scholarly journals Pre-injection of Zebrafish (Danio rerio) tnfb Polyclonal Antibody Decreases the Mortality of Vibrio vulnificus Infected Zebrafish

2021 ◽  
Vol 8 ◽  
Author(s):  
Suyi Li ◽  
Cong Jiang ◽  
Hua Chen ◽  
Lijuan Zhang ◽  
Ling Ke ◽  
...  

Tumor necrosis factor (TNF) plays an important role in an inflammatory cytokine storm. Over-secretion of TNF by the host in response to infection aggravates the disease. TNF expression level is positively correlated with the mortality caused by some bacterial infections. Therefore, using TNF antibody may alleviate the inflammation to resist bacterial infections. The function of fish TNF-b antibody in bacterial infection is still unclear. In this study, infection models of Vibrio vulnificus FJ03-X2 strain with high pathogenicity and strong virulence were established in zebrafish (Danio rerio) fibroblast cell line (ZF4 cells) and zebrafish. Zebrafish tnfb (Zetnf-b) gene was cloned and expressed by Escherichia coli BL21 (DE3), and Zetnf-b polyclonal antibody was prepared. Pre-injection of Zetnf-b polyclonal antibody and AG-126 before infecting with V. vulnificus could increase the survival rate of zebrafish by 36.6 and 46.7%, respectively. Pre-injection of Zetnf-b polyclonal antibody could effectively decrease the mortality of zebrafish infected by V. vulnificus. Thus, TNF polyclonal antibody therapy could be considered as an effective strategy to control V. vulnificus in fish.

2000 ◽  
Vol 279 (6) ◽  
pp. R2113-R2120 ◽  
Author(s):  
M. H. Porter ◽  
B. J. Hrupka ◽  
G. Altreuther ◽  
M. Arnold ◽  
W. Langhans

Cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) are assumed to mediate anorexia during bacterial infections. To improve our understanding of the role that these two cytokines serve in mediating infection during anorexia, we investigated the ability of pentoxifylline (PTX), a potent inhibitor of TNF-α production, to block the anorectic effects of the bacterial products lipopolysaccharide (LPS) and muramyl dipeptide (MDP) in rats. Intraperitoneally injected PTX (100 mg/kg body wt) completely eliminated the anorectic effect of intraperitoneally injected LPS (100 μg/kg body wt) and attenuated the anorectic effect of a higher dose of intraperitoneally injected LPS (250 μg/kg body wt). Concurrently, PTX pretreatment suppressed low-dose LPS-induced TNF-α production by more than 95% and IL-1β production 39%, as measured by ELISA. Similarly, high-dose LPS-induced TNF-α production was reduced by ∼90%. PTX administration also attenuated the tolerance that is normally observed with a second injection of LPS. In addition, PTX pretreatment attenuated the hypophagic effect of intraperitoneally injected MDP (2 mg/kg body wt) but had no effect on the anorectic response to intraperitoneally injected recombinant human TNF-α (150 ug/kg body wt). The results suggest that suppression of TNF-α production is sufficient to attenuate LPS- and MDP-induced anorexia. This is consistent with the hypothesis that TNF-α plays a major role in the anorexia associated with bacterial infection.


Author(s):  
Kouji Matsushima ◽  
Christian G. Larsen ◽  
Ajoy K. Samanta ◽  
Naofumi Mukaida ◽  
Arthur O. Anderson ◽  
...  

2000 ◽  
Vol 68 (3) ◽  
pp. 1243-1251 ◽  
Author(s):  
Yi-Xue Zhao ◽  
Ginette Lajoie ◽  
Hongwei Zhang ◽  
Basil Chiu ◽  
Ursula Payne ◽  
...  

ABSTRACT Tumor necrosis factor (TNF) has generally been regarded as a protective cytokine in host defense against bacterial infections. In the present study, we evaluated the role of TNF in the acute phase of infection by Yersinia enterocolitica by using mice rendered genetically deficient in TNF receptor p55 (TNFRp55−/−). Unexpectedly, TNFRp55−/− mice showed more effective resistance to the bacteria, reflected in enhanced bacterial clearance and less tissue damage, than did control C57BL/6 mice. C57BL/6 mice showed evidence of extensive apoptosis in the spleen accompanied by a selective decrease in the CD4+-T-cell population of splenocytes, whereas TNFRp55−/− mice were spared these changes. The splenocytes from TNFRp55−/− mice also maintained a robust gamma interferon IFN-γ response to mitogenic stimulation, while the comparable response in C57BL/6 mice was impaired. In addition, splenocytes harvested from infected mice demonstrated lower production of interleukin-10 IL-10 in TNFRp55−/− mice than in C57BL/6 mice. These findings suggest that Yersinia can induce TNFRp55-mediated apoptosis of splenocytes in the acute phase of the infection and that alteration of T-cell-generated cytokines can dramatically alter the early events in host defense against this pathogen.


2004 ◽  
Vol 200 (3) ◽  
pp. 367-376 ◽  
Author(s):  
Sofia Xanthoulea ◽  
Manolis Pasparakis ◽  
Stavroula Kousteni ◽  
Cord Brakebusch ◽  
David Wallach ◽  
...  

Tumor necrosis factor (TNF) is a potent cytokine exerting critical functions in the activation and regulation of immune and inflammatory responses. Due to its pleiotropic activities, the amplitude and duration of TNF function must be tightly regulated. One of the mechanisms that may have evolved to modulate TNF function is the proteolytic cleavage of its cell surface receptors. In humans, mutations affecting shedding of the p55TNF receptor (R) have been linked with the development of the TNFR-associated periodic syndromes, disorders characterized by recurrent fever attacks and localized inflammation. Here we show that knock-in mice expressing a mutated nonsheddable p55TNFR develop Toll-like receptor–dependent innate immune hyperreactivity, which renders their immune system more efficient at controlling intracellular bacterial infections. Notably, gain of function for antibacterial host defenses ensues at the cost of disbalanced inflammatory reactions that lead to pathology. Mutant mice exhibit spontaneous hepatitis, enhanced susceptibility to endotoxic shock, exacerbated TNF-dependent arthritis, and experimental autoimmune encephalomyelitis. These results introduce a new concept for receptor shedding as a mechanism setting up thresholds of cytokine function to balance resistance and susceptibility to disease. Assessment of p55TNFR shedding may thus be of prognostic value in infectious, inflammatory, and autoimmune diseases.


2006 ◽  
Vol 12 (10) ◽  
pp. 3099-3108 ◽  
Author(s):  
Anna Boula ◽  
Michael Voulgarelis ◽  
Stavroula Giannouli ◽  
George Katrinakis ◽  
Maria Psyllaki ◽  
...  

2007 ◽  
Vol 56 (6) ◽  
pp. 1754-1764 ◽  
Author(s):  
Sebastian Schneeweiss ◽  
Soko Setoguchi ◽  
Michael E. Weinblatt ◽  
Jeffrey N. Katz ◽  
Jerry Avorn ◽  
...  

2011 ◽  
Vol 84 (3) ◽  
pp. 426-428 ◽  
Author(s):  
Jun-Young Lee ◽  
Sook-In Jung ◽  
Kyung-Hwa Park ◽  
Hee Chang Jang ◽  
Na Ra Yun ◽  
...  

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