Inhibition of macrophage phagocytosis by Bacteroides fragilis in vivo and in vitro

Rodloff, Arne C.; Becker, Joan R.; Blanchard, D K; Klein, Thomas; Hahn, Helmut; Friedman, H

doi:10.1128/iai.52.2.488-492.1986

Cited by 11 publications

(1 citation statement)

References 20 publications

(30 reference statements)

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“…However, it also provides resistance to phagocytosis, thus playing an important role in bacterial fitness outside the colon. 87,88 The lipopolysaccharides of Bacteroides spp. lack O-antigen and are approximately 1000 times less virulent than the lipopolysaccharide of E. coli.…”

Section: Virulence Factors Of Bacteroidesmentioning

confidence: 99%

Gut Bacteroides species in health and disease

2021

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The functional diversity of the mammalian intestinal microbiome far exceeds that of the host organism, and microbial genes contribute substantially to the well-being of the host. However, beneficial gut organisms can also be pathogenic when present in the gut or other locations in the body. Among dominant beneficial bacteria are several species of Bacteroides, which metabolize polysaccharides and oligosaccharides, providing nutrition and vitamins to the host and other intestinal microbial residents. These topics and the specific organismal and molecular interactions that are known to be responsible for the beneficial and detrimental effects of Bacteroides species in humans comprise the focus of this review. The complexity of these interactions will be revealed.

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Section: Virulence Factors Of Bacteroidesmentioning

confidence: 99%

Gut Bacteroides species in health and disease

2021

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Induction of an atypical interferon by bacteroides fragilis and escherichia coli in experimental infections and in leukocyte cultures

et al. 1986

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Previous reports have shown that Bacteroides fragilis may enhance the pathogenicity of coinfecting enterobacteriaceae by interfering with the host's immune response. With the present study, we have investigated the possible role of interferons (IFN) in mediating these effects. Mice injected with B. fragilis developed moderate serum levels of IFN that appeared just prior to alterations of the animals' immunity described earlier. The IFN was neutralized by treatment with anti-IFN-alpha/beta-antibodies or hydrochloric acid; hence it displayed the same "atypical" characteristics as IFN found in patients with immuno-compromising diseases such as AIDS, systemic lupus erythematosus or rheumatoid arthritis. Escherichia coli displayed the same induction patterns as B. fragilis, while gram-positive bacteria induced "regular" IFN alpha/beta and gamma. Spleen cells, peritoneal macrophages, or liver leukocytes taken from B. fragilis or E. coli-injected animals 6 h post infection were refractory to IFN induction by E. coli lipopolysaccharide in vitro; cells from mice infected with gram-positive organisms showed normal or enhanced responsiveness.

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Reduced bacterial dissemination and liver injury in CD14-deficient mice following a chronic abscess-forming peritonitis induced by Bacteroides fragilis

Woltmann

Gangloff

Bruch

et al. 1999

Medical Microbiology and Immunology

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The CD14 myelomonocytic differentiation antigen plays a major role in acute Gram-negative infections with Escherichia coli; however, its role in chronic infections has not yet been analyzed. To address this question, we studied the role of CD14 in a chronic abscess-forming peritonitis, induced by Bacteroides fragilis. B. fragilis (3x10(8) CFU/ml) were resuspended in a liquid nutrient agar and injected into the peritoneal cavity of CD14-deficient (CD 14-/-) and normal C57BL/6J (CD 14+/+) mice, respectively. After 3 days there was a severe phlegmonous intra-abdominal inflammation in both groups. After 7 days an abscess-forming peritonitis developed and by 14 days the infectious foci were compartimentalized. These observations were indistinguishable between CD14-/- and CD14+/+ mice. Although no differences were seen in abscess formation, CD14-/- mice were able to clear B. fragilis more efficiently from the blood than CD14+/+ mice. After 3, 7, and 14 days blood cultures were B. fragilis positive in 11% (1/9), 20% (2/10), and 0% (0/9) in CD14-/-compared with 90% (9/10), 78% (7/9), and 20% (2/10) in CD14+/+ mice, respectively (P<0.05). Furthermore, although the infection resulted in hepatocellular necrosis and severe hepatitis in both groups, at day 14 the liver cell damage was more severe in CD14+/+ than in CD14-/- mice (P<0.05). These results show that the chronic abscess formation induced by B. fragilis capsular polysaccharides is CD14 independent; however, bacterial clearance and/or dissemination and liver cell damage are at least partially influenced by CD14-dependent mechanisms.

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Inhibition of macrophage phagocytosis by Bacteroides fragilis in vivo and in vitro

Cited by 11 publications

References 20 publications

Gut Bacteroides species in health and disease

Gut Bacteroides species in health and disease

Induction of an atypical interferon by bacteroides fragilis and escherichia coli in experimental infections and in leukocyte cultures

Reduced bacterial dissemination and liver injury in CD14-deficient mice following a chronic abscess-forming peritonitis induced by Bacteroides fragilis

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