scholarly journals Aeromonas hydrophila inhibits autophagy triggering cytosolic translocation of mtDNA which activates the pro-apoptotic caspase-1/IL-1β-nitric oxide axis in headkidney macrophages

Virulence ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 60-76
Author(s):  
Manmohan Kumar ◽  
Asha Shelly ◽  
Priyanka Dahiya ◽  
Atish Ray ◽  
Shibnath Mazumder
Keyword(s):  
Nitric Oxide ◽  
Aeromonas Hydrophila ◽  
Caspase 1

scholarly journals Diverse effects of nitric oxide reductase NorV on Aeromonas hydrophila virulence-associated traits under aerobic and anaerobic conditions

2019 ◽  
Vol 50 (1) ◽  
Author(s):  
Jin Liu ◽  
Yuhao Dong ◽  
Nannan Wang ◽  
Shuiyan Ma ◽  
Chengping Lu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Aeromonas Hydrophila ◽  
Dependent Manner ◽  
Nitric Oxide Reductase ◽  
Wild Type ◽  
Anaerobic Conditions ◽  
Aerobic Conditions ◽  
Significant Difference ◽  
Aerobic And Anaerobic ◽  
Aerobic And Anaerobic Conditions

Abstract NorV has been known to be an anaerobic nitric oxide reductase associated with nitric oxide (NO) detoxification. Recently, we showed that the norV gene of Aeromonas hydrophila was highly upregulated after co-culturing with Tetrahymena thermophila. Here, we demonstrated that the transcription and expression levels of norV were upregulated in a dose-dependent manner after exposure to NO under aerobic and anaerobic conditions. To investigate the roles of norV in resisting predatory protists and virulence of A. hydrophila, we constructed the norV gene-deletion mutant (ΔnorV). Compared to the wild type, the ΔnorV mutant showed no significant difference in growth at various NO concentrations under aerobic conditions but significantly stronger NO-mediated growth inhibition under anaerobic conditions. The deletion of norV exhibited markedly decreased cytotoxicity, hemolytic and protease activities under aerobic and anaerobic conditions. Also, the hemolysin co-regulated protein (Hcp) in the ΔnorV mutant showed increased secretion under aerobic conditions but decreased secretion under anaerobic conditions as compared to the wild-type. Moreover, the inactivation of norV led to reduced resistance to predation by T. thermophila, decreased survival within macrophages and highly attenuated virulence in zebrafish. Our data indicate a diverse role for norV in the expression of A. hydrophila virulence-associated traits that is not completely dependent on its function as a nitric oxide reductase. This study provides insights into an unexplored area of NorV, which will contribute to our understanding of bacterial pathogenesis and the development of new control strategies for A. hydrophila infection.

Involvement of Major Components from Sporothrix schenckii Cell Wall in the Caspase-1 Activation, Nitric Oxide and Cytokines Production During Experimental Sporotrichosis

2014 ◽  
Vol 179 (1-2) ◽  
pp. 21-30 ◽  
Author(s):  
Amanda Costa Gonçalves ◽  
Danielle Cardoso Geraldo Maia ◽  
Lucas Souza Ferreira ◽  
Luis Gustavo Silva Monnazzi ◽  
Pâmela Alegranci ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Wall ◽  
Sporothrix Schenckii ◽  
Caspase 1

scholarly journals Cytotoxins of the human pathogen Aeromonas hydrophila trigger, via the NLRP3 inflammasome, caspase-1 activation in macrophages

2010 ◽  
Vol 40 (10) ◽  
pp. 2797-2803 ◽  
Author(s):  
Andrea J. McCoy ◽  
Yukiko Koizumi ◽  
Claudia Toma ◽  
Naomi Higa ◽  
Vishva Dixit ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Aeromonas Hydrophila ◽  
Human Pathogen ◽  
Caspase 1

Piperine, a functional food alkaloid, exhibits inhibitory potential against TNBS-induced colitis via the inhibition of IκB-α/NF-κB and induces tight junction protein (claudin-1, occludin, and ZO-1) signaling pathway in experimental mice

2019 ◽  
Vol 39 (4) ◽  
pp. 477-491 ◽  
Author(s):  
G Guo ◽  
F Shi ◽  
J Zhu ◽  
Y Shao ◽  
W Gong ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tight Junction ◽  
Signaling Pathway ◽  
Nitrosative Stress ◽  
Nuclear Factor ◽  
Ultrastructural Studies ◽  
Caspase 1 ◽  
Tnf Α ◽  
Junction Protein ◽  
Cox 2

