Neutrophils and low-grade inflammation in the seemingly normal aging human lung

Meyer, Keith C.; Rosenthal, Nancy S.; Soergel, Paula; Peterson, Kimberly

doi:10.1016/s0047-6374(98)00065-7

Cited by 167 publications

(130 citation statements)

References 32 publications

Supporting

Mentioning

117

Contrasting

Unclassified

Order By: Relevance

“…The current data shows that inflammation in the larger airways is increased in the a 1 ATD subjects despite more using inhaled steroids (which would be expected to have a beneficial effect) [23] and the subjects being younger (which would also be associated with less inflammation in the larger airways) [31,32]. MPO concentrations were higher, as was the chemoattractant LTB 4 .…”

Section: Discussionmentioning

confidence: 66%

Airways inflammation in chronic bronchitis: the effects of smoking and alpha1-antitrypsin deficiency

Hill¹,

Bayley²,

Campbell³

et al. 2000

Eur Respir J

104

View full text Add to dashboard Cite

Airways inflammation in chronic bronchitis is thought predominantly to be a direct consequence of neutrophil recruitment and release of elastase in response to factors such as cigarette smoke. The aims of this study were to assess the role of smoking and determine whether the serum elastase inhibitor α1‐antitrypsin (α1AT) influenced the process. Airways inflammation was compared between patients with chronic obstructive bronchitis with (n=39) and without (n=42) severe α1AT deficiency. The authors assessed the sputum concentration of the neutrophil chemoattractants interleukin‐8 (IL‐8) and leukotriene (LT)B4, myeloperoxidase (MPO) as a marker of neutrophil influx, neutrophil elastase activity and its natural inhibitors, α1AT and secretory leukoprotease inhibitor (SLPI). Finally serum α1AT was measured to determine the degree of protein leakage (sputum sol serum α1AT ratio). Compared to current smokers, the exsmokers had a lower concentration of the chemoattractant IL‐8 (p<0.05) and a lower MPO concentration, although this failed to reach conventional statistical significance (p=0.06). Patients with α1AT deficiency had greater inflammation in the larger airways with increased LTB4 (p<0.005), MPO (p<0.001), neutrophil elastase activity (p<0.01), protein leak (p<0.001), and were found to have a lower anti‐proteinase screen with both reduced sputum α1AT (p<0.001) and SLPI concentrations (p<0.05). The reduction in sputum interleukin‐8 levels in exsmokers may decrease neutrophil influx and thus explain the slower rate of neutrophil mediated progression of lung disease compared to subjects who continue to smoke. Patients with α1‐antitrypsin deficiency had greater inflammation suggesting that α1‐antitrypsin plays an important role in protecting the larger airways from the inflammatory effects of elastase activity and may explain their more rapid progression of disease.

show abstract

Section: Discussionmentioning

confidence: 66%

Airways inflammation in chronic bronchitis: the effects of smoking and alpha1-antitrypsin deficiency

Hill¹,

Bayley²,

Campbell³

et al. 2000

Eur Respir J

104

View full text Add to dashboard Cite

show abstract

“…Although up-regulation of ECM protease expression is a unifying feature of age-related inflammatory conditions such as emphysema (Robbesom et al 2008), atherosclerosis (Robert et al 2008) and UVinduced photoageing (Fisher et al 1996), the constitutive expression of MMPs in non-inflamed lung, aorta and skin (Chen et al 2005;McNulty et al 2005;Meyer et al 1998) may be sufficient, given the longevity of ECM assemblies, to gradually degrade proteins over many years. To date, eight MMPs have been shown to degrade elastic fibre proteins in vitro: insoluble elastin is degraded to soluble fragments by MMP-2, -7, -9, -10, -12 and -14 (Chakraborti et al 2003;Taddese et al 2008), whilst fibrillin microfibrils and peptides are catabolised by MMP-2,-3,-9,-12 and -13 (Ashworth et al 1999;Tsuruga et al 2007).…”

Section: Degradationmentioning

confidence: 99%

“…In these systems, the pulmonary system undergoes progressive changes in mechanical properties with age which ultimately compromise lung function and therefore diminish quality of life. In the aged lung, the loss of elasticity simulates emphysema (Knudson et al 1977;Turner et al 1968), and both forced expiratory volume and forced vital capacity are reduced (Meyer et al 1998). This reduction in tissue elasticity (both compliance and recoil), which has been well characterised in both human (Lai-Fook and Hyatt 2000;Turner et al 1968) and rodent lungs (Janssens et al 1999;Nagase et al 1994), plays an important role in increasing the risk of mortality in the ageing population as a result of acute pulmonary diseases (Janssens et al 1999;Meyer et al 1998).…”

