Dissemination of Bacteria in Multiple Organs Associated with Apoptosis and Macrophage Activity in Different Stages of Experimental Sepsis

Tapfer, Helle; Liigant, Aive; Simovart, Helle-Evi; Põldoja, Elle; Kokk, Kersti; Naaber, Paul; Talvik, R.

doi:10.1177/145749690309200210

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…7b). This finding is consistent with several reports that indicate that the pathogen-mediated apoptosis of phagocytes is involved in the dissemination and severity of bacterial infection [37][38][39].…”

Section: Discussionsupporting

confidence: 82%

Synergistic effects of streptolysin S and streptococcal pyrogenic exotoxin B on the mouse model of group A streptococcal infection

Hung

Tsao

Zeng

et al. 2012

Med Microbiol Immunol

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Streptococcus pyogenes is a group A streptococcus (GAS) and an important human pathogen that causes a variety of diseases. Streptococcal pyrogenic exotoxin B (SPE B) and streptolysin S (SLS) are important virulence factors involved in GAS infection, but it is not clear which one is more virulent. Using an air pouch infection model, the wild-type strain NZ131, its isogenic mutants, and complementary mutants were used to examine the effects of SPE B and SLS on GAS infection. The results of the skin lesion and mouse mortality assays showed that although SPE B and SLS had a synergistic effect on GAS infection, SPE B played a more important role in local tissue damage while SLS had a more prominent effect on mouse mortality. Surveys of the exudates from the air pouch revealed that the expression of inflammatory cytokines was significantly inhibited in the sagB/speB-double-mutant JM4-infected mice. Furthermore, in vivo and in vitro studies showed that the isogenic mutant strains were more susceptible to the immune cell killing than the wild-type strain and that the sagB/speB-double-mutant JM4 was the most sensitive among these strains. Moreover, infection with the sagB/speB-double-mutant JM4 strain caused the least amount of macrophage apoptosis compared to infection with the wild-type NZ131 and the other complementary strains, which express only SPE B or SLS or both. Taken together, these results indicate that both SPE B and SLS contributed to GAS evasion from immune cell killing, local tissue damage, and mouse mortality.

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Section: Discussionsupporting

confidence: 82%

Synergistic effects of streptolysin S and streptococcal pyrogenic exotoxin B on the mouse model of group A streptococcal infection

Hung

Tsao

Zeng

et al. 2012

Med Microbiol Immunol

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“…Our results demonstrate that SRC-3 deficiency impaired phagocytosis of E. coli by macrophage through reducing the expression of SR-A, an important receptor for Fc receptor-independent phagocytosis (49). The apoptotic response of macrophages plays a vital role in the pathogenesis of sepsis (40, 50). For example, liver X receptors-null macrophages undergo accelerated apoptosis upon infection and exhibit defective bacterial clearance in vivo (38).…”

Section: Discussionmentioning

confidence: 99%

Steroid Receptor Coactivator 3 Is Required for Clearing Bacteria and Repressing Inflammatory Response in Escherichia coli-Induced Septic Peritonitis

Chen

et al. 2010

The Journal of Immunology

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Steroid receptor coactivator 3 (SRC-3) is a multifunctional protein that plays an important role in regulation of bacterial lipopolysaccharide-induced inflammation. However, its involvement in host defense against bacterial infection remains unclear. Herein we used SRC-3 knockout mice to assess the role of SRC-3 in antibacterial defense in E. coli-induced septic peritonitis. After E. coli bacteria were injected intraperitoneally, SRC-3 deficient mice exhibited excessive local and systemic inflammatory responses and more severe bacterial burdens, leading to a significantly higher mortality compared with wild-type mice. Peritoneal macrophages of SRC-3 deficient mice showed a decrease in bacterial phagocytosis in culture and an increase in apoptosis, which was consistent with the defective bacterial clearance observed in SRC-3-deficient mice. Accordingly, SRC-3 null macrophages expressed much lower levels of the scavenger receptor A, the antioxidant enzyme catalase, and anti-apoptotic gene Bcl-2. Collectively, our data demonstrate that SRC-3 is important in not only modulating the local and systemic inflammation but also intensifying bacterial clearance, which highlights a pivotal role of SRC-3 in the host defense system against bacterial infection.

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“…Apoptosis of macrophages correlates with decreased clearance of bacteria and progression of sepsis [19,20]. Inhibition of apoptosis in myeloid cells, by over-expression of Bcl-2, markedly decreased mortality in a mouse model of polymicrobial sepsis [21].…”

Section: Introductionmentioning

confidence: 99%

E. coli infection induces caspase dependent degradation of NF-κB and reduces the inflammatory response in macrophages

Albee

Perlman

2005

Inflamm. res.

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Dissemination of Bacteria in Multiple Organs Associated with Apoptosis and Macrophage Activity in Different Stages of Experimental Sepsis

Cited by 7 publications

References 23 publications

Synergistic effects of streptolysin S and streptococcal pyrogenic exotoxin B on the mouse model of group A streptococcal infection

Synergistic effects of streptolysin S and streptococcal pyrogenic exotoxin B on the mouse model of group A streptococcal infection

Steroid Receptor Coactivator 3 Is Required for Clearing Bacteria and Repressing Inflammatory Response in Escherichia coli-Induced Septic Peritonitis

E. coli infection induces caspase dependent degradation of NF-κB and reduces the inflammatory response in macrophages

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