Multi-organ damage resulting from experimental faecal peritonitis

1989 ◽  
Vol 76 (3) ◽  
pp. 269-276 ◽  
Author(s):  
D. Tighe ◽  
R. Moss ◽  
S. Boghossian ◽  
M. F. Heath ◽  
B. Chessum ◽  
...  
Keyword(s):  
Test Group ◽  
Organ Damage ◽  
Endothelial Damage ◽  
Sham Operation ◽  
Faecal Peritonitis ◽  
Alveolar Epithelial ◽  
Type Ii Pneumocytes ◽  
Specific Pathogen ◽  
Lung Capillaries ◽  
Micro Organisms

1. Using specific-pathogen-free New Zealand White rabbits, we have compared the effects of faecal peritonitis over a period of 5 h in eight test animals with eight controls in which a sham operation was performed. 2. There was morphological damage to lungs, liver and spleen of test animals. Lung capillaries and sinusoids of the liver showed occlusion by cell debris and leucocytes, with endothelial damage. The lungs also showed alveolar epithelial disruption, basement membrane exposure and type II pneumocytes lacking lamellar bodies. In the liver there was fibrin deposition and swollen Kupffer cells. The spleen showed degranulating neutrophils, fibrin deposits, platelet aggregates and activated macrophages, with no damage to the endothelium. 3. There was no morphological damage to the kidney or heart of test animals or to any organs of sham-operated animals. 4. There were mixed anaerobes and aerobes in faecal material used to induce peritonitis. Cultures of liver, spleen and kidney isolated four different types of micro-organisms. Blood cultures showed two types of micro-organisms. Cultures of lung and heart showed one type of micro-organism. 5. The presence of micro-organisms in an organ could not be correlated with the degree of histological damage to that organ. 6. In test animals an early significant reduction in circulating leucocytes and platelets was sustained for the duration of the experiment with significant diffuse intravascular coagulation. 7. There was no change in test animal neutrophil adhesiveness until 120 min, when significant reduction was observed. 8. Serum phospholipase A2 (EC 3.1.1.4) activity in the test group showed a threefold increase at 300 min.

scholarly journals Plutonium-induced Proliferative Lesions and Pulmonary Epithelial Neoplasms in the Rat: Immunohistochemical and Ultrastructural Evidence for Their Origin from Type II Pneumocytes

1994 ◽  
Vol 31 (3) ◽  
pp. 366-374 ◽  
Author(s):  
R. A. Herbert ◽  
B. S. Stegelmeier ◽  
N. A. Gillett ◽  
A. H. Rebar ◽  
W. W. Carlton ◽  
...  
Keyword(s):  
Clara Cell ◽  
Normal Lung ◽  
Type Ii ◽  
Epithelial Hyperplasia ◽  
Cell Antigen ◽  
Alveolar Epithelial ◽  
Type Ii Pneumocytes ◽  
Epithelial Neoplasms ◽  
Epithelial Lesions ◽  
Surfactant Apoprotein

Immunohistochemistry and transmission electron microscopy were used to clarify the cellular origin for plutonium-239-induced pulmonary proliferative (preneoplastic) epithelial lesions and epithelial neoplasms in F344 rats. Examples of each histologic type of proliferative lesion and neoplasm were stained by the avidin-biotin complex immunoperoxidase method using antibodies to rat surfactant apoprotein and Clara cell antigen. Rat surfactant apoprotein immunostaining was detected in type II pneumocytes in sections of normal lung, in the cells of the proliferative lesions classified histologically as alveolar epithelial hyperplasia (51) and mixed foci (alveolar epithelial hyperplasia with fibrosis) (30), and in adenomas (2), adenocarcinomas (3), and adenosquamous carcinomas (2). With the exception of one adenosquamous carcinoma, Clara cell antigen immunostaining was not detected in any of the pulmonary lesions but was detected in nonciliated cuboidal epithelial (Clara) cells in normal bronchioles. The epithelial cells of the proliferative lesions and neoplasms had ultrastructural features consistent with type II pneumocytes, i.e., the presence of cytoplasmic lamellar and multivesicular bodies. The results of these studies indicate that the majority of plutonium-induced proliferative epithelial lesions and neoplasms in the rat originate from alveolar type II pneumocytes.

scholarly journals Increased Extracellular Matrix Protein Production in Chronic Diabetic Complications: Implications of Non-Coding RNAs

