced cell changes. Atrophy, hypertrophy, hyperplasia, and metaplasia are the most common visibly evident adaptive modifications. These injured cells may store fat, cholesterol, protein, glycogen, or pigment. When cells die irreversibly, necrosis or apoptosis may occur, causing nuclear modifications like pyknosis, karyorrhexis, and karyolysis. In conclusion, microbial infection induces systemic inflammation, which affects several biological functions. Acute and chronic diseases can result from pathogen-induced systemic inflammation. It can damage the kidneys, liver, heart, lungs, and brain and has high-risk consequences. Microbial-induced cellular damage and systemic inflammation include several cell types. By causing apoptosis, pyroptosis, and necrosis, pro-inflammatory cytokines harm many immune cells.
Goal
The precise mechanism by which microbial infection leads to cellular adaptation or death is still not well understood. The ongoing research will investigate the relationship between the host and pathogen, specifically examining the pharmacological mechanism that limits the growth of microbial pathogens. Cellular homeostasis gaps can still exist even with the use of medications, antibodies, and other therapies. Our objective is to discover host-directed treatments (HDTs) that promote equilibrium between cell death and cellular adaptation in response to cell or tissue injury, with the goal of restoring the body's defense mechanisms. We will utilize state-of-the-art technologies such as advanced sequencing methods, multicolor flow cytometric assays, advanced imaging approaches, and pathological studies to enhance our comprehension of host-directed immunotherapies and the intricacies of cellular homeostasis during microbial infection.
Scope
We encourage the submission of original research, methodologies, reviews, mini-reviews, and graphical commentaries that contribute to our knowledge of microbial infection signals, processes, and their associated pathological consequences, such as cell/tissue injury/death and adaptation. This research theme covers a broad spectrum of subjects.
- The molecular mechanism behind cell damage, death, or adaptation.
- Immunological quincunxes
- The mechanisms that govern the interactions between a host and a pathogen.
- Novel therapeutic techniques
- A computational model for elucidating the inherent mechanisms of cell death, damage, or adaptation.
We strongly invite authors to provide innovative perspectives in these various fields, promoting a thorough comprehension of cell damage and death and cellular responses to microbial infection.
Keywords: Cell-death, necrosis, apoptosis, pyroptosis, cell/tissue injury, immunity
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.
