scholarly journals Expression of COX-2, HMGB-1 and CD68 in lung tissue in sheep fibrinous bronchopneumonia

2020 ◽  
Vol 76 (01) ◽  
pp. 6341-2020
Author(s):  
ORHAN YAVUZ ◽  
GÜNGÖR ÇAĞDAŞ DINÇEL
Keyword(s):  
Lung Tissue ◽  
Inflammatory Cell ◽  
High Mobility ◽  
Goblet Cells ◽  
Medicine Department ◽  
Respiratory Problems ◽  
Immunohistochemical Methods ◽  
Cox 2 ◽  
First Time ◽  
Interalveolar Septum

This study aimed to determine the expression of some cytokines, such as cyclooxygenase-2 (COX-2), High Mobility Group Box-1 (HMGB-1) and CD68, in the lung tissue of sheep with fibrinous bronchopneumonia by immunohistochemical methods. Forty sheep which had suffered from respiratory problems were brought for necropsy to the Faculty of Veterinary Medicine, Department of Pathology, Aksaray University, between November 2014 and December 2017. After necropsy, lung tissues grossly diagnosed with fibrinous bronchopneumonia were processed histologically, and stained histopathologically and immunohistochemically. Bacteriological culture was also applied to the lung tissues to isolate the agents. In histopathological examinations, congestion, red consolidation and grey consolidation stages were detected in the lung tissues. In such cases, we observed fibrin masses accumulated in some alveolar lumens, as well as inflammatory cell infiltrations of various extent in alveolar and bronchiolar lumens. In the interalveolar septum, a thickening was observed due to a fibrin mass and thrombotic vessels. Immunohistochemically, it was determined that COX-2 and HMGB-1 cytokines showed positive reactions, especially in bronchial, bronchiolar and alveolar epithelia, as well as goblet cells and macrophages. CD68 was found to be expressed in alveolar macrophages. COX-2 and HMGB-1, which have been implicated in the inflammatory response, were also shown to be expressed in fibrinous bronchopneumonia in sheep for the first time. Thus, these cytokines are thought to play a role in the pathogenesis of the disease. Moreover, their increased expression suggests that it may be helpful in the diagnosis of the disease.

scholarly journals Effect of Qinbai Qingfei Concentrated Pellets on substance P and neutral endopeptidase of rats with post-infectious cough

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Weigang Jia ◽  
Wei Wang ◽  
Rui Li ◽  
Quanyu Zhou ◽  
Ying Qu ◽  
...  
Keyword(s):  
Substance P ◽  
Inflammatory Cytokines ◽  
Lung Tissue ◽  
Inflammatory Cell ◽  
Neutral Endopeptidase ◽  
Inflammatory Cell Infiltration ◽  
Lung Damage ◽  
Cell Infiltration ◽  
Cough Frequency ◽  
Post Infectious

Abstract Background In recent years, it has been reported that Qinbai Qingfei Concentrated Pellet (QQCP) has the effect of relieving cough and reducing sputum. However, the therapeutic potentials of QQCP on post-infectious cough (PIC) rat models has not been elucidated. So the current study was aimed to scientifically validate the efficacy of QQCP in post infectious cough. Methods All rats were exposed to sawdust and cigarette smokes for 10 days, and intratracheal lipopolysaccharide (LPS) and capsaicin aerosols. Rats were treated with QQCP at dose of 80, 160, 320 mg/kg. Cough frequency was monitored twice a day for 10 days after drug administration. Inflammatory cell infiltration was determined by ELISA. Meanwhile, the histopathology of lung tissue and bronchus in rats were evaluated by hematoxylin-eosin staining (H&E). Neurogenetic inflammation were measured by ELISA and qRT-PCR. Results QQCP dose-dependently decreased the cough frequency and the release of pro-inflammatory cytokines TNF-α, IL-1β, IL-6 and IL-8, but exerted the opposite effects on the secretion of anti-inflammatory cytokines IL-10 and IL-13 in BALF and serum of PIC rats. The oxidative burden was effectively ameliorated in QQCP-treated PIC rats as there were declines in Malondialdehyde (MDA) content and increases in Superoxide dismutase (SOD) activity in the serum and lung tissue. In addition, QQCP blocked inflammatory cell infiltration into the lung as evidenced by the reduced number of total leukocytes and the portion of neutrophils in the broncho - alveolar lavage fluid (BALF) as well as the alleviated lung damage. Furthermore, QQCP considerable reversed the neurogenetic inflammation caused by PIC through elevating neutral endopeptidase (NEP) activity and reducing Substance P (SP) and Calcitonin gene related peptide (CGRP) expression in BALF, serum and lung tissue. Conclusions Our study indicated that QQCP demonstrated a protective role of PIC and may be a potential therapeutic target of PIC.