2019 ◽  
Vol 5 (1) ◽  
pp. 30 ◽  
Author(s):  
Saumik Biswas ◽  
Subrata Chakrabarti
Keyword(s):  
Extracellular Matrix ◽  
Diabetic Complications ◽  
Matrix Protein ◽  
Organ Damage ◽  
Endothelial Damage ◽  
Extracellular Matrix Protein ◽  
Quiescent State ◽  
Ecm Proteins ◽  
Non Coding Rnas ◽  
Characteristic Features

Management of chronic diabetic complications remains a major medical challenge worldwide. One of the characteristic features of all chronic diabetic complications is augmented production of extracellular matrix (ECM) proteins. Such ECM proteins are deposited in all tissues affected by chronic complications, ultimately causing organ damage and dysfunction. A contributing factor to this pathogenetic process is glucose-induced endothelial damage, which involves phenotypic transformation of endothelial cells (ECs). This phenotypic transition of ECs, from a quiescent state to an activated dysfunctional state, can be mediated through alterations in the synthesis of cellular proteins. In this review, we discussed the roles of non-coding RNAs, specifically microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), in such processes. We further outlined other epigenetic mechanisms regulating the biogenesis and/or function of non-coding RNAs. Overall, we believe that better understanding of such molecular processes may lead to the development of novel biomarkers and therapeutic strategies in the future.

scholarly journals Vascular Endothelial Damage: The Role of Syndecan-1 and Hyaluronan as Severity Indicators in COVID-19

2021 ◽  
Vol 2 (5) ◽  
Author(s):  
Azwar Anas ◽  
Arie Utariani ◽  
Bambang Pujo Semedi
Keyword(s):  
Distress Syndrome ◽  
Cell Damage ◽  
Organ Damage ◽  
Endothelial Damage ◽  
Vascular Endothelial ◽  
Vascular Integrity ◽  
Mural Cells ◽  
Coagulation Inhibitors ◽  
Hypoxic Respiratory Failure

SARS-CoV-2 was firstly found in bronchoalveloar lavage (BAL) of three suspected COVID-19 patients at Jinyintan Hospital, Wuhan, Hubei Province, China. The cases are still raisingwith2,12% global mortality rate. Hypoxic respiratory failure due to acute respiratory distress syndrome (ARDS) is the main cause of COVID-19 death. Endothelial cell damage has an important role in the pathogenesis of ARDS and multi-organ dysfuntion of COVID-19 patients. The endothelium is protected by mural cells, which keep vascular integrity. Inflammation is prevented by these cells by inhibiting the interaction of immune cells and platelets with endothelial cells. These cells also prevent coagulation by producing glycocalyx, coagulation inhibitors, and blood-clotting enzyme. Vascular glycocalyx has an important role to maintain endothelial function and is disrupted systemically in elderly and patients with various comorbidities, which can be a probable mechanism for the serious complications of COVID-19. Glycocalyx disruption in severe and critical COVID-19 patients causes increased levels of its components such assyndecan-1 and hyaluronan in the serum. Previous studies showed the significant increase ofsyndecan-1 and hyaluronan levels in septic, and severe Kawasaki and dengue patients. These biomarkers are also markers of organ damage. Therefore, hyaluronan and syndecan-1can be significant prognostic factors for morbidity and survival in patients with COVID-19.

scholarly journals Malignant hypertension and hypertensive emergencies.

1998 ◽  
Vol 9 (1) ◽  
pp. 133-142 ◽  
Author(s):  
C Kitiyakara ◽  
N J Guzman
Keyword(s):  
Damage Control ◽  
Organ Damage ◽  
Endothelial Damage ◽  
Target Organ ◽  
Malignant Hypertension ◽  
Organ Function ◽  
Hypertensive Urgency ◽  
Hypertensive Emergencies ◽  
Oral Agents ◽  
Hypertensive Urgencies

Hypertensive emergencies and urgencies are important causes of morbidity and mortality. Malignant hypertension is a hypertensive urgency characterized by grade III/IV retinopathy and widespread endothelial damage. Control of BP is essential in the treatment of these disorders. The effects of hypertension on target organ function need to be balanced against the risks of excessive BP lowering. In hypertensive emergencies, BP should be lowered within minutes with parenteral agents to prevent critical end-organ damage. In hypertensive urgencies, BP can be lowered more slowly over several hours, often with oral agents, to avoid a detrimental fall in BP. The absolute indications for treatment and the optimal therapy depend on the underlying condition.

