scholarly journals Immunobiotic and Paraprobiotic Potential Effect of Lactobacillus casei in a Systemic Toxoplasmosis Murine Model

2020 ◽  
Vol 8 (1) ◽  
pp. 113 ◽  
Author(s):  
Angel Gustavo Salas-Lais ◽  
Atzín Robles-Contreras ◽  
José Abraham Balderas-López ◽  
Victor Manuel Bautista-de Lucio

One of the main characteristics of probiotics is their ability to stimulate and modulate the immune response regardless of their viability. Lactobacillus casei (Lc) can stimulate local and systemic immunity, in addition to the activation of macrophages at sites distant from the intestine. Activated macrophages limit the replication of intracellular protozoa, such as Toxoplasma gondii, through the production of nitric oxide. The present study aimed to evaluate the protection generated by treatment with viable and non-viable Lc in the murine systemic toxoplasmosis model. CD1 male mice were treated with viable Lc (immunobiotic) and non-viable Lc (paraprobiotic), infected with tachyzoites of Toxoplasma gondii RH strain. The reduction of the parasitic load, activation of peritoneal macrophages, inflammatory cytokines, and cell populations was evaluated at 7 days post-infection, in addition to the survival. The immunobiotic and paraprobiotic reduced the parasitic load, but only the immunobiotic increased the activation of peritoneal macrophages, and the production of interferon-gamma (IFN-γ), tumor necrosis factor (TNF), and interleukin-6 (IL-6) while the paraprobiotic increased the production of monocyte chemoattractant protein-1 (MCP-1) and T CD4+CD44+ lymphocytes. Viable and non-viable Lc increases survival but does not prevent the death of animals. The results provide evidence about the remote immunological stimulation of viable and non-viable Lc in an in vivo parasitic model.

1994 ◽  
Vol 58 (2) ◽  
pp. 240-247 ◽  
Author(s):  
Isabelle Desbaillets ◽  
Mitsuhiro Tada ◽  
Nicolas De Tribolet ◽  
Annie-Claire Diserens ◽  
Marie-France Hamou ◽  
...  

Blood ◽  
1999 ◽  
Vol 93 (3) ◽  
pp. 857-865 ◽  
Author(s):  
Matthias Goebeler ◽  
Karin Kilian ◽  
Reinhard Gillitzer ◽  
Manfred Kunz ◽  
Teizo Yoshimura ◽  
...  

Abstract Monocyte chemoattractant protein-1 (MCP-1), a member of the C-C subfamily of chemokines, is important for the local recruitment of leukocytes to sites of inflammatory challenge. Here, we investigated endothelial signaling pathways involving members of the mitogen-activated protein (MAP) kinase superfamily and studied their role for MCP-1 expression in endothelium. We show that tumor necrosis factor- (TNF-), a potent inflammatory activator of endothelium, leads to activation of MAP kinases ERK, p38, and JNK in human umbilical vein endothelial cells (HUVEC). Contribution of MAP kinase pathways to TNF-–induced synthesis of endothelial MCP-1 was then studied by pharmacologic inhibition and transient expression of dominant negative or constitutively active kinase mutants using flow cytometry, Northern blot, and luciferase reporter gene assays. Inhibition of Raf/MEK/ERK or SEK/JNK pathways had no significant effect on MCP-1 levels, whereas blocking the MKK6/p38 pathway by p38 inhibitors SB203580 or SB202190 or by a dominant negative mutant of MKK6, the upstream activator of p38, strongly inhibited TNF-–induced expression of MCP-1. Consistent with that finding, expression of wild-type or constitutively active MKK6 significantly enhanced the effect of limiting TNF- concentrations on MCP-1 synthesis. These data suggest a crucial role for the MKK6/p38 stress kinase cascade in TNF-–mediated endothelial MCP-1 expression.


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