scholarly journals Streptococcus suis Induces Expression of Cyclooxygenase-2 in Porcine Lung Tissue

2021 ◽  
Vol 9 (2) ◽  
pp. 366
Author(s):  
Muriel Dresen ◽  
Josephine Schenk ◽  
Yenehiwot Berhanu Weldearegay ◽  
Désirée Vötsch ◽  
Wolfgang Baumgärtner ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Streptococcus Suis ◽  
Cyclooxygenase 2 ◽  
Economic Losses ◽  
Biological Processes ◽  
Alveolar Tissue ◽  
Cox 2 ◽  
Ciliated Epithelial Cells ◽  
Immunohistological Analysis

Streptococcus suis is a common pathogen colonising the respiratory tract of pigs. It can cause meningitis, sepsis and pneumonia leading to economic losses in the pig industry worldwide. Cyclooxygenase-2 (COX-2) and its metabolites play an important regulatory role in different biological processes like inflammation modulation and immune activation. In this report we analysed the induction of COX-2 and the production of its metabolite prostaglandin E2 (PGE2) in a porcine precision-cut lung slice (PCLS) model. Using Western blot analysis, we found a time-dependent induction of COX-2 in the infected tissue resulting in increased PGE2 levels. Immunohistological analysis revealed a strong COX-2 expression in the proximity of the bronchioles between the ciliated epithelial cells and the adjacent alveolar tissue. The morphology, location and vimentin staining suggested that these cells are subepithelial bronchial fibroblasts. Furthermore, we showed that COX-2 expression as well as PGE2 production was detected following infection with two prevalent S. suis serotypes and that the pore-forming toxin suilysin played an important role in this process. Therefore, this study provides new insights in the response of porcine lung cells to S. suis infections and serves as a basis for further studies to define the role of COX-2 and its metabolites in the inflammatory response in porcine lung tissue during infections with S. suis.

Rgx365, a Rare Protopanaxatriol-Type Ginsenoside Fraction from Black Ginseng, Suppresses Inflammatory Gene iNOS via the Iinhibition of p-STAT-1 and NF-κB

2020 ◽  
Vol 48 (05) ◽  
pp. 1091-1102
Author(s):  
So Yeon Jeong ◽  
Ji-Eun Kim ◽  
Gyu-Yong Song ◽  
Jong-Sup Bae
Keyword(s):  
Lung Tissue ◽  
Lavage Fluid ◽  
Heme Oxygenase 1 ◽  
Inos Protein ◽  
Protein Levels ◽  
Rna Transfection ◽  
Inos Protein Expression ◽  
Black Ginseng ◽  
Cox 2 ◽  
Human Pulmonary Artery

Black ginseng (BG), which is ginseng that has been steamed and dried nine times, and its main protopanaxatriol-type ginsenosides Rg4, Rg6, Rh4, and Rg2 have been reported to exhibit various forms of biological activity, including antiseptic, antidiabetic, wound-healing, immune-stimulatory, and anti-oxidant activity. The aim of the this study was to examine the effects of [Formula: see text] (a rare protopanaxatriol-type ginsenoside fraction; Rg2, Rg4, Rg6, Rh1, and Rh4) on heme oxygenase-1 (HO-1) induction and on the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-)2 in lipopolysaccharide (LPS)-activated human pulmonary artery endothelial cells (HPAECs). [Formula: see text] was tested to determine its effect on iNOS protein expression and inflammatory markers (interleukin [IL]-1[Formula: see text] and tumor necrosis factor [TNF]-[Formula: see text] in the lung tissue of LPS-treated mice. The results showed that [Formula: see text] induced the expression of HO-1, reduced LPS-activated NF-[Formula: see text]B-luciferase activity, and inhibited iNOS/NO and COX-2/PGE2, which contributed to the inhibition of STAT-1 phosphorylation. In particular, [Formula: see text] induced the translocation of Nrf2 from the cytosol to the nucleus by increasing Nrf2-ARE activity and decreased IL-1[Formula: see text] production in LPS-activated HPAECs. This reduction in iNOS/NO expression due to [Formula: see text] was reversed by siHO-1 RNA transfection. In LPS-treated mice, [Formula: see text] significantly reduced lung tissue iNOS protein levels and TNF-[Formula: see text] levels in the bronchoalveolar lavage fluid. In conclusion, these findings indicate that [Formula: see text] has a critical anti-inflammatory effect due to its ability to regulate iNOS via the inhibition of p-STAT-1 and NF-[Formula: see text]B, and thus it may be suitable for the treatment of inflammatory disease.

