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Microbes and the fate of neutrophils
Scott D Kobayashi1, Frank R DeLeo1, Mark T Quinn2
1Laboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA.
Abstract:
Neutrophils or polymorphonuclear neutrophils (PMNs) are an important component of innate host defense. These phagocytic leukocytes are recruited to infected tissues and kill invading microbes. There are several general characteristics of neutrophils that make them highly effective as antimicrobial cells. First, there is tremendous daily production and turnover of granulocytes in healthy adults-typically 1011 per day. The vast majority (~95%) of these cells are neutrophils. In addition, neutrophils are mobilized rapidly in response to chemotactic factors and are among the first leukocytes recruited to infected tissues. Most notably, neutrophils contain and/or produce an abundance of antimicrobial molecules. Many of these antimicrobial molecules are toxic to host cells and can destroy host tissues. Thus, neutrophil activation and turnover are highly regulated processes. To that end, aged neutrophils undergo apoptosis constitutively, a process that contains antimicrobial function and proinflammatory capacity. Importantly, apoptosis facilitates nonphlogistic turnover of neutrophils and removal by macrophages. This homeostatic process is altered by interaction with microbes and their products, as well as host proinflammatory molecules. Microbial pathogens can delay neutrophil apoptosis, accelerate apoptosis following phagocytosis, or cause neutrophil cytolysis. Here, we review these processes and provide perspective on recent studies that have potential to impact this paradigm.
Insights
Neutrophils, crucial for innate immunity, are potent antimicrobial cells. Their programmed cell death (apoptosis) is a regulated process vital for controlling inflammation and tissue repair, but can be manipulated by pathogens.
Area of Science:
- Immunology
- Cell Biology
- Microbiology
Background:
- Neutrophils (polymorphonuclear neutrophils, PMNs) are key phagocytic leukocytes in innate host defense, rapidly recruited to infection sites.
- They possess abundant antimicrobial molecules but can also cause host tissue damage, necessitating tight regulation of their activation and turnover.
- Aged neutrophils undergo apoptosis, a process critical for non-inflammatory clearance and maintaining homeostasis, which is influenced by microbial and host factors.
Purpose of the Study:
- To review the mechanisms regulating neutrophil apoptosis and its role in host defense and tissue homeostasis.
- To explore how microbial pathogens and host inflammatory molecules modulate neutrophil apoptosis.
- To provide perspective on recent research impacting the understanding of neutrophil turnover and programmed cell death.
Main Methods:
- Review of existing literature on neutrophil biology, apoptosis, and host-pathogen interactions.
- Analysis of studies investigating the modulation of neutrophil apoptosis by microbial products and inflammatory mediators.
- Synthesis of current knowledge on the physiological and pathological implications of altered neutrophil apoptosis.
Main Results:
- Neutrophil apoptosis is a tightly regulated process essential for limiting inflammation and facilitating efficient clearance by macrophages.
- Microbial pathogens can significantly alter neutrophil apoptosis kinetics, either delaying it to prolong antimicrobial activity or accelerating it post-phagocytosis.
- Host-derived inflammatory molecules also play a role in modulating neutrophil apoptosis, impacting the overall immune response.
Conclusions:
- Understanding the regulation of neutrophil apoptosis is crucial for comprehending innate immunity and developing therapeutic strategies.
- Pathogen-induced manipulation of neutrophil apoptosis represents a significant virulence mechanism.
- Further research into these processes holds potential for novel interventions in infectious and inflammatory diseases.
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