Comparison of the Susceptibilities of C57BL/6 and A/J Mouse Strains to<i>Streptococcus suis</i>Serotype 2 Infection

Domínguez-Punaro, María de la Cruz; Segura, Mariela; Radzioch, Danuta; Rivest, Serge; Gottschalk, Marcelo

doi:10.1128/iai.00350-08

Cited by 71 publications

(107 citation statements)

References 49 publications

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“…In agreement with the findings of previous studies (20,21,26), patterns of bacterial burdens observed in spleen and liver were similar to those observed in blood samples, with no significant differences being detected among strains (data not shown). These results suggest that the increased virulence of S. suis ST7 cannot be explained by an increase in blood bacterial burden and that other factors account for its pathogenic potential.…”

Section: Difference In Virulence Among North American European Andsupporting

confidence: 82%

“…For cytokine and chemokine analysis, mice were euthanized at 6 h postinfection. The dose of infection and postinfection times were selected on the basis of our previous work (21).…”

Section: Methodsmentioning

confidence: 99%

“…Our laboratory previously developed a mouse model of S. suis systemic infection (20,21). Infected animals can succumb rapidly, and this mortality can be associated with septic shock symptoms.…”

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confidence: 99%

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Exacerbated Type II Interferon Response Drives Hypervirulence and Toxic Shock by an Emergent Epidemic Strain of Streptococcus suis

et al. 2013

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b Streptococcus suis, a major porcine pathogen, can be transmitted to humans and cause severe symptoms. A large human outbreak associated with an unusual streptococcal toxic shock-like syndrome (STSLS) was described in China. Albeit an early burst of proinflammatory cytokines following Chinese S. suis infection was suggested to be responsible for STSLS case severity, the mechanisms involved are still poorly understood. Using a mouse model, the host response to S. suis infection with a North American intermediately pathogenic strain, a European highly pathogenic strain, and the Chinese epidemic strain was investigated by a whole-genome microarray approach. Proinflammatory genes were expressed at higher levels in mice infected with the Chinese strain than those infected with the European strain. The Chinese strain induced a fast and strong gamma interferon (IFN-␥) response by natural killer (NK) cells. In fact, IFN-␥-knockout mice infected with the Chinese strain showed significantly better survival than wild-type mice. Conversely, infection with the less virulent North American strain resulted in an IFN-␤-subjugated, low inflammatory response that might be beneficial for the host to clear the infection. Overall, our data suggest that a highly virulent epidemic strain has evolved to massively activate IFN-␥ production, mainly by NK cells, leading to a rapid and lethal STSLS.

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Section: Difference In Virulence Among North American European Andsupporting

confidence: 82%

“…For cytokine and chemokine analysis, mice were euthanized at 6 h postinfection. The dose of infection and postinfection times were selected on the basis of our previous work (21).…”

Section: Methodsmentioning

confidence: 99%

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Exacerbated Type II Interferon Response Drives Hypervirulence and Toxic Shock by an Emergent Epidemic Strain of Streptococcus suis

et al. 2013

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“…The appearance of clinical signs of meningitis was observed in 14% of the remaining infected mice between days 3 and 7 postinfection. The disease evolution was thus similar to that in previous studies (40,47,49). Blood bacterial loads were determined on days 1, 2, 3, and 4 postinfection.…”

Section: Different Features Of Protein-and Cps-specific Ab Responsesmentioning

confidence: 68%

Antibody Response Specific to the Capsular Polysaccharide Is Impaired in Streptococcus suis Serotype 2-Infected Animals

et al. 2015

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bStreptococcus suis serotype 2 is an extracellular encapsulated bacterium that causes severe septicemia and meningitis in swine and humans. Albeit crucial in the fight against encapsulated bacteria, the nature of the capsular polysaccharide (CPS)-specific antibody (Ab) response during S. suis type 2 infection is unknown. We compared for the first time the features of CPS-specific versus protein-specific Ab responses during experimental infections with live virulent S. suis type 2 in mice. The primary protein-specific Ab response was dominated by both type 1 and 2 IgG subclasses, whereas IgM titers were more modest. The secondary protein-specific Ab response showed all of the features of a memory response with faster kinetics and boosted the titers of all Ig isotypes. In contrast, the primary CPS-specific Ab response was either inexistent or had titers only slightly higher than those in noninfected animals and was essentially composed of IgM. A poor CPS-specific memory response was observed, with only a moderate boost in IgM titers and no IgG. Both protein-and CPS-specific Ab responses were Toll-like receptor 2 independent. By using S. suis type 2 strains of European or North American origin, the poor CPS-specific Ab response was demonstrated to be independent of the genotypic/phenotypic diversity of the strain within serotype 2. Finally, the CPS-specific Ab response was also impaired and lacked isotype switching in S. suis-infected pigs, the natural host of the bacterium. The better resistance of preinfected animals to reinfection with the same strain of S. suis type 2 might thus more likely be related to the development of a protein rather than CPS Ab response.

