scholarly journals Activated alveolar macrophages in subclinical pulmonary inflammation in collagen vascular diseases.

Thorax ◽  
1988 ◽  
Vol 43 (1) ◽  
pp. 24-30 ◽  
Author(s):  
B Wallaert ◽  
F Bart ◽  
C Aerts ◽  
A Ouaissi ◽  
P Y Hatron ◽  
...  
Pneumologie ◽  
2011 ◽  
Vol 65 (12) ◽  
Author(s):  
NC Habel ◽  
S Hirn ◽  
F Tian ◽  
O Eickelberg ◽  
T Stoeger

1987 ◽  
Vol 58 (02) ◽  
pp. 758-763 ◽  
Author(s):  
G Mombelli ◽  
R Monotti ◽  
A Haeberli ◽  
P W Straub

SummaryIncreased fibrinopeptide A (FPA) levels have been reported in various non-thrombotic disorders, including cancer, acute myocardial infarction, liver cirrhosis and collagen vascular diseases. To investigate the significance of these findings, the present study combined the radioimmunoassay of FPA with that of fibrinogen/fibrin degradation fragment E (FgE) in the aforementioned disorders and compared the results with those observed in healthy subjects as well as in patients with thromboembolism and overt disseminated intravascular coagulation (DIC). Mean FPA and FgE in malignancy were 6.3 and 305 ng/ml, in myocardial infarction 5.6 and 98 ng/ml, in liver cirrhosis 2.7 and 132 ng/ml and in collagen vascular diseases 5.6 and 142 ng/ml. All these values were significantly higher than in healthy controls (mean FPA 1.6 ng/ml, mean FgE 49 ng/ml) but significantly lower than in thromboembolism (mean FPA 10.7 ng/ml, mean FgE 639 ng/ ml) and DIC (mean FPA 22.0 ng/ml, mean FgE 1041 ng/ml). The overall correlation between FPA and FgE was highly significant. Elowever, different disorders showed peculiar patterns in FPA, FgE and fibrinogen levels. In malignancy, a definite increase of FPA, FgE and plasma fibrinogen levels was observed. This finding probably indicates a compensated state of (intra- or extravascular) fibrin formation and lysis. Acute myocardial infarction was characterized by a high FPA to FgE ratio, which is interpreted to reflect acute thrombin generation and fibrin formation. FPA in cirrhosis was only marginally elevated with most single values within the normal range, indicating that intravascular coagulation was infrequent and unimportant in quantitative terms.


Author(s):  
Bart De Naeyer ◽  
Gert De Meerleer ◽  
Sabine Braems ◽  
Luc Vakaet ◽  
John Huys

2021 ◽  
Vol 23 ◽  
Author(s):  
Pamelia N. Lim ◽  
Maritza M. Cervantes ◽  
Linh K. Pham ◽  
Alissa C. Rothchild

Abstract Alveolar macrophages (AMs) are lung-resident myeloid cells that sit at the interface of the airway and lung tissue. Under homeostatic conditions, their primary function is to clear debris, dead cells and excess surfactant from the airways. They also serve as innate pulmonary sentinels for respiratory pathogens and environmental airborne particles and as regulators of pulmonary inflammation. However, they have not typically been viewed as primary therapeutic targets for respiratory diseases. Here, we discuss the role of AMs in various lung diseases, explore the potential therapeutic strategies to target these innate cells and weigh the potential risks and challenges of such therapies. Additionally, in the context of the COVID-19 pandemic, we examine the role AMs play in severe disease and the therapeutic strategies that have been harnessed to modulate their function and protect against severe lung damage. There are many novel approaches in development to target AMs, such as inhaled antibiotics, liposomal and microparticle delivery systems, and host-directed therapies, which have the potential to provide critical treatment to patients suffering from severe respiratory diseases, yet there is still much work to be done to fully understand the possible benefits and risks of such approaches.


Author(s):  
Martina Bonifazi ◽  
Francesca Barbisan ◽  
Stefani Gasparini

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