Measurement of both native and inactivated forms of α<sub>1</sub> proteinase inhibitor in human inflammatory extracellular fluids

Πετροπούλου, Περιστέρα-Ιωάννα; Zhang, Z; Curtis, Michael J.; Johnson, Newell W.; Hughes, Francis J.; Winyard, Paul G.

doi:10.1034/j.1600-051x.2003.00369.x

Cited by 14 publications

(5 citation statements)

References 33 publications

(41 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nevertheless, this concept was further explored, with the theory that despite an increase of local AAT it could also be inactivated in periodontitis [85], leading to a functional imbalance and hence continued enzyme activity. Assays subsequently showed that inactivation of AAT was significantly greater in the crevicular fluid of patient with periodontitis although the mechanism underlying this was unknown [86]. In addition, the complexity of interactions with other enzymes and inhibitors, as in COPD, has also been proposed as relevant in periodontitis [87].…”

Section: Discussionmentioning

confidence: 99%

The link between chronic periodontitis and COPD: a common role for the neutrophil?

Usher

Stockley

2013

BMC Med

View full text Add to dashboard Cite

BackgroundThe possible relationship between chronic inflammatory diseases and their co-morbidities has become an increasing focus of research. Both chronic periodontitis and chronic obstructive pulmonary disease are neutrophilic, inflammatory conditions characterized by the loss of local connective tissue. Evidence suggests an association and perhaps a causal link between the two diseases. However, the nature of any relationship between them is unclear, but if pathophysiologically established may have wide-reaching implications for targeted treatments to improve outcomes and prognosis.DiscussionThere have been a number of epidemiological studies undertaken demonstrating an independent association between chronic periodontitis and chronic obstructive pulmonary disease. However, many of them have significant limitations, and drawing firm conclusions regarding causality may be premature. Although the pathology of both these diseases is complex and involves many cell types, such as CD8 positive cells and macrophages, both conditions are predominantly characterized by neutrophilic inflammation. Increasingly, there is evidence that the two conditions are underpinned by similar pathophysiological processes, especially centered on the functions of the neutrophil. These include a disturbance in protease/anti-protease and redox state balance. The association demonstrated by epidemiological studies, as well as emerging similarities in pathogenesis at the level of the neutrophil, suggest a basis for testing the effects of treatment for one condition upon the severity of the other.SummaryAlthough the evidence of an independent association between chronic periodontitis and chronic obstructive pulmonary disease grows stronger, there remains a lack of definitive studies designed to establish causality and treatment effects. There is a need for future research to be focused on answering these questions.

show abstract

Section: Discussionmentioning

confidence: 99%

The link between chronic periodontitis and COPD: a common role for the neutrophil?

Usher

Stockley

2013

BMC Med

View full text Add to dashboard Cite

show abstract

“…RA and PD have been reported to share numerous common pathogenic characteristics, and a number of studies have found a potential association between RA and PD (Mercado et al 2000, Mercado et al 2001, de Pablo et al 2008, Pischon et al 2008. Interestingly, common genetic variants are associated with both diseases (Ogrendik et al 2005), and other studies have shown a remarkably similar involvement of mediators, including prostaglandins, cytokines, matrix metalloproteinases, and cell types (Bozkurt et al 2000, Mercado et al 2003, Petropoulou et al 2003, leading to the stimulation of local osteoclastogenesis (Cochran, 2008).…”

mentioning

confidence: 99%

Mechanism of alveolar bone loss in a collagen-induced arthritis model in mice

Park

Jung

et al. 2010

Journal of Clinical Periodontology

View full text Add to dashboard Cite

show abstract

“…Notable concentration decreases of apoA-I or high-density lipoprotein (containing mostly apoA-I) have been observed during various inflammatory states [35,[37][38][39][40][41]. Research data suggested that apoA-I exerts its antiinflammatory activity by inhibiting contact-mediated activation of monocytes through binding to stimulated T cells [40,[42][43][44].…”

Section: Discussionmentioning

confidence: 99%

Serological Proteomics of Gastritis: Degradation of Apolipoprotein A-I and Alpha1-Antitrypsin Is a Common Response to Inflammation Irrespective of Helicobacter pylori Infection

Huai-yi

Wong

et al. 2008

Dig Dis Sci

View full text Add to dashboard Cite

Proteomic technology was employed to analyze serum samples from healthy subjects (10 cases) and gastritis patients with negative and positive Helicobacter pylori (Hp) infection (15 cases each). The serum proteins were separated by two-dimensional (2-D) gel electrophoresis and analyzed by a computer-aided program. The altered proteins in expression were then identified by mass spectrometry and validated by Western blotting. Compared to those in normal control, proteins in at least six areas of 2-D gels were found to significantly increase their expression levels in both Hp-negative and Hp-positive serum samples. These proteins were identified by mass peptide fingerprinting and confirmed by Western blotting to be the truncated or cleaved protein fragments of apolipoprotein A-I and alpha-1 antitrypsin, two well-known acute-phase proteins. We conclude that the degradation or metabolization of acute-phase proteins, apolipoprotein A-I, and alpha1-antitrypsin, is a common response to gastric inflammation irrespective of Hp infection.

show abstract

Measurement of both native and inactivated forms of α₁ proteinase inhibitor in human inflammatory extracellular fluids

Cited by 14 publications

References 33 publications

The link between chronic periodontitis and COPD: a common role for the neutrophil?

The link between chronic periodontitis and COPD: a common role for the neutrophil?

Mechanism of alveolar bone loss in a collagen-induced arthritis model in mice

Serological Proteomics of Gastritis: Degradation of Apolipoprotein A-I and Alpha1-Antitrypsin Is a Common Response to Inflammation Irrespective of Helicobacter pylori Infection

Contact Info

Product

Resources

About

Measurement of both native and inactivated forms of α1 proteinase inhibitor in human inflammatory extracellular fluids

Cited by 14 publications

References 33 publications

The link between chronic periodontitis and COPD: a common role for the neutrophil?

The link between chronic periodontitis and COPD: a common role for the neutrophil?

Mechanism of alveolar bone loss in a collagen-induced arthritis model in mice

Serological Proteomics of Gastritis: Degradation of Apolipoprotein A-I and Alpha1-Antitrypsin Is a Common Response to Inflammation Irrespective of Helicobacter pylori Infection

Contact Info

Product

Resources

About

Measurement of both native and inactivated forms of α₁ proteinase inhibitor in human inflammatory extracellular fluids