Background: Inflammatory bowel disease is a chronic immunoinflammatory disease of the gastrointestinal tract. Piperine, an alkaloid, has been reported to possess antioxidant, anti-inflammatory, antiapoptotic, and antiulcer potential. Aim: To elucidate the plausible mechanisms of action of piperine on experimental trinitrobenzenesufonic acid (TNBS)-induced colitis by assessing various biochemical, molecular, histological, and ultrastructural modifications. Methods: Colitis was induced in male Sprague–Dawley rats via intrarectal instillation of TNBS. Then, the rats were treated with piperine (10, 20, and 40 mg/kg, p.o.) for 14 days. Results: TNBS induced significant ( p < 0.05) colonic damage, which was assessed by disease activity index, macroscopic score, and stool consistency. The administration of piperine (20 and 40 mg/kg) significantly inhibited ( p < 0.05) these damages. Treatments with piperine (20 and 40 mg/kg) notably inhibited ( p < 0.05) the TNBS-induced elevation of oxido-nitrosative stress (superoxide dismutase, glutathione, malondialdehyde, and nitric oxide), 5-hydroxytryptamine, and hydroxyproline content in the colon. Furthermore, colonic inducible nitric oxide synthase (iNOs), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, interferon-gamma, and cyclooxygenase-2 (COX-2) messenger RNA (mRNA) expressions were upregulated after TNBS instillation and piperine (20 and 40 mg/kg) significantly attenuated ( p < 0.05) these elevated mRNA expressions. TNBS decreased the expressions of tight junction (TJ) protein (claudin-1, occludin, and zonula occludens-1 (ZO-1)) and increased the expressions of proapoptotic (caspase-1) protein. These expressions were markedly inhibited ( p < 0.05) by piperine treatment. Histological and ultrastructural studies of transmission electron microscopy suggested that piperine significantly ameliorated ( p < 0.05) TNBS-induced colonic aberrations. Conclusion: Piperine ameliorated the progression of TNBS-induced colitis by modulating the nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha/nuclear factor-kappa B signaling pathway, thus inhibiting the overexpression of proinflammatory cytokines (TNF-α and IL’s), COX-2, iNOs, oxido-nitrosative stress, and proapoptotic proteins (caspase-1) that may improve the expression of TJ protein (claudin-1, occludin, and ZO-1).

TLR22-mediated activation of TNF-α-caspase-1/IL-1β inflammatory axis leads to apoptosis of Aeromonas hydrophila-infected macrophages

2021 ◽  
Vol 137 ◽  
pp. 114-123
Author(s):  
Manmohan Kumar ◽  
Jai Kumar ◽  
Shagun Sharma ◽  
Md. Arafat Hussain ◽  
Asha Shelly ◽  
...  
Keyword(s):  
Aeromonas Hydrophila ◽  
Caspase 1 ◽  
Tnf Α

scholarly journals Nitric Oxide Induces Thymocyte Apoptosis Via a Caspase-1-Dependent Mechanism

2000 ◽  
Vol 165 (3) ◽  
pp. 1252-1258 ◽  
Author(s):  
Xin Zhou ◽  
Sherilyn A. Gordon ◽  
Young-Myeong Kim ◽  
Rosemary A. Hoffman ◽  
Yue Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Caspase 1 ◽  
Thymocyte Apoptosis ◽  
Dependent Mechanism

scholarly journals How Does Colistin-Induced Nephropathy Develop and Can It Be Treated?

2013 ◽  
Vol 57 (8) ◽  
pp. 3463-3469 ◽  
Author(s):  
Gulsum Ozkan ◽  
Sukru Ulusoy ◽  
Asım Orem ◽  
Mehmet Alkanat ◽  
Sevdegül Mungan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Bacterial Infections ◽  
Histopathological Examination ◽  
Kidney Tissue ◽  
Grape Seed ◽  
Multidrug Resistant ◽  
Control Group ◽  
Caspase 1 ◽  
Oxide Synthase

ABSTRACTColistin is an old antibiotic used in the treatment of Gram-negative infections. It was once suspended because of its nephrotoxic effect but has since been reintroduced due to multidrug-resistant bacterial infections. The pathogenesis of colistin-associated nephropathy has not been clarified, and there is currently no effective therapeutic or prophylactic agent available. The aim of this study was to investigate the roles of caspase-associated apoptosis and caspase 1, calpain 1, inducible nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS) expression in the pathogenesis of colistin-associated nephrotoxicity and the effect of grape seed proanthocyanidin extract (GSPE) in preventing it. Twenty-four rats were divided into three groups: control, colistin, and colistin plus GSPE (colistin+GSPE). Colistin-associated nephropathy was induced by the administration of 300,000 IU/kg of body weight/day colistin intraperitoneally for 7 days. The experiment was discontinued on the seventh day. Blood was collected for measurements of blood urea nitrogen (BUN) and creatinine levels. Histopathological examination of kidney tissue and caspase 1 and 3, iNOS, eNOS, terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL), and calpain 1 staining was also performed. Significant increases in BUN levels; creatinine levels; renal histopathological scores; and TUNEL, caspase 1 and 3, calpain 1, iNOS, and eNOS staining were observed for the colistin group compared to the control group. Significant decreases in BUN levels; creatinine levels; renal histopathological scores; and TUNEL, caspase 1 and 3, calpain 1, iNOS, and eNOS staining were observed in the colistin+GSPE group compared to the colistin group. Our study shows, for the first time in the literature, that caspase-mediated apoptosis, iNOS, caspase 1, and calpain 1 are involved in the pathogenesis of colistin-associated nephropathy. GSPE had a renoprotective effect, as shown by the lowered levels of these mediators.

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