Ehrlichiosis pathophysiology
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Pathophysiology
- Ehrlichia are transported between cells through the host cell filopodia during initial stages of infection, whereas, in the final stages of infection the pathogen ruptures the host cell membrane.[1]
- Most of the symptoms of Ehrlichiosis can likely be ascribed to the immune dysregulation that it causes.
- Early in infection, production of TNF-alpha, a cellular product that promotes inflammation and immune response, is suppressed. Experiments in mouse models further supports this hypothesis, as mice lacking TNF-alpha I/II receptors are resistant to liver injury caused by ehrlichia infection.[2]
- Late in infection, however, production of this substance can be upregulated by 30 fold, which is likely responsible for the "toxic shock-like" syndrome seen in some severe cases of ehrlichiosis.
References
- ↑ Thomas S, Popov VL, Walker DH (2010). Kaushal, Deepak, ed. "Exit Mechanisms of the Intracellular Bacterium Ehrlichia". PLoS ONE. 5 (12): e15775. doi:10.1371/journal.pone.0015775. PMC 3004962. PMID 21187937.
- ↑ McBride, Jere W. (31 January 2011). "Molecular and cellular pathobiology of Ehrlichia infection: targets for new therapeutics and immunomodulation strategies". Expert Reviews in Molecular Medicine. 13. doi:10.1017/S1462399410001730. Unknown parameter
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