scholarly journals Krebs von den Lungen 6 levels in COVID-19 ICU Patients are Associated with Mortality

2021 ◽  
Author(s):  
Giuliana Scarpati ◽  
Daniela Baldassarre ◽  
Graziella Lacava ◽  
Filomena Oliva ◽  
Gabriele Pascale ◽  
...  
Keyword(s):  
Cox Regression ◽  
Icu Patients ◽  
Cox Regression Analysis ◽  
Alveolar Epithelial ◽  
Type Ii Pneumocytes ◽  
Group A ◽  
Predictive Role ◽  
Fraction Of Inspired Oxygen ◽  
Group B

Rationale Krebs von den Lungen 6 (KL-6) is a high molecular weight mucin-like glycoprotein produced by type II pneumocytes and bronchial epithelial cells. Elevated circulating levels of KL-6 may denote disorder of the alveolar epithelial lining. Objective Aim of this study was to verify if KL-6 values may help to risk stratify and triage severe COVID-19 patients. Methods We performed a retrospective prognostic study on 110 COVID-19 ICU patients, evaluating the predictive role of KL-6 for mortality. Measurements and Main Results The study sample was divided in two groups related according to the median KL-6 value [Group A (KL-6 lower than the log-transformed median (6.73)) and Group B (KL-6 higher than the log-transformed median)]. In both linear and logistic multivariate analyses, ratio of arterial partial pressure of oxygen to fraction of inspired oxygen (P/F) was significantly and inversely related to KL-6. Death rate was higher in group B than in group A (80.3 versus 45.9%) (p<0.001), Accordingly, the Cox regression analysis showed a significant prognostic role of KL-6 on mortality in the whole sample as well as in the subgroup with SOFA lower than its median value. Conclusions At ICU admission, KL-6 serum level was significantly lower in the survivors group. Our findings shown that, in severe COVID19 patients, elevated KL-6 was strongly associated with mortality in ICU.

scholarly journals Seroconversion stages COVID19 into distinct pathophysiological states

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Matthew D Galbraith ◽  
Kohl T Kinning ◽  
Kelly D Sullivan ◽  
Ryan Baxter ◽  
Paula Araya ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Medical Condition ◽  
Organ Damage ◽  
Endothelial Damage ◽  
Targeted Therapeutics ◽  
Cross Sectional ◽  
Ifn Alpha ◽  
Antibody Titers ◽  
Clinical Trial Results ◽  
B Cell Subsets

COVID19 is a heterogeneous medical condition involving diverse underlying pathophysiological processes including hyperinflammation, endothelial damage, thrombotic microangiopathy, and end-organ damage. Limited knowledge about the molecular mechanisms driving these processes and lack of staging biomarkers hamper the ability to stratify patients for targeted therapeutics. We report here the results of a cross-sectional multi-omics analysis of hospitalized COVID19 patients revealing that seroconversion status associates with distinct underlying pathophysiological states. Low antibody titers associate with hyperactive T cells and NK cells, high levels of IFN alpha, gamma and lambda ligands, markers of systemic complement activation, and depletion of lymphocytes, neutrophils, and platelets. Upon seroconversion, all of these processes are attenuated, observing instead increases in B cell subsets, emergency hematopoiesis, increased D-dimer, and hypoalbuminemia. We propose that seroconversion status could potentially be used as a biosignature to stratify patients for therapeutic intervention and to inform analysis of clinical trial results in heterogenous patient populations.

Stimulation of phosphatidylcholine hydrolysis in type II alveolar epithelial cells

1992 ◽  
Vol 263 (1) ◽  
pp. L42-L50
Author(s):  
L. C. Dubrovin ◽  
L. A. Brown
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Kinase C ◽  
Type Ii Pneumocytes ◽  
Stimulation Of ◽  
In Cells

The effects of phorbol 12-myristate 13-acetate (TPA) or ATP on phosphatidylcholine (PC) hydrolysis were investigated in cultured type II pneumocytes prelabeled with [3H]choline or 1-O-[3H]octadecyl-sn-glycero-3-phosphocholine ([3H]lyso-PAF). In cells prelabeled with [3H]choline, TPA or ATP stimulated an increase in [3H]choline, [3H]phosphocholine, and [3H]glycerophosphocholine. The formation of these choline metabolites was associated with a concomitant loss of [3H]PC but not from disaturated PC or phosphatidylinositol. In cells prelabeled with [3H]lyso-PAF, the formation of [3H]phosphatidic acid (PA) and then [3H]1,2-DG was stimulated by TPA or ATP and was associated with a loss of 3H from PC but not from disaturated PC or phosphatidylinositol. There was a concentration-dependent formation of [3H]1,2-DG and [3H]PA in response to ATP. Downregulation of protein kinase C with TPA abolished the stimulation of PC hydrolysis. In addition to the generation of metabolites indicative of phospholipase C and/or D activity, [3H]lyso-PC, a product of phospholipase A2, was also generated in response to TPA. These findings suggest an important role for PC breakdown in signal transduction in type II pneumocytes.