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“…Earlier studies using immunocompetent strains have indicated that mice exhibit a spectrum of resistance to bacterial infection linked to neutrophil recruitment (7,9,12). We hypothesized that genetic variation in the capacity of alveolar macrophage-mediated bacterial killing may also exist.…”

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confidence: 99%

Analysis of Murine Genetic Predisposition to Pneumococcal Infection Reveals a Critical Role of Alveolar Macrophages in Maintaining the Sterility of the Lower Respiratory Tract

2011

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The study of pathogenic mechanisms of disease can be greatly facilitated by studying genetic differences in susceptibility to infection. In the present study, we compared the severity of pneumococcal infection in C57BL/6 (B6) and 129Sv mice. The results showed that 129Sv mice were remarkably more susceptible to pneumococcal infection than B6 mice. Bacterial clearance, proinflammatory mediators, leukocyte recruitment, and phagocyte activities were measured to examine potential immune factors associated with differences in susceptibility to pneumococcal infection. The greater susceptibility of 129Sv mice was associated only with inadequate alveolar macrophage bacterial killing, as indicated by significantly decreased initial bacterial clearance from the respiratory tract. Effective pneumococcal clearance was not dependent upon Toll-like receptor 2 (TLR2) expression, oxidative stress, or matrix metallopeptidase 12 (MMP-12) expression. Furthermore, phagocytosis analysis suggested that the deficiency found in 129Sv alveolar macrophages was not due to a lack of bacterial recognition but, rather, to reduced bacterial uptake. In conclusion, our findings indicate a crucial role of alveolar macrophage phagocytosis during innate defense against pneumococcal infection, which may explain the association of host genetic risk factors with predisposition to pneumococcal infection.There are over 90 Streptococcus pneumoniae serotypes, based on their capsular polysaccharide, and different serotypes vary in the ability to cause disease on the basis of the virulent factors expressed (19,20). On the other hand, host genetic components are also involved in the outcome of pneumococcal infection (2, 4, 22), and host immune status associated with age, respiratory viral infection, chronic diseases, and immunosuppression are all significant risk factors for the development of severe pneumococcal infection (13,16).Although pneumococcus is a major human pathogen, the majority of information about pathogenesis and disease has resulted from mouse studies. It is recognized that there are significant variations in susceptibility to pneumococcal infection among inbred mouse strains (9, 12), and understanding the underlying immune protective mechanisms may explain the association of genetic risk factors with predisposition of the human host to pneumococcal infection.Earlier studies using immunocompetent strains have indicated that mice exhibit a spectrum of resistance to bacterial infection linked to neutrophil recruitment (7, 9, 12). We hypothesized that genetic variation in the capacity of alveolar macrophage-mediated bacterial killing may also exist. Our previous studies have demonstrated a pivotal role of alveolar macrophages in pneumococcal clearance, especially after a sublethal bacterial inoculation (24). However, the overall importance of alveolar macrophages in maintaining the sterility of the lower respiratory tract remains to be firmly established, and the impact of genetic variation on alveolar macrophage function against extracellular...

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Comparison of the Susceptibilities of C57BL/6 and A/J Mouse Strains toStreptococcus suisSerotype 2 Infection

Cited by 71 publications

References 49 publications

Exacerbated Type II Interferon Response Drives Hypervirulence and Toxic Shock by an Emergent Epidemic Strain of Streptococcus suis

Exacerbated Type II Interferon Response Drives Hypervirulence and Toxic Shock by an Emergent Epidemic Strain of Streptococcus suis

Antibody Response Specific to the Capsular Polysaccharide Is Impaired in Streptococcus suis Serotype 2-Infected Animals

Analysis of Murine Genetic Predisposition to Pneumococcal Infection Reveals a Critical Role of Alveolar Macrophages in Maintaining the Sterility of the Lower Respiratory Tract

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