Streptococcus suis induces expression of cyclooxygenase-2 in porcine lung tissue

Streptococcus suis is a common pathogen colonizing 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 modulation of inflammation 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 infection with S. suis.

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

Microorganisms ◽

10.3390/microorganisms9020366 ◽

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.

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The role of cyclooxygenase-2 on endurance exercise training in female LDL-receptor knockout ovariectomized mice

Anais da Academia Brasileira de Ciências ◽

10.1590/s0001-37652013005000046 ◽

2013 ◽

Vol 85 (3) ◽

pp. 1157-1164 ◽

Cited By ~ 3

Author(s):

FLAVIA DE OLIVEIRA ◽

LAURA B.M. MAIFRINO ◽

GUSTAVO P.P. DE JESUS ◽

JULIANA G. CARVALHO ◽

CLAUDIA MARCHON ◽

...

Keyword(s):

Cardiovascular Risk ◽

Exercise Training ◽

Ldl Receptor ◽

Density Lipoprotein ◽

Cyclooxygenase 2 ◽

Sedentary Control ◽

Down Regulation ◽

Ovariectomized Mice ◽

Cox 2

Estrogen deprivation in postmenopausal women increases cardiovascular risk. Cardiovascular risk as a result of atherosclerosis is able to induce an inflammatory disease as far as cyclooxygenase-2 ( COX-2) expression. The purpose of the study was to investigate the role of COX-2 on exercise training in female mice low-density lipoprotein receptor knockout ( LDL-KO) with or without ovariectomy. A total of 15 female C57BL/6 mice and 15 female LDL-KO mice were distributed into 6 groups: sedentary control, sedentary control ovariectomized, trained control ovariectomized, LDL-KO sedentary, LDL-KO sedentary ovariectomized and LDL-KO trained ovariectomized. The ascending part of the aorta was stained with H&E and COX-2 expression was assessed by immunohistochemistry. Results revealed that ovariectomy as well as exercise training were not able to induce histopathological changes in mouse aorta for all groups investigated. LDL-KO mice demonstrated plaque containing cholesterol clefts, foamy histiocytes and mild inflammatory process for all groups indistinctly. Ovariectomy induced a strong immunoexpression in atherosclerosis lesion of LDL-KO mice. Nevertheless, a down-regulation of COX-2 expression was detected in LDL-KO trained ovariectomized when compared to LDL-KO sedentary. Our results are consistent with the notion that exercise training is able to modulate COX-2 expression in LDL-KO mice as a result of COX-2 down-regulation.

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The Role of Propolis in Pulp Pain by Inhibiting Cyclooxygenase-2 Expression

Conservative Dentistry Journal ◽

10.20473/cdj.v11i1.2021.11-18 ◽

2021 ◽

Vol 11 (1) ◽

pp. 11

Author(s):

Ira Widjiastuti ◽

Widya Saraswati ◽

Annisa Rahma

Keyword(s):

Side Effects ◽

Pain Relief ◽

Inflammatory Pain ◽

Cyclooxygenase 2 ◽

Propolis Extract ◽

In Silico Studies ◽

Cox 2

Background: Inflammation of the pulp can lead to elicit pain. Pain in inflammation is induced by the cyclooxygenase-2 enzyme (COX-2) which induces prostaglandin E2 (PGE2) resulting in pain. Pain in the pulp can be relieved by eugenol. In its application, eugenol is toxic to pulp fibroblasts. Due to the side effect, it is worth considering other biocompatible materials with minimal side effects, such as propolis. Flavonoids and phenolic acids that contained in propolis can inhibit COX-2. Therefore, an analysis outlined in the literature review is needed to examine the results of research related to the role of propolis as pulp pain relief by inhibiting COX-2 expression. Purpose: To analyze the role of propolis in pulp pain by inhibiting COX-2 expression. Reviews: Propolis extract that extracted by ethanol, water, and hydroalcohol has pain relief properties in the pulp by inhibiting COX-2 by directly binding to the COX-2 receptors and by reducing the production of proinflammatory cytokines which are COX-2 inducers, proven through in vivo, in vitro, and in silico studies in various target cell organs. Conclusion: Propolis extract has high prospect as inflammatory pain inhibitor in the pulp by inhibit COX-2 expression.

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Role of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) derived prostaglandins (PG) in adaptive cytoprotection induced by mild stress

Gastroenterology ◽

10.1016/s0016-5085(98)80332-6 ◽

1998 ◽

Vol 114 ◽

pp. A82

Author(s):

T. Brzozowski ◽

P.C. Konturek ◽

R. Pajdo ◽

N. Nagraba ◽

A. Szczeklik ◽

...

