scholarly journals Efficacy of the antimicrobial peptide TP4 against Helicobacter pylori infection: in vitro membrane perturbation via micellization and in vivo suppression of host immune responses in a mouse model

Oncotarget ◽  
2015 ◽  
Vol 6 (15) ◽  
pp. 12936-12954 ◽  
Author(s):  
Jayaram Lakshmaiah Narayana ◽  
Han-Ning Huang ◽  
Chang-Jer Wu ◽  
Jyh-Yih Chen
PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0148353 ◽  
Author(s):  
Sílvia Fontenete ◽  
Marina Leite ◽  
Davie Cappoen ◽  
Rita Santos ◽  
Chris Van Ginneken ◽  
...  

2000 ◽  
Vol 118 (4) ◽  
pp. A732-A733
Author(s):  
Gerardo Nardone ◽  
Eileen Holicky ◽  
Jim R. Uhl ◽  
Vittorio Colantuoni ◽  
Lina Sabatino ◽  
...  

Molecules ◽  
2015 ◽  
Vol 20 (3) ◽  
pp. 3972-3985 ◽  
Author(s):  
Xiao-Lin Zhang ◽  
An-Min Jiang ◽  
Zhong-You Ma ◽  
Xian-Bao Li ◽  
You-Yi Xiong ◽  
...  

1998 ◽  
Vol 114 ◽  
pp. A987
Author(s):  
T. Gotoh ◽  
A. Nishizono ◽  
J. Ikewaki ◽  
M. Kimoto ◽  
K. Mifune ◽  
...  

2002 ◽  
Vol 4 (7) ◽  
pp. 713-722 ◽  
Author(s):  
Hassan Ashktorab ◽  
Mattew Neapolitano ◽  
Chandara Bomma ◽  
Cornel Allen ◽  
Amel Ahmed ◽  
...  

Helicobacter ◽  
1999 ◽  
Vol 4 (4) ◽  
pp. 260-265 ◽  
Author(s):  
Paul D. Hammond ◽  
Fred J. Stutzenberger ◽  
Ross N. Butler ◽  
Leanna C. Read ◽  
Geoffrey P. Davidson

2021 ◽  
Author(s):  
Vivian Vasconcelos Costa ◽  
Michelle A Sugimoto ◽  
Josy Hubner ◽  
Caio S Bonilha ◽  
Celso Martins Queiroz-Junior ◽  
...  

Host immune responses contribute to dengue's pathogenesis and severity, yet the possibility that failure in endogenous inflammation resolution pathways could characterise the disease has not been contemplated. The pro-resolving protein Annexin A1 (AnxA1) is known to counterbalance overexuberant inflammation and mast cell (MC) activation. We hypothesised that inadequate AnxA1 engagement underlies the cytokine storm and vascular pathologies associated with dengue disease. Levels of AnxA1 were examined in the plasma of dengue patients and infected mice. Immunocompetent, IFNα/βR-/-, AnxA1-/- and FPR2/ALX-/- mice were infected with Dengue virus (DENV) and treated with the AnxA1 mimetic peptide Ac2-26 for analysis. Additionally, the effect of Ac2-26 on DENV-induced MC degranulation was assessed in vitro and in vivo. We observed that circulating levels of AnxA1 were reduced in dengue patients and DENV-infected mice. While the absence of AnxA1 or its receptor FPR2/ALX aggravated illness in infected mice, treatment with AnxA1 agonistic peptide attenuated disease manifestations. Both clinical outcomes were attributed to modulation of DENV-mediated viral load-independent MC degranulation. We have thereby identified that altered levels of the pro-resolving mediator AnxA1 are of pathological relevance in DENV infection, suggesting FPR2/ALX agonists as a therapeutic target for dengue disease.


2021 ◽  
Author(s):  
Xi Zhang ◽  
Jingjing Chen ◽  
Huimin Cheng ◽  
Jinying Zhu ◽  
Qiao Dong ◽  
...  

Abstract Infection by Brucella is characterized by the inhibition of host immune responses. MicroRNA-155 (miR-155) has been implicated in the immune response to many diseases. In this study, miR-155 expression during Brucella 16M infection of macrophages and mice were analyzed. Expression of miR-155 was significantly induced in macrophages at 24 hours post infection. Analysis of infected mice showed that miR-155 was inhibited at 7 and 14 days, but induced at 28 days. Very interestingly, the induction or inhibition trend was reversed at 7 and 14 days in 16M△virB-infected mice. This suggested that decreased expression of miR-155 at an early stage of infection was dependent on intracellular replication. In humans with brucellosis, serum levels of miR-155 were significantly decreased compared to those without brucellosis and healthy volunteers. Significant correlations were observed between serum level of miR-155 and serum anti-Brucella antibody titers and symptom of sweat. The decrease in miR-155 with Brucella infection contrasts with the increase in miR-155 observed in Mycobacterium tuberculosis infection. This contrasting effect suggests that Brucella interferes with miR-155-regulated immune responses through a unique mechanism. Taken together, data from this study indicate that Brucella infection affects miR-155 expression, and that human brucellosis patients show decreased serum levels of miR-155.


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