scholarly journals Morpho-Functional Alterations in the Gills of a Seawater Teleost, the Ornate Wrasse (Thalassoma pavo L.), after Short-Term Exposure to Chlorpyrifos

Toxics ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 97
Author(s):  
Rachele Macirella ◽  
Vittoria Curcio ◽  
Elvira Brunelli
Keyword(s):  
Goblet Cells ◽  
High Concentration ◽  
Short Term ◽  
Cell Degeneration ◽  
Widespread Species ◽  
Pillar Cell ◽  
Secondary Lamellae ◽  
Short Term Exposure ◽  
First Time ◽  
Sublethal Concentrations

Chlorpyrifos (CPF) is an organophosphorus insecticide commonly used for domestic and agricultural purposes. The risk posed by environmental contamination from CPF is well acknowledged, and it has been detected worldwide in aquatic habitats and coastal areas. In addition, due to its slower degradation in seawater compared to freshwater, CPF is of particular concern for marine environments. Here, we investigated for the first time the morpho-functional alterations induced by CPF on the gills of Thalassoma pavo, a widespread species in the Mediterranean Sea. We tested the effects of two sublethal concentrations (4 and 8 µg/L) after 48 and 96 h. Our study demonstrates that the alterations induced by CPF are dose and time-dependent and highlight the harmful properties of this insecticide. After exposure to the low tested concentration, the more frequent alteration is an intense proliferation of the primary epithelium, whereas after exposure to the high concentration, the primary epithelium proliferation is less extensive, and the most evident effects are the thinning of secondary lamellae and the ectopia of chloride and goblet cells. CPF also modulated the expression of Na+/K+-ATPase. Dilation of lamellar apical tips, pillar cell degeneration, and appearance of aneurysms are often observed.

scholarly journals Structural Basis of Enantioselective Inhibition of Cyclooxygenase-1 by S-α-Substituted Indomethacin Ethanolamides

2007 ◽  
Vol 282 (38) ◽  
pp. 28096-28105 ◽  
Author(s):  
Christine A. Harman ◽  
Melissa V. Turman ◽  
Kevin R. Kozak ◽  
Lawrence J. Marnett ◽  
William L. Smith ◽  
...  
Keyword(s):  
Binding Pocket ◽  
Drug Binding ◽  
Structural Basis ◽  
Cyclooxygenase 1 ◽  
Cox 2 ◽  
The Impact ◽  
First Time ◽  
Side Pocket ◽  
Cox 1 ◽  
Equal Efficacy

The modification of the nonselective nonsteroidal anti-inflammatory drug, indomethacin, by amidation presents a promising strategy for designing novel cyclooxygenase (COX)-2-selective inhibitors. A series of α-substituted indomethacin ethanolamides, which exist as R/S-enantiomeric pairs, provides a means to study the impact of stereochemistry on COX inhibition. Comparative studies revealed that the R- and S-enantiomers of the α-substituted analogs inhibit COX-2 with almost equal efficacy, whereas COX-1 is selectively inhibited by the S-enantiomers. Mutagenesis studies have not been able to identify residues that manifest the enantioselectivity in COX-1. In an effort to understand the structural impact of chirality on COX-1 selectivity, the crystal structures of ovine COX-1 in complexes with an enantiomeric pair of these indomethacin ethanolamides were determined at resolutions between 2.75 and 2.85Å. These structures reveal unique, enantiomer-selective interactions within the COX-1 side pocket region that stabilize drug binding and account for the chiral selectivity observed with the (S)-α-substituted indomethacin ethanolamides. Kinetic analysis of binding demonstrates that both inhibitors bind quickly utilizing a two-step mechanism. However, the second binding step is readily reversible for the R-enantiomer, whereas for the S-enantiomer, it is not. These studies establish for the first time the structural and kinetic basis of high affinity binding of a neutral inhibitor to COX-1 and demonstrate that the side pocket of COX-1, previously thought to be sterically inaccessible, can serve as a binding pocket for inhibitor association.

scholarly journals Sociodemography and Clinical Profile of COVID 19 Positive Physicians at a Tertiary Level Hospital, Dhaka