Keyword(s):

Cyclooxygenase 2 ◽

Mild Stress ◽

Adaptive Cytoprotection ◽

Cyclooxygenase 1 ◽

Cox 2 ◽

Cox 1

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A role for cyclooxygenase-2 in lipopolysaccharide-induced anorexia in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00200.2002 ◽

2002 ◽

Vol 283 (4) ◽

pp. R862-R868 ◽

Cited By ~ 59

Author(s):

F. Lugarini ◽

B. J. Hrupka ◽

G. J. Schwartz ◽

C. R. Plata-Salaman ◽

W. Langhans

Keyword(s):

Cerebrospinal Fluid ◽

Cyclooxygenase 2 ◽

Major Metabolite ◽

Time Dependent ◽

Selective Inhibitors ◽

Cox 2 ◽

Cox 1

Because nonselective cycloooxygenase (COX) inhibition attenuated anorexia after lipopolysaccharide (LPS) administration, we tested the ability of resveratrol (2.5, 10, and 40 mg/kg) and NS-398 (2.5, 10, and 40 mg/kg), selective inhibitors of the two COX isoforms COX-1 and -2, respectively, to attenuate LPS (100 μg/kg ip)-induced anorexia. NS-398 (10 and 40 mg/kg) administered with LPS at lights out attenuated LPS-induced anorexia, whereas resveratrol at all doses tested did not. Because prostaglandin (PG) E2 is considered the major metabolite synthesized by COX, we measured plasma and cerebrospinal fluid (CSF) PGE2levels after LPS administration. LPS induced a time-dependent increase of PGE2 in CSF but not in plasma. NS-398 (5, 10, and 40 mg/kg) blocked the LPS-induced increase in CSF PGE2, whereas resveratrol (10 mg/kg) did not. These results support a role of COX-2 in mediating the anorectic response to peripheral LPS and point at PGE2 as a potential neuromodulator involved in this response.

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Cyclooxygenase-2 expression in Warthin's tumour

The Journal of Laryngology & Otology ◽

10.1258/0022215054352117 ◽

2005 ◽

Vol 119 (7) ◽

pp. 515-518 ◽

Cited By ~ 2

Author(s):

A H C Loy ◽

T C Putti ◽

L K S Tan

Keyword(s):

Quantitative Analysis ◽

Parotid Gland ◽

Immunohistochemical Staining ◽

Cyclooxygenase 2 ◽

Duct System ◽

Salivary Duct ◽

Epithelial Component ◽

Warthin’S Tumour ◽

Cox 2

Objectives: To determine whether cyclooxygenase-2 (COX-2) is overexpressed in Warthin's tumours, and to characterize its pattern of expression.Methods: Twenty-one paraffin-embedded Warthin's tumour specimens were analysed by immunohistochemical staining for expression of human COX-2. Semi-quantitative analysis of the staining was performed.Results: In all of the specimens, we found that there was overexpression of COX-2 within the epithelial component of the tumours, with no expression in the lymphoid components. There was also overexpression of COX-2 in the salivary duct system of normal parotid tissue.Conclusions: Our results suggest that COX-2 is up-regulated in the epithelial component of Warthin's tumours. Our findings support the hypothesis that Warthin's tumours originate from heterotopic ductal epithelial cells of the parotid gland. The role of COX-2 expression in the pathogenesis of Warthin's tumours remains to be determined.

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ApoL1 renal risk variants induce aberrant THP-1 monocyte differentiation and increase eicosanoid production via enhanced expression of cyclooxygenase-2

AJP Renal Physiology ◽

10.1152/ajprenal.00254.2017 ◽

2018 ◽

Vol 315 (1) ◽

pp. F140-F150 ◽

Cited By ~ 9

Author(s):

Hewang Lee ◽

Hila Roshanravan ◽

Ying Wang ◽

Koji Okamoto ◽

Junghwa Ryu ◽

...

Keyword(s):

Gene Expression ◽

Specific Inhibitor ◽

Cyclooxygenase 2 ◽

Prostaglandin E ◽

Monocyte Differentiation ◽

Eicosanoid Production ◽

Gene And Protein Expression ◽

Cox 2 ◽

Tgf Β1

Apolipoprotein L1 ( ApoL1) genetic variants are strongly associated with kidney diseases. We investigated the role of ApoL1 variants in monocyte differentiation and eicosanoid production in macrophages, as activated tissue macrophages in kidney might contribute to kidney injury. In human monocyte THP-1 cells, transient overexpression of ApoL1 (G0, G1, G2) by transfection resulted in a 5- to 11-fold increase in CD14 and CD68 gene expression, similar to that seen with phorbol-12-myristate acetate treatment. All ApoL1 variants caused monocytes to differentiate into atypical M1 macrophages with marked increase in M1 markers CD80, TNF, IL1B, and IL6 and modest increase in the M2 marker CD163 compared with control cells. ApoL1-G1 transfection induced additional CD206 and TGFB1 expression, and ApoL1-G2 transfection induced additional CD204 and TGFB1 expression. Gene expression of prostaglandin E2 (PGE2) synthase and thromboxane synthase and both gene and protein expression of cyclooxygenase-2 (COX-2) were increased by ApoL1-G1 and -G2 variants compared with -G0 transfection. Higher levels of PGE2 and thromboxane B2, a stable metabolite of thromboxane A2, and transforming growth factor (TGF)-β1 were released into the supernatant of cultured THP-1 cells transfected with ApoL1-G1 and -G2, but not -G0. The increase in PGE2, thromboxane B2, and TGF-β1 was inhibited by COX-2-specific inhibitor CAY10404 but not by COX-1-specific inhibitor SC-560. These results demonstrate a novel role of ApoL1 variants in the regulation of monocyte differentiation and eicosanoid metabolism, which could modify the immune response and promote inflammatory signaling within the local targeted organs and tissues including the kidney.

