C-Reactive Protein and Serum Amyloid A Overexpression in Lung Tissues of Chronic Obstructive Pulmonary Disease Patients: A Case-Control Study

Lόpez-Campos, José Luís; Calero, Carmen; Rojano, Belen; Porras, Marta López; Sáenz-Coronilla, Javier; Blanco, Ana; Sánchez-López, Verónica; Tobar, Daniela; Montes-Worboys, Ana; Arellano, Elena

doi:10.7150/ijms.6152

Cited by 26 publications

(21 citation statements)

References 38 publications

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“…Conversely, recent work has indicated that the proinflammatory effects of A-SAA are diminished when bound to HDL (76,77); therefore, the functional relevance of increased circulating HDL-bound A-SAA on neutrophil recruitment remains to be determined. Further characterization of A-SAA functions in the lungs may have clinical relevance, as A-SAA is increased in both the lungs and serum of patients with COPD (34)(35)(36).…”

Section: Discussionmentioning

confidence: 99%

“…Conversely, A-SAA fragments form fibrils in amyloid A amyloidosis (33). A-SAA is elevated in the blood and lungs of patients with chronic obstructive pulmonary disease (COPD) (34)(35)(36), which is associated with and exacerbated by O 3 exposure (37,38). Furthermore, A-SAA induces glucocorticoid-resistant airway neutrophilia that is dependent on IL-6 and IL-17A (36).…”

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confidence: 99%

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Serum amyloid A: an ozone‐induced circulating factor with potentially important functions in the lung‐brain axis

et al. 2017

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Accumulating evidence suggests that O 3 exposure may contribute to CNS dysfunction. Here, we posit that inflammatory and acute-phase proteins in the circulation increase after O 3 exposure and systemically convey signals of O 3 exposure to the CNS. To model acute O 3 exposure, female Balb/c mice were exposed to 3 ppm O 3 or forced air for 2 h and were studied after 6 or 24 h. Of 23 cytokines and chemokines, only KC/CXCL1 was increased in blood 6 h after O 3 exposure. The acute-phase protein serum amyloid A (A-SAA) was significantly increased by 24 h, whereas C-reactive protein was unchanged. A-SAA in blood correlated with total leukocytes, macrophages, and neutrophils in bronchoalveolar lavage from O 3 -exposed mice. A-SAA mRNA and protein were increased in the liver. We found that both isoforms of A-SAA completely crossed the intact blood-brain barrier, although the rate of SAA2.1 influx was approximately 5 times faster than that of SAA1.1. Finally, A-SAA protein, but not mRNA, was increased in the CNS 24 h post-O 3 exposure. Our findings suggest that A-SAA is functionally linked to pulmonary inflammation in our O 3 exposure model and that A-SAA could be an important systemic signal of O 3 exposure to the CNS.-Erickson,

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Serum amyloid A: an ozone‐induced circulating factor with potentially important functions in the lung‐brain axis

et al. 2017

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“…Our finding that AngIIinduced increases in IL-1β are significantly blunted in mice lacking acute phase SAAs underscores the fact that SAA has proinflammatory effects in pathological settings, such as experimental AAA. SAA concentrations can be dramatically elevated in tissues due to local injury, infection or inflammation (15,(71)(72)(73)(74). The relative contribution of locally produced SAA versus HDL-bound SAA that has deposited in tissues at the site of injury or inflammation is not known, and merits further investigation.…”

Section: Discussionmentioning

confidence: 99%

High-density lipoprotein inhibits serum amyloid A–mediated reactive oxygen species generation and NLRP3 inflammasome activation

