Neutrophil immunity of the elderly

Schröder, AC; Rink, Lothar

doi:10.1016/s0047-6374(03)00017-4

Cited by 83 publications

(60 citation statements)

References 62 publications

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“…However, MPO+ neutrophils are significantly reduced in the aged injured striatum at all survival times, in agreement with a previous study reporting diminished neutrophil infiltration in aged rats after intracerebral hemorrhage [37]. Reduced presence of MPO+ neutrophils at sites of neuroinflammation in the aged may be attributed to several factors: A first explanation could be an age decrease in circulating neutrophils [38]; however, it has been shown that the number of bone marrow precursor cells remain unaltered in human aging, and the number of circulating polymorphonuclear cells has been claimed to be either significantly increased in the elderly [39], or remain unchanged with age [40,41].…”

Section: Aged-induced Changes In Neutrophil Densitysupporting

confidence: 91%

Decreased myeloperoxidase expressing cells in the aged rat brain after excitotoxic damage

Campuzano¹,

Castillo-Ruiz²,

Acarín³

et al. 2011

Experimental Gerontology

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Brain aging is associated to several morphological and functional alterations that influence the evolution and outcome of CNS damage. Acute brain injury such as an excitotoxic insult induces initial tissue damage followed by associated inflammation and oxidative stress, partly attributed to neutrophil recruitment and the expression of oxidative enzymes such as myeloperoxidase (MPO), among others. However, to date, very few studies have focused on how age can influence neutrophil infiltration after acute brain damage. Therefore, to evaluate the age-dependent pattern of neutrophil cell infiltration following an excitotoxic injury, intrastriatal injection of Nmethyl-D-aspartate was performed in young and aged male Wistar rats. Animals were sacrificed at different times between 12 hours post-lesion (hpl) to 14 days post-lesion (dpl). Cryostat sections were processed for myeloperoxidase (MPO) immunohistochemistry, and double labeling for either neuronal cells (NeuN), astrocytes (GFAP), perivascular macrophages (ED-2), or microglia/macrophages (tomato lectin histochemistry). Our observations showed that MPO+ cells were observed in the injured striatum from 12 hpl (when maximum values were found) until 7 dpl, when cell density was strongly diminished. However, at all survival times analyzed, the overall density of MPO+ cells was lower in the aged versus the adult injured striatum. MPO+ cells were mainly identified as neutrophils (especially at 12 hpl and 1 dpl), but it should be noted that MPO+ neurons and microglia/macrophages were also found. MPO+ neurons were most commonly observed at 12 hpl and reduced in the aged. MPO+ microglia/macrophages were the main population expressing MPO from 3 dpl, when density was also reduced in aged subjects.These results point to neutrophil infiltration as another important factor contributing to the different response of the adult and aged brain to damage, highlighting the need of using aged animals for the study of acute agerelated brain insults.

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Section: Aged-induced Changes In Neutrophil Densitysupporting

confidence: 91%

Decreased myeloperoxidase expressing cells in the aged rat brain after excitotoxic damage

Campuzano¹,

Castillo-Ruiz²,

Acarín³

et al. 2011

Experimental Gerontology

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“…These changes include reduction in response and modulation in regulatory and immune effector cells leading to changes in expression of various chemokines and cytokines (27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37). Shurin et al (37) investigated the effect of age on 30 different serum biomarkers involved in pro-and anti-inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

Multiplexed measurements of immunomodulator levels in peripheral blood of healthy subjects: Effects of analytical variables based on anticoagulants, age and gender

et al. 2013

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“…For example, the effect of aging on the immune response to traumatic injury has been studied. The inflammatory response becomes radically altered during the process of aging [38][39][40][41]. Indeed, the two processes (inflammation and aging), have prompted some authors to coin the term "inflamm-aging" for this complex process [39].…”

Section: Human Studies Of T/hsmentioning

confidence: 99%

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

Namas¹,

Ghuma²,

Hermus

et al. 2008

Libyan Journal of Medicine

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Abstract; Traumatic injury/hemorrhagic shock (T/HS) elicits an acute inflammatory response that may result in death. Inflammation describes a coordinated series of molecular, cellular, tissue, organ, and systemic responses that drive the pathology of various diseases including T/HS and traumatic brain injury (TBI). Inflammation is a finely tuned, dynamic, highly-regulated process that is not inherently detrimental, but rather required for immune surveillance, optimal post-injury tissue repair, and regeneration. The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP's). DAMPs perpetuate inflammation through the release of pro-inflammatory cytokines, but may also inhibit anti-inflammatory cytokines. Various animal models of T/HS in mice, rats, pigs, dogs, and non-human primates have been utilized in an attempt to move from bench to bedside. Novel approaches, including those from the field of systems biology, may yield therapeutic breakthroughs in T/HS and TBI in the near future.

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Neutrophil immunity of the elderly

Cited by 83 publications

References 62 publications

Decreased myeloperoxidase expressing cells in the aged rat brain after excitotoxic damage

Decreased myeloperoxidase expressing cells in the aged rat brain after excitotoxic damage

Multiplexed measurements of immunomodulator levels in peripheral blood of healthy subjects: Effects of analytical variables based on anticoagulants, age and gender

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

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