Aging Reduces the Expression of Lung CINC and MCP-1 mRNA in a P. aeruginosa Rat Model of Infection

Wen, Jie; Li, Chengmei; Gu, Li; Yin, Shi; Li, Wei; Yang, Rong

doi:10.1007/s10753-014-9813-5

Cited by 11 publications

(13 citation statements)

References 20 publications

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“…Neutrophil migration into the lung was also shown to be impaired in aged mice and rats (e.g. aged 18–24 months) following infectious challenges such as Francisella tularenesis , Pseudomonas aeruginosa, influenza A (Mares, et al 2010; Wen, et al 2014; Chen, et al 2014; Birmingham, et al 2014). This impairment might be attributed to a delay in the kinetics of neutrophil responses.…”

Section: Discussionmentioning

confidence: 99%

Age Impacts Pulmonary Inflammation and Systemic Bone Response to Inhaled Organic Dust Exposure

Poole

Romberger

Wyatt

et al. 2015

Journal of Toxicology and Environmental Health, Part A

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Agricultural workers have high rates of airway and skeletal health disease. Studies recently demonstrated that inhaled agricultural organic dust extract (ODE) induced-airway injury is associated with bone deterioration in an animal model. However, the effect of age in governing these responses to organic dusts is unclear, but might be important in future approaches. Young (7–9 weeks) and older (12–14 months) male C57BL/6 mice received intranasal (i.n.) inhalation exposure to ODE from swine confinement facilities once or daily for 3 weeks. Acute ODE-induced neutrophil influx and cytokine and chemokine (TNF-α, IL-6, CXCL1, CXCL2) airway production was reduced in older compared to young mice. Repetitive ODE treatment, however, increased lymphocyte recruitment and alveolar compartment histopathologic inflammatory changes in older mice. Whole lung cell infiltrate analysis revealed that young, but not older mice, repetitively treated with ODE demonstrated an elevated CD4:CD8 lymphocyte response. Acute inhalant ODE exposure resulted in a 4-fold and 1.5-fold rise in blood neutrophils in young and older mice, respectively. Serum IL-6 and CXCL1 levels were elevated in young and older mice i.n. exposed once to ODE, with increased CXCL1 levels in younger compared to older mice. Although older mice displayed reduced bone measurements compared to younger mice, younger rodents demonstrated ODE-induced decrease in bone mineral density, bone volume and bone micro-architecture quality as determined by CT analysis. Collectively, age impacts the airway injury, and systemic inflammatory and bone loss response to inhalant ODE, suggesting an altered and enhanced immunologic response in younger as compared to older counterparts.

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Section: Discussionmentioning

confidence: 99%

Age Impacts Pulmonary Inflammation and Systemic Bone Response to Inhaled Organic Dust Exposure

Poole

Romberger

Wyatt

et al. 2015

Journal of Toxicology and Environmental Health, Part A

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“…studies reported lower expression of inflammatory mediators and higher levels of antioxidants in infants/juveniles 44,58 and a more activated inflammatory milieu in the middle aged/elderly 73,75,82,83,85,88 when compared with adults. Data on the number of resident alveolar macrophages and neutrophils were conflicting.…”

Section: Critical Care Medicinementioning

confidence: 98%

“…40,65,68,75,77,80,82,83 Given that each model produces different lung injury modifying the molecular mechanisms activated, 29 we present results on the pulmonary response to injury stratified by type of pulmonary insult (tables 4 and 5). 73,78,82,83,88 In addition, macrophage function in the pneumonia models was impaired in these age groups and associated with a decreased clearance of bacteria (tables 4 and 5). Independent of the model used, in most studies, the recruitment of neutrophils into the lung was lower in infants/juveniles 44,46,51,52,54,[56][57][58]60,61 (table 4) and higher in the middle aged/elderly 40,[65][66][67]69,[72][73][74][76][77][78][79][80][81]86,87,89 (table 5), compared with adults.…”

Section: Critical Care Medicinementioning

confidence: 98%

“…In all age groups, cell influx was predominated by neutrophils. [60][61][62][63]77,80,81,85,86,88 The pulmonary inflammatory mediator response in infants/juveniles was mainly studied in VILI and hyperoxia models, which showed decreased levels compared with adults 43,44,46,53,54 (table 4). Some studies reported a delayed recruitment of neutrophils in both extremes of age: infants 52,54,57,58 and elderly.…”

Section: Critical Care Medicinementioning

confidence: 99%

“…Some studies reported a delayed recruitment of neutrophils in both extremes of age: infants 52,54,57,58 and elderly. 41,65,67,74,76,89,90 In contrast, no clear trend was seen in the pneumonia models [80][81][82][83][85][86][87][88] (table 5). [60][61][62][63]77,80,81,85,86,88 The pulmonary inflammatory mediator response in infants/juveniles was mainly studied in VILI and hyperoxia models, which showed decreased levels compared with adults 43,44,46,53,54 (table 4).…”

Section: Critical Care Medicinementioning

confidence: 99%

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Association between Maturation and Aging and Pulmonary Responses in Animal Models of Lung Injury

et al. 2015

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Increasing age seems to be correlated with exaggerated pulmonary responses to injury, ultimately leading to more severe lung injury. Pulmonary inflammation seems relatively suppressed in infants/juveniles, whereas in the middle aged/elderly, the inflammatory response seems delayed but aggravated. This implies that investigators and clinicians need to use caution about extrapolating results from adolescent or youngadult animals to pediatric or elderly patients in clinical practice.

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Immunosenescence in monocytes, macrophages, and dendritic cells: Lessons learned from the lung and heart

Linton

Thoman

2014

Immunology Letters

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In the absence of an immune challenge, healthy, aged individuals have a significantly higher basal inflammatory state where circulating levels of cytokines, including IL-6, TNF-α and IL-1β, are elevated[1]. This progressive pro-inflammatory state, termed “inflamm-aging,” affects the phenotype/function of cells present in the aged as well as renders the older individuals more susceptible to a poor prognosis after systemic insults. Although it is important to understand the mechanisms that underlie the progression of disease, most preclinical analyses of disease therapies are performed in young adult mice that have an intact, functional immune system. Oftentimes, this is not necessarily representative of the immune disposition in the aged, let alone diseased, aged. Herein, two distinct responses that are not only commonly associated with aging but that also have dendritic cells and/or monocytes and macrophages as key players are discussed: pulmonary infection and myocardial infarction. Although studies of pulmonary infection in the aged have progressed significantly, studies of monocytes and macrophages in inflammation and cardiac injury following ischemia in the aged have not been as forthcoming. Nonetheless, several elegant studies have established the dynamic role of monocytes and macrophages post infarction. These will be discussed in light of what is known with aging.

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Aging Reduces the Expression of Lung CINC and MCP-1 mRNA in a P. aeruginosa Rat Model of Infection

Cited by 11 publications

References 20 publications

Age Impacts Pulmonary Inflammation and Systemic Bone Response to Inhaled Organic Dust Exposure

Age Impacts Pulmonary Inflammation and Systemic Bone Response to Inhaled Organic Dust Exposure

Association between Maturation and Aging and Pulmonary Responses in Animal Models of Lung Injury

Immunosenescence in monocytes, macrophages, and dendritic cells: Lessons learned from the lung and heart

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