Section: Pulmonarymentioning

confidence: 99%

“…In the aged lung, the loss of elasticity simulates emphysema (Knudson et al 1977;Turner et al 1968), and both forced expiratory volume and forced vital capacity are reduced (Meyer et al 1998). This reduction in tissue elasticity (both compliance and recoil), which has been well characterised in both human (Lai-Fook and Hyatt 2000;Turner et al 1968) and rodent lungs (Janssens et al 1999;Nagase et al 1994), plays an important role in increasing the risk of mortality in the ageing population as a result of acute pulmonary diseases (Janssens et al 1999;Meyer et al 1998). The mechanical properties of the lung are highly complex and depend on: the relative mechanical properties of the constituent ECM components (Fredberg and Kamm 2006), the arrangement of these molecules within the alveolar wall, and the geometrical construction of the alveolus itself (Kitaoka et al 2007;Wilson and Bachofen 1982).…”

Section: Pulmonarymentioning

confidence: 99%

See 1 more Smart Citation

Tissue elasticity and the ageing elastic fibre

Sherratt

2009

AGE

270

189

View full text Add to dashboard Cite

The ability of elastic tissues to deform under physiological forces and to subsequently release stored energy to drive passive recoil is vital to the function of many dynamic tissues. Within vertebrates, elastic fibres allow arteries and lungs to expand and contract, thus controlling variations in blood pressure and returning the pulmonary system to a resting state. Elastic fibres are composite structures composed of a cross-linked elastin core and an outer layer of fibrillin microfibrils. These two components perform distinct roles; elastin stores energy and drives passive recoil, whilst fibrillin microfibrils direct elastogenesis, mediate cell signalling, maintain tissue homeostasis via TGFβ sequestration and potentially act to reinforce the elastic fibre. In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality. This review considers how the unique molecular structure, tissue distribution and longevity of elastic fibres pre-disposes these abundant extracellular matrix structures to the accumulation of damage in ageing dermal, pulmonary and vascular tissues. As compromised elasticity is a common feature of ageing dynamic tissues, the development of strategies to prevent, limit or reverse this loss of function will play a key role in reducing age-related morbidity and mortality.

show abstract

“…In conjunction with this decline in lung function, over 45% of elderly humans demonstrate an increase in airway responsiveness to nonspecific agonists such as histamine 6. Moreover, elderly humans have been shown to have increased airway inflammation 7, 8…”

mentioning

confidence: 99%

Age Effects on Blood Gas, Spirometry, Airway Reactivity, and Bronchoalveolar Lavage Fluid Cytology in Clinically Healthy Horses

Pacheco

Paradis

Hoffman

et al. 2014

Veterinary Internal Medicne

View full text Add to dashboard Cite

BackgroundDespite the increasing number of geriatric horses attended by veterinarians, there is a lack of understanding of aging‐related changes on the respiratory system of horses.ObjectiveTo identify aging‐related changes on the respiratory function and bronchoalveolar lavage fluid (BALF) cytology of horses.AnimalsFifteen healthy young adult (2–11 years) and 16 healthy aged (≥20 years) horses.MethodsThe respiratory system was examined by measurement of arterial blood gases (ABG), use of respiratory inductive plethysmography (RIP) for assessment of breathing pattern and ventilatory parameters, histamine bronchoprovocation, and BALF cytology.ResultsNo significant differences were detected with regard to values obtained by ABG or bronchoprovocation of young adult and aged healthy horses. In aged horses, there were significant differences in mean ± SD of the following parameters when compared to young horses: prolonged expiratory time (Te) measured by RIP (3.9 ± 1.5 s versus 3.0 ± 0.6 s), decreased percentage of alveolar macrophages (40.6 ± 11.3% versus 53.5 ± 9.6%), and increased percentage of lymphocytes (53.4 ± 9.5% versus 43.9 ± 11.0%). No correlations between airway reactivity and ventilatory parameters, ABG, or BALF cytology were found in this asymptomatic population.ConclusionsThese results suggest that aging does not cause changes in the results obtained by ABG, most RIP‐derived variables, and bronchoprovocation in the horse. A decreased percentage of macrophage and an increased percentage of lymphocytes in the BALF cytology may be expected in the asymptomatic geriatric horse and may be a result of aging.

show abstract

Neutrophils and low-grade inflammation in the seemingly normal aging human lung

Cited by 167 publications

References 32 publications

Airways inflammation in chronic bronchitis: the effects of smoking and alpha1-antitrypsin deficiency

Airways inflammation in chronic bronchitis: the effects of smoking and alpha1-antitrypsin deficiency

Tissue elasticity and the ageing elastic fibre

Age Effects on Blood Gas, Spirometry, Airway Reactivity, and Bronchoalveolar Lavage Fluid Cytology in Clinically Healthy Horses

Contact Info

Product

Resources

About