Inflammatory reaction patterns of the lung as a response to alveolar hypoxia and their significance for the diagnosis of asphyxiation

Gutjahr, Ewgenija; Madea, Burkhard

doi:10.1016/j.forsciint.2019.02.026

Cited by 16 publications

(9 citation statements)

References 32 publications

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“…Another animal study described similar findings a few hours after endotoxin challenge [21]. Activation and differentiation of alveolar monocytes into MRP-8/14-positive mature macrophages with the progress of asphyxia duration have been detected in specimens of suffocated human lungs [23]. Human data on the kinetics of CLP are scarce.…”

Section: The Expression Of Clp In Lung Tissue and Potential Mechanismmentioning

confidence: 80%

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Calprotectin in Lung Diseases

Kotsiou

Papagiannis

Papadopoulou

et al. 2021

IJMS

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Calprotectin (CLP) is a heterodimer formed by two S-100 calcium-binding cytosolic proteins, S100A8 and S100A9. It is a multifunctional protein expressed mainly by neutrophils and released extracellularly by activated or damaged cells mediating a broad range of physiological and pathological responses. It has been more than 20 years since the implication of S100A8/A9 in the inflammatory process was shown; however, the evaluation of its role in the pathogenesis of respiratory diseases or its usefulness as a biomarker for the appropriate diagnosis and prognosis of lung diseases have only gained attention in recent years. This review aimed to provide current knowledge regarding the potential role of CLP in the pathophysiology of lung diseases and describe how this knowledge is, up until now, translated into daily clinical practice. CLP is involved in numerous cellular processes in lung health and disease. In addition to its anti-microbial functions, CLP also serves as a molecule with pro- and anti-tumor properties related to cell survival and growth, angiogenesis, DNA damage response, and the remodeling of the extracellular matrix. The findings of this review potentially introduce CLP in daily clinical practice within the spectrum of respiratory diseases.

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Section: The Expression Of Clp In Lung Tissue and Potential Mechanismmentioning

confidence: 80%

“…In long alveolar asphyxia cases, a 2-fold up to a 4-fold increase of MRP-14/MRP-8 was shown compared to short asphyxia [23]. In freshly isolated monocytes during prolonged cultivation, a strong upregulation of CLP was only observed during the first 3-4 days, and then declined [26].…”

Section: The Expression Of Clp In Lung Tissue and Potential Mechanismmentioning

confidence: 99%

Calprotectin in Lung Diseases

Kotsiou

Papagiannis

Papadopoulou

et al. 2021

IJMS

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“…Several approaches have been proposed 1 – 7 , mainly focused on the effects of asphyxial mechanisms, while little is known about the real-time biological modifications that occur during hypoxic-ischaemic insult. It was recently demonstrated 8 that only exceptionally long asphyxial periods can produce lungs histological modifications, whilst alterations can be observed at cellular and, especially, molecular level. The consequences of mechanical asphyxia not only affect the cellular compartments but also peripheral blood homeostasis, so investigate the metabolic status of an individual exposed to this insult might improve the comprehension of asphyxial CA.…”

Section: Introductionmentioning

confidence: 99%

Metabolomics improves the histopathological diagnosis of asphyxial deaths: an animal proof-of-concept model

Locci

Chighine

Noto

et al. 2021

Sci Rep

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The diagnosis of mechanical asphyxia remains one of the most difficult issues in forensic pathology. Asphyxia ultimately results in cardiac arrest (CA) and, as there are no specific markers, the differential diagnosis of primitive CA and CA secondary to asphyxiation relies on circumstantial details and on the pathologist experience, lacking objective evidence. Histological examination is currently considered the gold standard for CA post-mortem diagnosis. Here we present the comparative results of histopathology versus those previously obtained by 1H nuclear magnetic resonance (NMR) metabolomics in a swine model, originally designed for clinical purposes, exposed to two different CA causes, namely ventricular fibrillation and asphyxia. While heart and brain microscopical analysis could identify the damage induced by CA without providing any additional information on the CA cause, metabolomics allowed the identification of clearly different profiles between the two groups and showed major differences between asphyxiated animals with good and poor outcomes. Minute-by-minute plasma sampling allowed to associate these modifications to the pre-arrest asphyxial phase showing a clear correlation to the cellular effect of mechanical asphyxia reproduced in the experiment. The results suggest that metabolomics provides additional evidence beyond that obtained by histology and immunohistochemistry in the differential diagnosis of CA.

