Expanding roles of neutrophils in aging hosts

Tseng, Ching Wen; Liu, George Y.

doi:10.1016/j.coi.2014.03.009

Cited by 65 publications

(58 citation statements)

References 54 publications

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“…Because the effects of age on neutrophil function seem to be multifaceted (i.e., some functions have been reported to be decreased and others might be augmented, which remains a matter of debate [20][21][22]), this aspect needs to be specifically explored further in a dedicated study of age-matched patients and controls. First, because of the difficulty in conducting such functional tests in the clinic, the sample size of our cohort was relatively modest.…”

Section: Discussionmentioning

confidence: 99%

Marked alterations of neutrophil functions during sepsis-induced immunosuppression

Demaret

Venet

Friggeri

et al. 2015

Journal of Leukocyte Biology

157

120

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Severe septic syndromes deeply impair innate and adaptive immunity and are responsible for sepsis-induced immunosuppression. Although neutrophils represent the first line of defense against infection, little is known about their phenotype and functions a few days after sepsis, when the immunosuppressive phase is maximal (i.e., between d 3 and 8). The objective of the present study was to perform, for the first time, a global evaluation of neutrophil alterations in immunosuppressed septic patients (at d 3-4 and d 6-8) using phenotypic and functional studies. In addition, the potential association of these parameters and deleterious outcomes was assessed. Peripheral blood was collected from 43 septic shock patients and compared with that of 23 healthy controls. In the septic patients, our results highlight a markedly altered neutrophil chemotaxis (functional and chemokine receptor expressions), oxidative burst, and lactoferrin content and an increased number of circulating immature granulocytes (i.e., CD10(dim)CD16(dim)). These aspects were associated with an increased risk of death after septic shock. In contrast, phagocytosis and activation capacities were conserved. To conclude, circulating neutrophils present with phenotypic, functional, and morphologic alterations a few days after sepsis onset. These dysfunctions might participate in the deleterious role of sepsis-induced immunosuppression. The present results open new perspectives in the mechanisms favoring nosocomial infections after septic shock. They deserve to be further investigated in a larger clinical study and in animal models recapitulating these alterations.

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Section: Discussionmentioning

confidence: 99%

Marked alterations of neutrophil functions during sepsis-induced immunosuppression

Demaret

Venet

Friggeri

et al. 2015

Journal of Leukocyte Biology

157

120

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“…Neutrophils have a short lifespan and die by apoptosis if unstimulated, but pro-inflammatory stimuli such as lipopolysaccharide (LPS) can increase their lifespan [18, 19]. The number of neutrophils has been shown to be relatively high in the elderly with altered effector functions [20–22]. Changes in innate and adaptive immunity with age contribute to decreased efficiency of responses to new infections, poorer immunity to previously encountered pathogens and the development of chronic, low-grade inflammation and autoimmunity.…”

Section: Age-related Changes In the Immune Systemmentioning

confidence: 99%

Immune senescence, epigenetics and autoimmunity

Ray

Yung

2018

Clinical Immunology

156

110

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Aging of the immune system in humans and animals is characterized by a decline in both adaptive and innate immune responses. Paradoxically, aging is also associated with a state of chronic inflammation ("inflammaging") and an increased likelihood of developing autoimmune diseases. Epigenetic changes in non-dividing and dividing cells, including immune cells, due to environmental factors contribute to the inflammation and autoimmunity that characterize both the state and diseases of aging. Here, we review the epigenetic mechanisms involved in the development of immune senescence and autoimmunity in old age.

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“…An additional factor that may contribute to the reduced antimicrobial activity is the increased susceptibility of neutrophils from older individuals to apoptotic signals . Finally, age‐specific changes appear in the antimicrobial arsenal of neutrophils, rendering them less capable of killing pathogens as well as altering the necessary cross‐talk with other immune cells necessary for the resolution of inflammation . Although mechanisms associated with the age‐associated defects in neutrophil effector function cannot be linked to changes in expression of receptors , because of the age‐associated decrease in cell‐membrane fluidity as a result of increased cholesterol content of the lipid rafts, alterations in receptor engagement have been proposed to contribute to these altered functions .…”

Section: Innate Immune Cell Compartmentmentioning

confidence: 99%

Aging, inflammation, immunity and periodontal disease

Ebersole¹,

Graves²,

González³

et al. 2016

Periodontology 2000

186

184

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The increased prevalence and severity of periodontal disease have long been associated with aging, such that this oral condition affects the majority of the adult population over 50 years of age. Although the immune system is a critical component for maintaining health, aging can be characterized by quantitative and qualitative modifications of the immune system. This process, termed 'immunosenescence', is a progressive modification of the immune system that leads to greater susceptibility to infections, neoplasia and autoimmunity, presumably reflecting the prolonged antigenic stimulation and/or stress responses that occur across the lifespan. Interestingly, the global reduction in the host capability to respond effectively to these challenges is coupled with a progressive increase in the general proinflammatory status, termed 'inflammaging'. Consistent with the definition of immunosenescence, it has been suggested that the cumulative effect of prolonged exposure of the periodontium to microbial challenge is, at least in part, a contributor to the effects of aging on these tissues. Thus, it has also been hypothesized that alterations in the function of resident immune and nonimmune cells of the periodontium contribute to the expression of inflammaging in periodontal disease. Although the majority of aging research has focused on the adaptive immune response, it is becoming increasingly clear that the innate immune compartment is also highly affected by aging. Thus, the phenomenon of immunosenescence and inflammaging, expressed as age-associated changes within the periodontium, needs to be more fully understood in this era of precision and personalized medicine and dentistry.

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Expanding roles of neutrophils in aging hosts

Cited by 65 publications

References 54 publications

Marked alterations of neutrophil functions during sepsis-induced immunosuppression

Marked alterations of neutrophil functions during sepsis-induced immunosuppression

Immune senescence, epigenetics and autoimmunity

Aging, inflammation, immunity and periodontal disease

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