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Immunohistochemical Expression of Cyclooxygenase 2 in Follicular Carcinomas of the Thyroid

Archives of Pathology & Laboratory Medicine ◽

10.5858/2005-129-736-ieocif ◽

2005 ◽

Vol 129 (6) ◽

pp. 736-741 ◽

Cited By ~ 5

Author(s):

Denise M. Haynik ◽

Richard A. Prayson

Keyword(s):

Follicular Adenoma ◽

Immunohistochemical Analysis ◽

Cyclooxygenase 2 ◽

Positive Staining ◽

Limited Data ◽

Immunohistochemical Expression ◽

Cox 2 ◽

Disease Free

Abstract Context.—Cyclooxygenase 2 (COX-2) has been shown to be up-regulated and/or overexpressed in a variety of human neoplasms. However, limited data exist on the role of COX-2 in follicular carcinomas of the thyroid. Studies in this area are potentially significant, since therapeutic agents that inhibit COX-2 are currently available and could play a role in treatment. Design.—A retrospective clinicopathologic review with COX-2 immunohistochemical staining of 34 follicular carcinomas and 7 follicular adenomas with incomplete capsular penetration was performed. Results.—The study included 41 patients (25 women; mean age, 50.9 years). All patients underwent gross total resection of the neoplasm. Fifteen carcinoma patients received adjuvant radiotherapy. Seven patients with follicular carcinomas developed recurrent disease: 3 patients were alive (mean follow-up, 10.1 years) and 4 patients died of metastatic disease (mean follow-up, 3.5 years). All remaining patients were disease free (mean follow-up, 5.9 years). Only 1 follicular adenoma with incomplete capsular penetration recurred (patient alive at 9 years). The remaining patients were disease free (mean follow-up, 4.9 years). The COX-2 staining was positive in 11 tumors (9 of 34 follicular carcinomas, 2 of 7 follicular adenomas with incomplete capsular penetration). A greater percentage of recurrences (36% COX-2 positive vs 13% COX-2 negative) and fatal tumors (18% COX-2 positive vs 7% COX-2 negative) occurred in patients who had COX-2–positive staining neoplasms. Conclusion.—Only a few follicular carcinomas (26%) and follicular adenomas with incomplete capsular penetration (29%) express COX-2 by immunohistochemical analysis. The data suggest that such expression of COX-2 may correlate with increased tumor recurrence and death; however, studies with larger numbers of patients will be needed to establish this.

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Interleukin (IL)-6, But Not IL-1, Induction in the Brain Downstream of Cyclooxygenase-2 Is Essential for the Induction of Febrile Response against Peripheral IL-1α

Endocrinology ◽

10.1210/en.2004-0054 ◽

2004 ◽

Vol 145 (11) ◽

pp. 5044-5048 ◽

Cited By ~ 26

Author(s):

Kyoko Kagiwada ◽

Dai Chida ◽

Tomoya Sakatani ◽

Masahide Asano ◽

Aya Nambu ◽

...

Keyword(s):

Prostaglandin E2 ◽

Cyclooxygenase 2 ◽

Signaling Cascade ◽

Endogenous Pyrogen ◽

Febrile Response ◽

Cox 2 ◽

The Brain ◽

Deficient Mice

Abstract IL-1 is an endogenous pyrogen produced upon inflammation or infection. Previously, we showed that, upon injection with turpentine, IL-1 is induced in the brain in association with the development of fever. The role of endogenous IL-1 in the brain and the signaling cascade to activate thermosensitive neurons, however, remain to be elucidated. In this report, febrile response was analyzed after peripheral injection of IL-1α. We found that a normal febrile response was induced even in IL-1α/β-deficient mice, indicating that production of IL-1 in the brain is not necessarily required for the response. In contrast, IL-6-deficient mice did not exhibit a febrile response. Cyclooxygenase (Cox)-2 expression in the brain was strongly induced 1.5 h after injection of IL-1α, whereas IL-6 expression was observed 3 h after the injection. Cox-2 expression in the brain was not influenced by IL-6 deficiency, whereas indomethacin, an inhibitor of cyclooxygenases, completely inhibited induction of IL-6. These observations suggest a mechanism of IL-1-induced febrile response in which IL-1 in the blood activates Cox-2, with the resulting prostaglandin E2 inducing IL-6 in the brain, leading to the development of fever.

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