Expression of heat-shock protein 70 (Hsp70) in the respiratory tract and lungs of fire victims

Marschall, Sabine; Rothschild, Markus A.; Bohnert, Michael

doi:10.1007/s00414-006-0105-y

Cited by 38 publications

(22 citation statements)

References 37 publications

(41 reference statements)

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“…An important member of the Hsp family is Hsp 70. Hsp 70 is known to play a role in modulating protein biosynthesis and ensures cell protection and survival at high temperatures, presumably by binding to ribosomal subunits (13). In the present study, we noted that Hsp 70 appeared to be overexpressed in rats pretreated with both vitamin C and catechins following OSE.…”

Section: Discussionsupporting

confidence: 58%

Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Li¹,

Chen²,

Chang³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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Li P-C, Chen W-C, Chang L-C, Lin S-C. Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure. Am J Physiol Lung Cell Mol Physiol 294: L912-L920, 2008. First published March 7, 2008 doi:10.1152/ajplung.00443.2007.-This study aimed to 1) assess whether substance P (SP) acts via neurokinin (NK)-1 and NK-2 receptors to stimulate neurogenic inflammation (indicated by formation of ICAM-1 expression and oxidative stress) following oil smoke exposure (OSE) in rats; and 2) determine if pretreatment with antioxidants ameliorates the deleterious effects of OSE. Rats were pretreated with NK-1 receptor antagonist CP-96345, NK-2 receptor antagonist SR-48968, vitamin C, or catechins. OSE was for 30 -120 min. Rats were killed 0 -8 h later. Total lung resistance (RL), airway smooth muscle activity (ASMA), lung ICAM-1 expression, neurogenic plasma extravasation (via India ink and Evans blue dye), bronchoalveolar lavage fluid SP concentrations, and reactive oxygen species formation [via lucigenin-and luminalamplified chemiluminescence (CL)] were assessed. Lung histology was performed. SP concentrations increased significantly in nonpretreated rats following OSE in a dose-dependent manner. RL and total ASMA increased over time after OSE. Vitamin C and catechin pretreatments were associated with significantly reduced lucigenin CL 2 and 4 h after OSE. Pretreatment with catechins significantly reduced luminal CL counts 4 and 8 h after OSE. Evans blue levels were significantly reduced following 60 and 120 min of OSE in catechinand CP-96345-pretreated rats. ICAM-1 protein expression was significantly decreased in all pretreatment groups after OSE. Thickening of the alveolar capillary membrane, focal hemorrhaging, interstitial pneumonitis, and peribronchiolar inflammation were apparent in OSE lungs. These findings suggest that SP acts via the NK-1 receptor to provoke neurogenic inflammation, oxidative stress, and ICAM-1 expression after OSE in rats.reactive oxygen species; intracellular adhesion molecule-1; acute lung injury ACTIVATION OF NONMYELINATED bronchopulmonary C-fiber endings by various stimuli [including cigarette smoke (9), airway surface osmolality changes (14), and fire smoke (22)] causes the release of tachykinins and calcitonin gene-related peptide neuropeptides stored in the peripheral nerve terminals, eliciting both central nervous system (CNS) and local axon reflex responses (4). The CNS reflex consists of bronchoconstriction, expiratory apnea, rapid shallow breathing, cough, hypotension, and bradycardia, whereas the axon reflex response initiates local inflammation, increased mucous secretion, and bronchoconstriction. Substance P (SP), a tachykinin neuropeptide, induces a range of neuroimmunogenic effects on target smooth muscle or parasympathetic ganglia cells expressing neurokinin (NK)-1 or NK-2 receptors (1, 2). These effects, collectively termed neurogenic airway inflammation, comprise bronchoconstriction, microvasc...

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Section: Discussionsupporting

confidence: 58%

Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Li¹,

Chen²,

Chang³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The molecular and cellular pathophysiology of the wound healing process is applied for wound age determination. Recently, the immunohistochemical detection and RNA analyses of several molecules (e.g., extracellular matrix components, growth factors, cytokines, and adhesion molecules) has become a powerful method for forensic practices such as wound age determination or postmortem diagnosis [3][4][5][6][7][8][9][10][11][12][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45]. To the best of our knowledge, there have been only two forensic studies on thrombus age estimation Fig.…”

Section: Discussionmentioning

confidence: 99%

Time-dependent appearance of intrathrombus neutrophils and macrophages in a stasis-induced deep vein thrombosis model and its application to thrombus age determination

et al. 2009

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We immunohistochemically examined neutrophils and macrophages in venous thrombi, which developed in the ligation of the inferior vena cava (IVC). Myeloperoxidase (MPO)-positive neutrophils and F4/80-positive macrophages were detected in the whole course of thrombi after IVC ligation. Morphometrically, the number of neutrophils was greatest at 1 day after IVC ligation and, thereafter, gradually decreased with an increase of the post-ligation interval. In contrast, the number of macrophages peaked at 7 days after ligation. The number of intrathrombus neutrophils was significantly higher than that of intrathrombus macrophages at 1 and 3 days, and the average ratios of neutrophils to macrophages (N/M ratios) were 6.8 +/- 1.1 (4.8-9.0) and 2.5 +/- 0.4 (1.7-4.2) at 1 and 3 days, respectively. After more than 5 days, all samples had N/M ratios of <2.0 (0.2-1.4). These observations suggest that an N/M ratio of >2.0 indicates a thrombus age of 1-3 days. To differentiate between 1- and 3-day-old thrombi, an N/M ratio markedly exceeding 5.0 strongly indicates an age of 1 day. Furthermore, an N/M ratio of 1.0 or less probably indicates an age of more than 5 days. The present study demonstrated that the immunohistochemical detection of intrathrombus neutrophils and macrophages was suitable to determine the age of venous thrombi.

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“…Macro-and microscopic signs of vitality in fire death include soot deposits and thermal injury in the upper airways, but these findings may partly be sparse or even absent, especially in peracute deaths, making the diagnosis difficult (Bohnert et al, 2003). Recent immunohistochemical studies of the respiratory tract and lungs demonstrated intravital reactions in fatal burns (Boehm et al, 2010;Bohnert et al, 2010;Marschall et al, 2006); however, the pathophysiological process leading to death is still unclear. In particular, the influences of toxic gases usually do not leave significant pathology that is detectable after death, except that bilateral pallidum necrosis is occasionally seen in CO intoxication.…”

Section: Burnsmentioning

confidence: 99%

Immunohistochemistry of Neuronal Apoptosis in Fatal Traumas: The Contribution of Forensic Molecular Pathology in Medical Science

Wang¹,

Michiue²,

Maeda³

2012

Apoptosis and Medicine

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Expression of heat-shock protein 70 (Hsp70) in the respiratory tract and lungs of fire victims

Cited by 38 publications

References 37 publications

Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Time-dependent appearance of intrathrombus neutrophils and macrophages in a stasis-induced deep vein thrombosis model and its application to thrombus age determination

Immunohistochemistry of Neuronal Apoptosis in Fatal Traumas: The Contribution of Forensic Molecular Pathology in Medical Science

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