PubMed · 15303267
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Lisa Crossman, Matthew Holden, Arnab Pain, Julian Parkhill. 2004. Genomes beyond compare.. https://doi.org/10.1038/nrmicro961
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The bacterial pathogen Bartonella henselae (Bh) is responsible for a broad range of clinical manifestations, including the formation of vascular tumours as the result of pathogen-triggered vasoproliferation. In vitro, the interaction of Bh with human umbilical vein endothelial cells (Huvec) involves (i) cytoskeletal rearrangements in conjunction with bacterial internalization, (ii) nuclear factor kappaB (NFkappaB)-dependent proinflammatory activation, (iii) the inhibition of apoptosis, and (iv) the modulation of angiogenic properties such as proliferation, migration, and tubular differentiation. To study the transcriptional signature of these pathogen-triggered changes of Huvec, we performed transcriptional profiling with Affymetrix U133 GeneChips. At 6 h or 30 h of infection, a total of 706 genes displayed a clear and statistically significant change of expression (>2.5-fold, t-test p-value<0.05). These included 314 up-regulated genes dominated by the innate immune response. The gene list comprises subsets of tumour necrosis factor alpha (TNFalpha, 99 genes) and interferon alpha (IFNalpha, 30 genes) inducible genes, which encode components of the NF-kappaB-dependent proinflammatory response and the type I IFN-dependent anti-infective response, respectively. The remaining set of 197 up-regulated genes mirrors other cellular changes induced by Bh, in particular proliferation and proangiogenic activation. The set of 362 down-regulated genes includes 41TNFalpha - or IFNalpha-suppressible genes, and 52 genes involved in cell cycle control or progression. This comprehensive analysis of Bh-triggered changes of the Huvec transcriptome identified candidate genes putatively involved in controlling innate immune responses, cell cycle, and vascular remodelling, and may thus provide the basis for functional studies of the molecular mechanisms underlying these pathogen-induced cellular processes.
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We report a case of cat-scratch disease neuroretinitis for which systemic and ocular investigations proved the responsibility of Bartonella henselae. An 11-year-old boy was referred to the hospital in November 2002 for severe visual loss in the left eye over the preceding 2 weeks. At the same time, he also developed a flu-like illness. The best corrected acuity in the left eye was counting fingers at 30 cm. Posterior segment examination on the left eye showed an optic disk edema with papillary and peripapillary hemorrhages and serous retinal detachment, mild vitreous inflammation, and two little perivascular white spots. The medical history was unremarkable except for a cat scratch on his left forearm 2 months before. Four weeks of antibiotic therapy including oral rifampin and doxycycline was used. Bartonella henselae immunoglobulin M were first detected with Bartonella henselae immunoglobulin G testing negative at this time. A 3-week serum showed immunoglobulin M seroreversion, while Bartonella henselae immunoglobulin G appeared. Other causes of optic disk edema with macular star were excluded by biological data. Bartonella antibodies to both Bartonella henselae and Bartonella clarridgeiae were detected in the cat. Ophthalmic follow-up showed progressive resorption of the neuroretinitis and the visual acuity increased to 5/10. The significance of this case report lies in the reminder that this pathology can be the cause of neuroretinitis; the prognosis can be improved by earlier treatment.