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“…Several studies on human lung tissue described a significant increase in alveolar macrophages and giant cells, especially in protracted asphyxia [ 10 , 28 – 31 ]. Betz et al [ 32 , 33 ] and Grellner et al [ 34 ], conversely, described in their studies that there is no significant giant cell formation or alveolar macrophage proliferation in deaths by asphyxia, which could also be substantiated in 2019 by Gutjahr et al [ 27 , 35 ] (“pre-existence hypothesis”). The agony times in these studies correspond to the “realistic” times in the cases of asphyxiation in everyday forensic medicine.…”

Section: Introductionmentioning

confidence: 90%

“…Brinkmann et al described a specific combination of emphysema, microembolism syndrome, alveolar septal edema, and hemorrhagic-dysoric syndrome as "pathognomonic of obstructive asphyxia" [17]. However, this conclusion was refuted by other authors, since this constellation of findings was also found in control groups, e.g., in cases of shock or resuscitation [26,27]. Several studies on human lung tissue described a significant increase in alveolar macrophages and giant cells, especially in protracted asphyxia [10,[28][29][30][31].…”

Section: Introductionmentioning

confidence: 99%

Acute or chronic pulmonary emphysema? Or both?—A contribution to the diagnosis of death due to violent asphyxiation in cases with pre-existing chronic emphysema

et al. 2021

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The diagnosis of death due to violent asphyxiation may be challenging if external injuries are missing, and a typical acute emphysema (AE) “disappears” in pre-existing chronic emphysema (CE). Eighty-four autopsy cases were systematically investigated to identify a (histo-) morphological or immunohistochemical marker combination that enables the diagnosis of violent asphyxiation in cases with a pre-existing CE (“AE in CE”). The cases comprised four diagnostic groups, namely “AE”, “CE”, “acute and chronic emphysema (AE + CE)”, and “no emphysema (NE)”. Samples from all pulmonary lobes were investigated by conventional histological methods as well as with the immunohistochemical markers Aquaporin 5 (AQP-5) and Surfactant protein A1 (SP-A). Particular attention was paid to alveolar septum ends (“dead-ends”) suspected as rupture spots, which were additionally analyzed by transmission electron microscopy. The findings in the four diagnostic groups were compared using multivariate analysis and 1-way ANOVA analysis. All morphological findings were found in all four groups. Based on histological and macroscopic findings, a multivariate analysis was able to predict the correct diagnosis “AE + CE” with a probability of 50%, and the diagnoses “AE” and “CE” with a probability of 86% each. Three types of “dead-ends” could be differentiated. One type (“fringed ends”) was observed significantly more frequently in AE. The immunohistochemical markers AQP-5 and SP-A did not show significant differences among the examined groups. Though a reliable identification of AE in CE could not be achieved using the examined parameters, our findings suggest that considering many different findings from the macroscopical, histomorphological, and molecular level by multivariate analysis is an approach that should be followed.

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Inflammatory reaction patterns of the lung as a response to alveolar hypoxia and their significance for the diagnosis of asphyxiation

Cited by 16 publications

References 32 publications

Calprotectin in Lung Diseases

Calprotectin in Lung Diseases

Metabolomics improves the histopathological diagnosis of asphyxial deaths: an animal proof-of-concept model

Acute or chronic pulmonary emphysema? Or both?—A contribution to the diagnosis of death due to violent asphyxiation in cases with pre-existing chronic emphysema

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