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Interaction of fibrinogen and muramidase-released protein promotes the development of Streptococcus suis meningitis.

Wang J, Kong D, Zhang S, Jiang H, Zheng Y, Zang Y, Hao H, Jiang Y - Front Microbiol (2015)

Bottom Line: Muramidase-released protein (MRP) is as an important virulence marker of Streptococcus suis (S. suis) serotype 2.In this study, we found that the deletion of mrp significantly impairs the hFg-mediated adherence and traversal ability of S. suis across human cerebral microvascular endothelial cells (hCMEC/D3).Measurement of the permeability to Lucifer yellow in vitro and Evans blue extravasation in vivo show that the MRP-hFg interaction significantly increases the permeability of the blood-brain barrier (BBB).

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Pathogen and Biosecurity, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences , Beijing, China ; Urumqi Ethnic Cadres' College , Urumqi, China.

ABSTRACT
Muramidase-released protein (MRP) is as an important virulence marker of Streptococcus suis (S. suis) serotype 2. Our previous works have shown that MRP can bind human fibrinogen (hFg); however, the function of this interaction in S. suis meningitis is not known. In this study, we found that the deletion of mrp significantly impairs the hFg-mediated adherence and traversal ability of S. suis across human cerebral microvascular endothelial cells (hCMEC/D3). Measurement of the permeability to Lucifer yellow in vitro and Evans blue extravasation in vivo show that the MRP-hFg interaction significantly increases the permeability of the blood-brain barrier (BBB). In the mouse meningitis model, wild type S. suis caused higher bacterial loads in the brain and more severe histopathological signs of meningitis than the mrp mutant at day 3 post-infection. Western blot analysis and immunofluorescence observations reveal that the MRP-hFg interaction can destroy the cell adherens junction protein p120-catenin of hCMEC/D3. These results indicate that the MRP-hFg interaction is important in the development of S. suis meningitis.

No MeSH data available.


Related in: MedlinePlus

MRP contributes to the occurrence of S. suis meningitis. (A) Bacterial loads in the blood and brain from CD1 mice infected with S. suis 05ZYH33 or 05ZYH33Δmrp mutant. The difference between the two groups was determined by a Mann-Whitney test. (B,C) Histopathology of representative brain tissues from CD1 mice infected with S. suis 05ZYH33 (B) and Δmrp mutant (C).
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Figure 4: MRP contributes to the occurrence of S. suis meningitis. (A) Bacterial loads in the blood and brain from CD1 mice infected with S. suis 05ZYH33 or 05ZYH33Δmrp mutant. The difference between the two groups was determined by a Mann-Whitney test. (B,C) Histopathology of representative brain tissues from CD1 mice infected with S. suis 05ZYH33 (B) and Δmrp mutant (C).

Mentions: We next evaluated the effects of the MRP-Fg interaction on the pathogenesis of S. suis meningitis. In this study, CD1 mice were challenged intravenously with wild type S. suis 05ZYH33 (3.31 × 106 CFU) and the Δmrp mutant strain (2.94 × 106 CFU). Bacterial loads in the blood of 05ZYH33 and Δmrp mutant infected mice were comparable from day 1 to day 3 post-infection, but bacterial counts in the brains of 05ZYH33 infected mice at 72 h were significantly higher than that of Δmrp mutant infected mice (Figure 4A). Histopathological lesions such as meningeal thickening and neutrophil infiltration were found in the brains of 05ZYH33 infected mice (Figure 4B) 3 days post-infection, but not of Δmrp mutant infected mice (Figure 4C). These data indicate that MRP promotes the development of S. suis meningitis.


Interaction of fibrinogen and muramidase-released protein promotes the development of Streptococcus suis meningitis.

Wang J, Kong D, Zhang S, Jiang H, Zheng Y, Zang Y, Hao H, Jiang Y - Front Microbiol (2015)

MRP contributes to the occurrence of S. suis meningitis. (A) Bacterial loads in the blood and brain from CD1 mice infected with S. suis 05ZYH33 or 05ZYH33Δmrp mutant. The difference between the two groups was determined by a Mann-Whitney test. (B,C) Histopathology of representative brain tissues from CD1 mice infected with S. suis 05ZYH33 (B) and Δmrp mutant (C).
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4585153&req=5

Figure 4: MRP contributes to the occurrence of S. suis meningitis. (A) Bacterial loads in the blood and brain from CD1 mice infected with S. suis 05ZYH33 or 05ZYH33Δmrp mutant. The difference between the two groups was determined by a Mann-Whitney test. (B,C) Histopathology of representative brain tissues from CD1 mice infected with S. suis 05ZYH33 (B) and Δmrp mutant (C).
Mentions: We next evaluated the effects of the MRP-Fg interaction on the pathogenesis of S. suis meningitis. In this study, CD1 mice were challenged intravenously with wild type S. suis 05ZYH33 (3.31 × 106 CFU) and the Δmrp mutant strain (2.94 × 106 CFU). Bacterial loads in the blood of 05ZYH33 and Δmrp mutant infected mice were comparable from day 1 to day 3 post-infection, but bacterial counts in the brains of 05ZYH33 infected mice at 72 h were significantly higher than that of Δmrp mutant infected mice (Figure 4A). Histopathological lesions such as meningeal thickening and neutrophil infiltration were found in the brains of 05ZYH33 infected mice (Figure 4B) 3 days post-infection, but not of Δmrp mutant infected mice (Figure 4C). These data indicate that MRP promotes the development of S. suis meningitis.

Bottom Line: Muramidase-released protein (MRP) is as an important virulence marker of Streptococcus suis (S. suis) serotype 2.In this study, we found that the deletion of mrp significantly impairs the hFg-mediated adherence and traversal ability of S. suis across human cerebral microvascular endothelial cells (hCMEC/D3).Measurement of the permeability to Lucifer yellow in vitro and Evans blue extravasation in vivo show that the MRP-hFg interaction significantly increases the permeability of the blood-brain barrier (BBB).

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Pathogen and Biosecurity, Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences , Beijing, China ; Urumqi Ethnic Cadres' College , Urumqi, China.

ABSTRACT
Muramidase-released protein (MRP) is as an important virulence marker of Streptococcus suis (S. suis) serotype 2. Our previous works have shown that MRP can bind human fibrinogen (hFg); however, the function of this interaction in S. suis meningitis is not known. In this study, we found that the deletion of mrp significantly impairs the hFg-mediated adherence and traversal ability of S. suis across human cerebral microvascular endothelial cells (hCMEC/D3). Measurement of the permeability to Lucifer yellow in vitro and Evans blue extravasation in vivo show that the MRP-hFg interaction significantly increases the permeability of the blood-brain barrier (BBB). In the mouse meningitis model, wild type S. suis caused higher bacterial loads in the brain and more severe histopathological signs of meningitis than the mrp mutant at day 3 post-infection. Western blot analysis and immunofluorescence observations reveal that the MRP-hFg interaction can destroy the cell adherens junction protein p120-catenin of hCMEC/D3. These results indicate that the MRP-hFg interaction is important in the development of S. suis meningitis.

No MeSH data available.


Related in: MedlinePlus