2020 ◽  
pp. 56-60
Author(s):  
Mohammad Rafiqul Islam ◽  
Khondaker Abul Bashar ◽  
Shariful Matin ◽  
Tahmid Tanveer ◽  
Atiqur Rahman ◽  
...  
Keyword(s):  
College Hospital ◽  
Personal Protection Equipment ◽  
Medicine Department ◽  
Medical College ◽  
First Case ◽  
Care Workers ◽  
High Infection ◽  
Epidemiological Characteristics ◽  
First Time ◽  
Body Ache

Introduction: On 11th March, 2020 COVID19 was declared as a pandemic and it currently involves 210 countries worldwide. Bangladesh declared its first case on 8th March 2020. Currently, the highest case detection of COVID is in the Dhaka district. Due to a lack of quality PPE (personal protection equipment) and proper knowledge of donning, doffing and transmission dynamics of COVID 19 thought to be high infection rate among physicians. Material and Methods: A pretested questionnaire was set and distributed among COVID 19 infected physicians working at Shaheed Suhrawardy Medical College Hospital through internet to know about the clinical and epidemiological characteristics. Results: 65.3% of the respondents were male and had a mean age were 35.7 years. Among all the respondents, the highest number of physicians involved were from medicine department (26.9%). Lethargy, body ache and fever were observed in 57.69%, 50% and 30.7% patients respectively. Among 52 infected physicians, first time RT-PCR for COVID 19 yield 78.8% positive results. Prophylactic dose of hydroxychloroquine taken by 15.3% patients before being infected with COVID19. Conclusion: Health care workers are getting infected in a alarming number but fortunately at Shaheed Suhrawardy Medical college all the cases were in mild form. J Bangladesh Coll Phys Surg 2020; 38(0): 56-60

Mucin secretion and PKC isoforms in SPOC1 goblet cells: differential activation by purinergic agonist and PMA

2003 ◽  
Vol 285 (1) ◽  
pp. L149-L160 ◽  
Author(s):  
Lubna H. Abdullah ◽  
Jason T. Bundy ◽  
Camille Ehre ◽  
C. William Davis
Keyword(s):  
Goblet Cells ◽  
Independent Effect ◽  
Rt Pcr ◽  
Mucin Secretion ◽  
Binding Partner ◽  
Pkc Isoforms ◽  
C1 Domain ◽  
Phorbol Ester Receptor ◽  
Enzyme Mapping ◽  
First Time

SPOC1 cells, which are a mucin-secreting model of rat airway goblet cells, possess a luminal P2Y2 purinoceptor through which UTP, ATP, and ATPγS stimulate secretion with EC50 values of ∼3 μM. PMA elicits mucin secretion with high EC50 (75 nM) and saturation (300 nM) values. For the first time in airway mucin-secreting cells, the PKC isoforms expressed and activated by a secretagogue were determined using RT-PCR/restriction-enzyme mapping and Western blotting. Five isoforms were expressed: cPKCα, nPKCδ and -η, and aPKCζ and -ι/λ. PMA caused cPKCα and nPKCδ to translocate to the membrane fraction of SPOC1 cells; only nPKCδ so responded to ATPγS. Membrane-associated nPKCδ and mucin secretion increased in parallel with ATPγS concentration and yielded EC50 values of 2–3 μM and maximum values of 100 μM. Effects of PMA to increase membrane-associated cPKCα and nPKCδ saturated at 30 nM, whereas mucin secretion saturated at 300 nM, which suggests a significant PKC-independent effect of PMA on mucin secretion. A prime alternate phorbol ester-receptor candidate is the C1-domain protein MUNC13. RT-PCR revealed the expression of ubiquitous (ub)MUNC13-2 and its binding partner, DOC2-γ. Hence, P2Y2 agonists activate nPKCδ in SPOC1 cells. PMA activates cPKCα and nPKCδ at high affinity and stimulates a lower affinity PKC-independent pathway that leads to mucin secretion.

scholarly journals Protein S is Protective in Acute Lung Injury by Inhibiting Cell Apoptosis

2019 ◽  
Vol 20 (5) ◽  
pp. 1082 ◽  
Author(s):  
Prince Baffour Tonto ◽  
Taro Yasuma ◽  
Tetsu Kobayashi ◽  
Corina D’Alessandro-Gabazza ◽  
Masaaki Toda ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Transgenic Mice ◽  
Lung Tissue ◽  
Cell Apoptosis ◽  
Inflammatory Cell ◽  
Protein S ◽  
Inflammatory Cell Infiltration ◽  
Human Protein ◽  
Wild Type

