Markers of mechanical asphyxia: immunohistochemical study on autoptic lung tissues

Abstract

Forensic pathologists are often asked to provide evidence of asphyxia death in the trial and a histological marker of asphyxiation would be of great help. Data from the literature indicate that the reaction of lung tissue cells to asphyxia may be of more interest for forensic purposes than migrating cells. The lungs of 62 medico-legal autopsy cases, 34 acute mechanical asphyxia (AMA), and 28 control cases (CC), were immunostained with anti-P-selectin, anti-E-selectin, anti-SP-A, and anti-HIF1-α antibodies, in order to verify if some of them may be used as markers of asphyxia death. Results show that P- and E-selectins expression in lung vessels, being activated by several types of trigger stimuli not specific to hypoxia, cannot be used as indicator of asphyxia. Intra-alveolar granular deposits of SP-A seem to be related to an intense hypoxic stimulus, and when massively present, they can suggest, together with other elements, a severe hypoxia as the mechanism of death. HIF1-α was expressed in small-, medium-, and large-caliber lung vessels of the vast majority of mechanical asphyxia deaths and CO intoxications, with the number and intensity of positive-stained vessels increasing with the duration of the hypoxia. Although further confirmation studies are required, these preliminary data indicate an interesting potential utility of HIF1-α as a screening test for asphyxia deaths.

HIF1α protein and mRNA expression as a new marker for post mortem interval estimation in human gingival tissue

“…); in the lungs in cases of mechanical asphyxia (Cecchi et al. ); and in the kidneys, especially in cases of acute circulatory failure (Zhao et al. ).…”

“…Indeed, HIF expression has been related to different causes of death in different organs, specific targets of hypoxia. In particular, increases in HIF expression have been observed: in myocardial tissue in cases of myocardial ischaemia (Blanco Pamp ın et al 2006) or cardiac death (Zhu et al 2008); in the lungs in cases of mechanical asphyxia (Cecchi et al 2014); and in the kidneys, especially in cases of acute circulatory failure (Zhao et al 2006). However, to the best of our knowledge, gingival tissue is not a specific target of hypoxia in the peri mortem period; thus, there is no reason to hypothesize a different pattern of hypoxia related to HIF-1a expression in gingival tissue that is associated with a specific cause of death.…”

G6PC3, ALDOA and CS induction accompanies mir-122 down-regulation in the mechanical asphyxia and can serve as hypoxia biomarkers

“…And an increase of SP-A in mechanical asphyxia cases demonstrates that hypoxia is the distinguishing feature of death in such cases [24]. In addition, Cecchi et al have demonstrated that HIF-1a (hypoxia-induced factor 1-a), a target of mir-122 expressed in response to hypoxia, was up-regulated in mechanical asphyxia compared with craniocerebral injury, natural death and other causes of death [25, 26]. Our findings thus indicate that mir-122 reduction might be the response to hypoxia in mechanical asphyxia.…”

Immunohistochemical expression of P-selectin, SP-A, HSP70, aquaporin 5, and fibronectin in saltwater drowning and freshwater drowning

“…This protein is produced by type II alveolar cells and physiologically lines the alveoli and smallest bronchioles. As it is the major surfactant protein, its deficiency causes respiratory distress [19][20]. Hypoxia increases its production, causing its precipitation and formation of aggregates of SP-A in the alveolar spaces, likely due to the exertions of forced breathing [20].…”