RESUMO
Bacteroides fragilis is an anaerobic bacteria component of human intestinal microbiota and agent of infections. In the host B. fragilis interacts with macrophages, which produces toxic radicals like NO. The interaction of activated mice peritoneal macrophages with four strains of B. fragilis was evaluated on this study. Previously was shown that such strains could cause metabolic and morphologic alterations related to macrophage death. In this work propidium iodide staining showed the strains inducing macrophage necrosis in that the labeling was evident. Besides nitroblue tetrazolium test showed that B. fragilis stimulates macrophage to produce oxygen radicals. In vivo assays performed in BalbC mice have results similar to those for in vitro tests as well as scanning electron microscopy, which showed the same surface pore-like structures observed in vitro before. The results revealed that B. fragilis strains studied lead to macrophage death by a process similar to necrosis.
Assuntos
Infecções por Bacteroides/microbiologia , Infecções por Bacteroides/patologia , Bacteroides fragilis/patogenicidade , Macrófagos Peritoneais/microbiologia , Macrófagos Peritoneais/patologia , Animais , Feminino , Macrófagos Peritoneais/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Necrose/microbiologia , Necrose/patologia , Espécies Reativas de Oxigênio/metabolismoRESUMO
Metronidazole is widely used to treat protozoan and fungal infections. As an antibacterial drug, it is used mainly against anaerobes. Among anaerobes, the Bacteroides fragilis group is the most relevant in terms of frequency of recovery and antimicrobial resistance patterns. The use of metronidazole and other antimicrobial drugs induces morphological changes in this bacterial group. The present study investigated in vivo if these morphological modifications were accompanied by changes in virulence patterns by using germfree mice experimentally challenged with metronidazole-resistant Bacteroides strains before and after exposure to metronidazole. It was observed that metronidazole-resistant strains were more virulent after contact with the drug, as demonstrated by anatomicopathologic data for spleen, liver, and small intestine samples. These results suggest that long-term therapy and high metronidazole concentrations could interfere with microbial pathogenicity, resulting in changes to host-bacterium relationships.
Assuntos
Antibacterianos/farmacologia , Infecções por Bacteroides/microbiologia , Infecções por Bacteroides/patologia , Bacteroides/efeitos dos fármacos , Metronidazol/farmacologia , Antibacterianos/uso terapêutico , Bacteroides/patogenicidade , Infecções por Bacteroides/tratamento farmacológico , Infecções por Bacteroides/fisiopatologia , Progressão da Doença , Resistência Microbiana a Medicamentos , Vida Livre de Germes , Humanos , Metronidazol/uso terapêutico , Virulência/efeitos dos fármacosRESUMO
1. The influence of some components of the normal human intestinal flora on the acute phase of experimental infection with strain CL of Trypanosoma cruzi was studied in 30-day-old germ-free or gnotobiotic CFW (LOB) mice monoassociated with Bacteroides fragilis, Peptostreptococcus sp or Clostridium sp by intragastric inoculation of 10(6) bacteria 10 days before the intraperitoneal infection with 5 x 10(3) trypomastigotes/g body weight. 2. Significantly earlier parasitemia peak and mortality were observed in Bacteroides fragilis- and Clostridium-associated mice (16.75 +/- 0.96 and 15.00 +/- 1.15 days, respectively) when compared with germfree animals (18.83 +/- 1.17 days). More precocious mortality (10.40 +/- 2.06 days) and, curiously, much lower blood parasitemia were observed in Peptostreptococcus-associated mice than in other gnotobiotic mice. 3. The extent of cardiac tissue parasitism decreased in the following order: germfree, B. fragilis-associated, Clostridium-associated, and Peptostreptococcus-associated animals. The levels of inflammatory reaction decreased in the following order: germfree, Peptostreptococcus-associated, Clostridium-associated, and B. fragilis-associated mice. 4. These results show that the acute phase of experimental infection with T. cruzi was more severe in mice associated with strict anaerobic bacteria when compared with germfree animals. This suggests that a normal intestinal flora may be another factor, in addition to nutritional and genetic factors, responsible for the different susceptibility of organisms of the same species infected with T. cruzi.