Acute lung injury is a fatal disease characterized by inflammatory cell infiltration, alveolar-capillary barrier disruption, protein-rich edema, and impairment of gas exchange. Protein S is a vitamin K-dependent glycoprotein that exerts anticoagulant, immunomodulatory, anti-inflammatory, anti-apoptotic, and neuroprotective effects. The aim of this study was to evaluate whether human protein S inhibits cell apoptosis in acute lung injury. Acute lung injury in human protein S transgenic and wild-type mice was induced by intratracheal instillation of lipopolysaccharide. The effect of human protein S on apoptosis of lung tissue cells was evaluated by Western blotting. Inflammatory cell infiltration, alveolar wall thickening, myeloperoxidase activity, and the expression of inflammatory cytokines were reduced in human protein S transgenic mice compared to the wild-type mice after lipopolysaccharide instillation. Apoptotic cells and caspase-3 activity were reduced while phosphorylation of extracellular signal-regulated kinase was enhanced in the lung tissue from human protein S transgenic mice compared to wild-type mice after lipopolysaccharide instillation. The results of this study suggest that human protein S is protective in lipopolysaccharide-induced acute lung injury by inhibiting apoptosis of lung cells.

Cyclooxygenase-2 Expression in Canine Mammary Tumors

2003 ◽  
Vol 40 (2) ◽  
pp. 207-212 ◽  
Author(s):  
M. Doré ◽  
I. Lanthier ◽  
J. Sirois
Keyword(s):  
Potential Role ◽  
Mammary Tumorigenesis ◽  
Mammary Tumors ◽  
Cyclooxygenase 2 ◽  
Benign Tumors ◽  
Normal Mammary Gland ◽  
Normal Gland ◽  
Canine Mammary Tumors ◽  
Cox 2 ◽  
First Time

Mammary tumors are the most common neoplasms in female dogs. Induction of cyclooxygenase-2 (COX-2) has been implicated in various cancers in humans. However, expression of COX-2 has not been investigated in canine mammary tumors. Normal mammary gland ( n = 4), simple or complex adenomas ( n = 63), and simple or complex adenocarcinomas ( n = 84) were studied by immunohistochemistry. Results showed that COX-2 was not expressed in the normal gland but was detected in 24% of adenomas and in 56% of adenocarcinomas ( P < 0.001). The incidence of COX-2 expression and the intensity of the COX-2 signal were higher in adenocarcinomas than in adenomas ( P < 0.001). These results demonstrate for the first time that COX-2 is induced in a proportion of canine mammary tumors and that COX-2 expression is more frequent and more intense in malignant than in benign tumors, suggesting a potential role for COX-2 in canine mammary tumorigenesis.

scholarly journals Comparative Analysis of Pharmacologic and/or Genetic Disruption of Cyclooxygenase-1 and Cyclooxygenase-2 Function in Female Reproduction in Mice*

Endocrinology ◽  
2001 ◽  
Vol 142 (7) ◽  
pp. 3198-3206 ◽  
Author(s):  
Jeff Reese ◽  
Xuemei Zhao ◽  
Wen-Ge Ma ◽  
Naoko Brown ◽  
Timothy J. Maziasz ◽  
...  
Keyword(s):  
Early Pregnancy ◽  
Synergistic Effects ◽  
Female Reproduction ◽  
Cox Inhibitors ◽  
Cyclooxygenase 1 ◽  
Simultaneous Inhibition ◽  
Cox 2 ◽  
Alternative Sources ◽  
First Time ◽  
Cox 1

Abstract Cyclooxygenase (COX)-derived prostaglandins are critical in female reproduction. Gene targeting studies show that ovulation, fertilization, implantation, and decidualization are defective in COX-2 deficient mice. We used genetic and pharmacologic approaches to perturb COX function and examine the differential and synergistic effects of inhibition of COX-1, COX-2, or of both isoforms on reproductive outcomes during early pregnancy in mice. The results demonstrate that simultaneous inhibition of COX-1 and COX-2 produces more severe effects on early pregnancy events than inhibition of either isoform alone. The effects of pharmacological inhibition of COX-2 on female reproductive functions were less severe than the null mutation of the COX-2 gene. A combined approach showed that COX-2 inhibition in COX-1−/− mice induced complete reproductive failure, suggesting a lack of alternative sources of prostaglandin synthesis. This investigation raises caution regarding the indiscriminate use of COX inhibitors and shows for the first time the distinct and overlapping pathways of the cyclooxygenase systems in female reproduction.

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