Inner surface ultrastructure of the lungs of frog and lizard

1978 ◽  
Vol 36 (2) ◽  
pp. 504-505
Author(s):  
R. F. Bils ◽  
G. M. Hughes
Keyword(s):  
Epithelial Cells ◽  
Random Network ◽  
Lung Surfactant ◽  
Cell Types ◽  
Alveolar Epithelial Cells ◽  
Lung Cells ◽  
Alveolar Epithelial ◽  
Inner Surface ◽  
Mammalian Lung ◽  
Lung Capillaries

Mammalian lung cells and tissues have been studied extensively, resulting in a voluminous literature. In comparison, the ultrastructure study of the respiratory systems of the lower vertebrates is incomplete. Lung surfactant and the related osmiophilic lamellar inclusions were observed in bird lung by Lambson and Cohn and in cultured frog lung cells by Soloff and Burns. This report compares the inner surface structure, cell types and vascularization in the lungs of frog and lizard.Mature Rana pipiens and Lacerta viviparus lungs were fixed at normal volumes (approximately 0. 3 ml and 0. 05 ml, respectively) with cacodylate-buffered glutaraldehyde, post-fixed with OsO4 and processed for both TEM and SEM.Frog LungLooking outward from the central duct, the septa divide the respiratory regions into smaller and smaller compartments, ending in closed sacs or alveoli, ranging from 150 to 300 mμ in diameter (Fig. 1). The largest or primary septa are covered by ciliated epithelium, whereas a squamous microvillous epithelium covers the minor septa and alveolar walls (Fig. 2). In section, the microvillous epithelial cells appear as a combination of type 1 and type 2 alveolar epithelial cells of the mammalian lung. Capillaries appeared as a random network through the septa and alveolar walls.

17β-Estradiol inhibits keratinocyte-derived chemokine production following trauma-hemorrhage

2007 ◽  
Vol 292 (2) ◽  
pp. L585-L591 ◽  
Author(s):  
Michael Frink ◽  
Bjoern M. Thobe ◽  
Ya-Ching Hsieh ◽  
Mashkoor A. Choudhry ◽  
Martin G. Schwacha ◽  
...  
Keyword(s):  
Kupffer Cell ◽  
Neutrophil Infiltration ◽  
Organ Damage ◽  
Sham Operation ◽  
Myeloperoxidase Activity ◽  
Edema Formation ◽  
Chemokine Production ◽  
Cell Production ◽  
Tnf Α ◽  
17Β Estradiol

Neutrophil infiltration is a key step in the development of organ dysfunction following trauma-hemorrhage (T-H). Although we have previously shown that 17β-estradiol (E2) prevents neutrophil infiltration and organ damage following T-H, the mechanism by which E2 inhibits neutrophil transmigration remains unknown. We hypothesized that E2 prevents neutrophil infiltration via modulation of keratinocyte-derived chemokine (KC), a major attractant for neutrophils. To examine this, male C3H/HeN mice were subjected to T-H or sham operation and thereafter resuscitated with Ringer lactate and E2 (1 mg/kg body wt) or vehicle. Animals were killed 2 h after resuscitation, and Kupffer cells were isolated. Plasma levels and Kupffer cell production capacities of KC, TNF-α, and IL-6 were determined by BD Cytometric Bead Arrays; lung mRNA expression of KC was measured with real-time PCR; myeloperoxidase activity assays were performed to determine neutrophil infiltration, and organ damage was assessed by edema formation. Treatment with E2 decreased systemic levels and restored Kupffer cell production of KC, TNF-α, and IL-6, as well as KC gene expression and protein in the lung. This was accompanied with a decrease in neutrophil infiltration and edema formation in the lung. These results suggest that E2 prevents lung neutrophil infiltration and organ damage in part by decreasing KC during posttraumatic immune response.

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