Abstract
Bartonella henselae is a gram-negative facultative intracellular bacterium and is the causative agent of cat-scratch disease. Our previous data have established that Bacteroides fragilis colonization is able to prevent B. henselae damages through the polysaccharide A (PSA) in an experimental murine model. In order to determine whether the PSA is essential for the protection against pathogenic effects of B. henselae in immunocompromised hosts, SCID mice were co-infected with B. fragilis wild type or its mutant B. fragilis ΔPSA and the effects of infection on murine tissues have been observed by High-Frequency Ultrasound (HFUS), histopathological examination, and Transmission Electron Microscopy (TEM). For the first time, echostructure, hepatic lobes length, vascular alterations, and indirect signs of hepatic dysfunctions, routinely used as signs of disease in humans, have been analyzed in an immunocompromised murine model. Our findings showed echostructural alterations in all infected mice compared with the Phosphate Buffer Solution (PBS) control group; further, those infected with B. henselae and co-infected with B. henselae/B. fragilis ΔPSA presented the major echostructural alterations. Half of the mice infected with B. henselae and all those co-infected with B. henselae/B. fragilis ΔPSA have showed an altered hepatic echogenicity compared with the renal cortex. The echogenicity score of co-infected mice with B. henselae/B. fragilis ΔPSA differed significantly compared with the PBS control group (p < 0.05). Moreover the inflammation score of the histopathological evaluation was fairly concordant with ultrasound findings. Ultrastructural analysis performed by TEM revealed no significant alterations in liver samples of SCID mice infected with B. fragilis wild type while those infected with B. fragilis ΔPSA showed the presence of collagen around the main vessels compared with the PBS control group. The liver samples of mice infected with B. henselae showed macro-areas rich in collagen, stellate cells, and histiocytic cells. Interestingly, our data demonstrated that immunocompromised SCID mice infected with B. henselae and co-infected with B. henselae/B. fragilis ΔPSA showed the most severe morpho-structural liver damage. In addition, these results suggests that the HFUS together with histopathological evaluation could be considered good imaging approach to evaluate hepatic alterations.
Highlights
Bartonella henselae, a facultative intracellular gram-negative bacterium, causes cat-scratch disease, a self-limiting infection often characterized by lymphadenopathy or by an asymptomatic course in immunocompetent patients (Eicher and Dehio, 2012; Harms and Dehio, 2012)
In order to investigate whether B. fragilis can ameliorate inflammatory disease caused by B. henselae in an immunocompromised Specific pathogens free C.B-17/IcrHsd-PrkdcSCID (SCID) mouse model we evaluated the effect on tissues of co-infected mice with B. henselae and B. fragilis wild type or B. fragilis PSA by in vivo High-Frequency
In order to determine whether PSA was essential for protection against pathogenic effects induced by B. henselae, SCID mice were inoculated with either B. fragilis wild type or its mutant B. fragilis PSA
Summary
Bartonella henselae, a facultative intracellular gram-negative bacterium, causes cat-scratch disease, a self-limiting infection often characterized by lymphadenopathy or by an asymptomatic course in immunocompetent patients (Eicher and Dehio, 2012; Harms and Dehio, 2012). B. henselae infections occur more frequently in immunocompromised patients (Maguiña et al, 2009) that may develop bacillary angiomatosis (BA) or peliosis (BP), vasoproliferative tumor lesions of the skin or the inner organs (Mosepele et al, 2012). Bartonella infections in the immunocompromised host may be characterized by fever, osteomyelitis, or angioproliferative lesions that may affect virtually any organ system, but have a predilection for highly vascularized tissues such a heart valves, liver, and spleen (Maguiña et al, 2009; Mosepele et al, 2012). B. henselae can infect and damage endothelial progenitors cells (EPCs) reducing the endothelium regenerating potential (Salvatore et al, 2008, 2015; Costa et al, 2010)
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