Neutrophil accumulation within tissues: A damage x healing dichotomy

Oliveira-Costa, Karen Marques; Menezes, Gustavo B.; Neto, Heitor A. Paula

doi:10.1016/j.biopha.2021.112422

Cited by 12 publications

(21 citation statements)

References 105 publications

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“…[26][27][28] These observations support the concept that the innate immune system has developed to not only protect the host from infection or damaging insult, but also to confine this response and resolve it as soon as possible and thereby avoid collateral host tissue damage. [26][27][28] The circulating pool of PMNs is freely able to move through tissues in their role as sentinels, and it has been estimated that PMNs migrating into tissues under homeostatic conditions may reside there for 2-3 days before they undergo apoptosis and are removed by the reticuloendothelial system. 29 Although apoptosis and clearance of apoptotic cells was proposed by Kerr et al, the removal process for neutrophils was characterized by Newman et al, 30,31 who demonstrated that aged or senescent neutrophils are ingested by inflammatory macrophages.…”

Section: Apoptosis and Turnoversupporting

confidence: 62%

Microbes and the fate of neutrophils

Kobayashi

DeLeo

Quinn

2022

Immunological Reviews

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Summary 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.

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Section: Apoptosis and Turnoversupporting

confidence: 62%

Microbes and the fate of neutrophils

Kobayashi

DeLeo

Quinn

2022

Immunological Reviews

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“…Neutrophils are the first cells to be recruited to injured human or mouse skin, and are critical for preventing microbe invasion after epidermal barrier disruption. 8 However, uncontrolled inflammation triggered by neutrophils impairs the wound healing process. 9 In response to infection and injury, neutrophils form neutrophil extracellular traps (NETs), consisting of a network of extruding nuclear material, lined with cytotoxic proteins such as myeloperoxidase (MPO) and citrullinated histone 3.…”

Section: Introductionmentioning

confidence: 99%

“…Neutrophils are the first cells to be recruited to injured human or mouse skin, and are critical for preventing microbe invasion after epidermal barrier disruption 8 . However, uncontrolled inflammation triggered by neutrophils impairs the wound healing process 9 .…”

Section: Introductionmentioning

confidence: 99%

Neutrophils and their extracellular traps impair ablative fractional carbon dioxide laser‐induced dermal remolding in mice

et al. 2022

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Objectives: Ablative fractional CO 2 laser (AFL) therapy is an effective intervention to induce dermal remodeling. AFL treatment of the skin triggers the recruitment of immune cells, with neutrophils dominating the early phase. However, the role of recruited neutrophils in AFL-induced microinjuries and their subsequent dermal remodeling capacity remains elusive. Materials and Methods: A mouse model of AFL-induced dermal remodeling was established. RNA sequencing was used to identify the prominent features of AFL-treated tissues. Histological analysis, including H&E and Masson staining, ultrastructure observation by transmission microscopy, immunofluorescence, and quantitative real-time polymerase chain reaction were used for dermal remodeling analysis. Moreover, AFL-treated mice were intraperitoneally injected with antimouse Ly6G antibodies to deplete neutrophils. Neutrophil extracellular traps (NETs) were explored using immunofluorescence, transmission microscopy, and in vitro coculture experiments. Results: Dermal remodeling, characterized by an increased number of CD31-positve vessels and elevated messenger RNA (mRNA) expression of genes encoding transforming growth factor-β (TGF-β), collagen I, and collagen III, was observed at 15 days after AFL treatment. In the AFL-induced inflammation phase, RNA sequencing identified neutrophil chemotaxis, and degranulation genes were significantly enriched. Histology and immunofluorescence staining of human and mouse tissues harvested at Day 1 after AFL treatment revealed significant neutrophil infiltration surrounding thermal-induced microinjuries. Neutrophil depletion decreased the expression of stressrelated genes such as S100A8 and S100A9 in the early phase following AFL treatment. Importantly, neutrophil depletion enhanced dermal remodeling at Day 15, as reflected by enrichment of the extracellular matrix and collagen biosynthesis genes based on RNA sequencing. Moreover, increased collagen I, collagen III, and TGF-β mRNA expression, increased cell proliferation, and vascularity were observed. Interestingly, NETs, which could be induced by AFL-treated fibroblasts in vitro, were identified in both human and mouse tissues on Day 1 after AFL treatment. Conclusions: AFL-treated human and mouse skin recruited a large number of neutrophils. The neutrophil surge impaired dermal remodeling in mice. The microenvironment and fibroblast functional modulation mediated by neutrophil degranulation and NET formation were determined to be the underlying mechanisms. Our results indicate that modification of infiltrated neutrophil activity might be a potential therapeutic target for AFL-induced dermal remodeling.

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“…The exact role of neutrophils in the dynamics of immune cell infiltration in stroke is under ongoing research. 14,15 We aimed to measure the percentage of neutrophils showing spontaneous oxidative burst in patients with acute ischemic stroke (samples collected at baseline and on day 3 of stroke) in comparison to age and gender matched controls, and to determine the incidence and severity of infection, as well as the length of hospital stay in patients with stroke.…”

Section: Discussionmentioning

confidence: 99%

Neutrophil Respiratory Burst: an immunological indicator of post stroke infection

Okba

Farres

Shahin

et al. 2022

EJI

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Stroke is long known to be followed by a series of immunosuppressive events, and infections might be a cause of death after an acute insult of stroke. The aim of our work was to assess the percentage of neutrophils showing spontaneous oxidative burst in patients with acute ischemic stroke. The study included 30 patients with acute cerebral infarction subjected to the following: magnetic resonance imaging of the brain immediately on admission, and blood sampling on day one of admission (baseline) and after 3 days of admission. Blood samples were used for the assessment of: differential leucocyte count and percentage of neutrophils showing spontaneous oxidative burst, performed by flow cytometry. Thirty age and gender matched controls were also recruited. Neutrophil respiratory burst percentage was significantly lower in stroke patients in comparison to controls (P<0.001), and stroke patients had significantly lower neutrophil respiratory burst percent on day 3 of admission compared to the baseline (P<0.001). Stroke-induced immune alterations including impairment of the first-line defense performed by neutrophils against bacteria. The hypothesis that these changes enhance susceptibility to acquired infections is supported by our observation that oxidative burst in neutrophils was more impaired in patients with stroke who exhibited subsequent stroke-associated infections.

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Neutrophil accumulation within tissues: A damage x healing dichotomy

Cited by 12 publications

References 105 publications

Microbes and the fate of neutrophils

Microbes and the fate of neutrophils

Neutrophils and their extracellular traps impair ablative fractional carbon dioxide laser‐induced dermal remolding in mice

Neutrophil Respiratory Burst: an immunological indicator of post stroke infection

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