Shridas

Beer

Webb

2018

Journal of Biological Chemistry

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Serum amyloid A (SAA) is a high-density apolipoprotein whose plasma levels can increase more than 1000-fold during a severe acute-phase inflammatory response and are more modestly elevated in chronic inflammation. SAA is thought to play important roles in innate immunity, but its biological activities have not been completely delineated. We previously reported that SAA deficiency protects mice from developing abdominal aortic aneurysms (AAAs) induced by chronic angiotensin II (AngII) infusion. Here, we report that SAA is required for AngII-induced increases in interleukin-1 beta (IL-1β), a potent proinflammatory cytokine that is tightly controlled by the Nod-like receptor protein 3 (NLRP3) inflammasome and caspase-1 and has been implicated in both human and mouse AAAs. We determined that purified SAA stimulates IL-1β secretion in murine J774 and bone marrow-derived macrophages through a mechanism that depends on NLRP3 expression and caspase-1 activity, but is independent of P2X7 nucleotide receptor (P2X7R) activation. Inhibiting reactive oxygen species (ROS) by N-acetyl-Lcysteine or mito-TEMPO and inhibiting activation of cathepsin B by CA-074 blocked SAA-mediated inflammasome activation and IL-1β secretion. Moreover, inhibiting cellular potassium efflux with glyburide or increasing extracellular potassium also significantly reduced SAA-mediated IL-1β secretion. Of note, incorporating SAA into high-density lipid (HDL) prior to its use in cell treatments completely http://www.jbc.org/cgi

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“…CRP is an acute-phase protein that is produced in the liver and whose main biologic function is to recognize pathogens and damaged cells in the host, as well as to mediate their elimination by recruiting the complement system and phagocytic cells (17). CRP is suggested as a prognostic factor for the risk of several cancers (35), including lung cancer (14,20,24) and chronic lung disease (18,36). We hypothesized that CRP concentrations may provide an integrative biomarker of inflammatory responses of the host to tobacco and other environmental factors, which may predict those at greater risk of death from lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Prospective evaluation of C-reactive protein, smoking and lung cancer death in the Third National Health and Nutrition Examination Survey

Bittoni

Focht

Clinton

et al. 2015

International Journal of Oncology

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Abstract.Chronic inflammation plays an important role in lung carcinogenesis. Few prospective studies have examined associations between lung cancer, serum C-reactive protein (CRP), a measure of systemic inflammation, and inflammatory lifestyle factors, such as smoking and obesity. This study prospectively examined the relationship between CRP and lung cancer death and its interrelationships with several lifestyle factors. Baseline data on smoking and other lifestyle variables were collected for 8,950 participants in the Third National Health and Nutrition Examination Survey (NHANES III: 1988-1994. Baseline CRP levels were measured in serum samples by nephelometry. Mortality status was ascertained through probabilistic record matching using the National Death Index through 2006. Cox proportional hazard regression models were used to estimate hazard ratios (HRs) for CRP and lung cancer death, with adjustment for smoking and other variables. During 18 years of follow-up, 219 individuals died from lung cancer. Multivariate regression models revealed a dose-response effect for elevated CRP and risk of lung cancer death when adjusting for age, gender, BMI and smoking. Compared to individuals with CRP <3 mg/l, lung cancer death was significantly associated with elevated levels of CRP: HR=1.63 (95% CI=1.15-2.26) for 3-7 mg/l and HR=2.44 (95% CI=1.81-3.45) for CRP >7 mg/l, P-trend <0.0001). The risk of lung cancer death for smokers increased 9-fold in adjusted models (P<0.0001). When stratified by gender and smoking status the effects of CRP were similar for smokers and males but did not reach statistical significance for females and non-smokers. This study supports a dose-dependent relationship between lung cancer death and CRP for males and smokers, but additional efforts are needed to better elucidate these relationships in women and non-smokers. The results suggest that CRP may emerge as a valuable tool in identifying high-risk subgroups of smokers for lung cancer prevention strategies.

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C-Reactive Protein and Serum Amyloid A Overexpression in Lung Tissues of Chronic Obstructive Pulmonary Disease Patients: A Case-Control Study

Cited by 26 publications

References 38 publications

Serum amyloid A: an ozone‐induced circulating factor with potentially important functions in the lung‐brain axis

Serum amyloid A: an ozone‐induced circulating factor with potentially important functions in the lung‐brain axis

High-density lipoprotein inhibits serum amyloid A–mediated reactive oxygen species generation and NLRP3 inflammasome activation

Prospective evaluation of C-reactive protein, smoking and lung cancer death in the Third National Health and Nutrition Examination Survey

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