News Journal of Clinical Investigation Online Early: March 15, 2010
stem cells known as Drug inhibitors of receptor tyrosine kinase (RTKIs) are commonly used to treat various cancers, but may be used to effectively treat infectious diseases has not been determined. Paul Kaye and his colleagues at the University of York, UK, have begun to address this issue, showing that the cancer drug sunitinib maleate (which is a RTKI) blocks of various symptoms disease in mouse models of visceral leishmaniasis, a neglected tropical disease caused by parasites Leishmania donovani and Leishmania infantum.
In the study, although the sunitinib maleate treatment only prevented the development of various symptoms of visceral leishmaiasis that does not cause a reduction in tissue parasite burden. However, the sequential administration of sunitinib maleate and conventional antileishmanial drugs led to parasite clearance, effective with ten times less than conventional drugs normally required to achieve this effect. This, the authors suggest that using a RTKI before administration los medicamentos convencionales antileishmanial puede ser clínicamente útil en el tratamiento de la leishmaniasis visceral.
TÍTULO: La inhibición del receptor de la tirosina quinasas inmunocompetencia restaura y mejora la inmunidad dependiente de la quimioterapia contra la leishmaniasis experimental en ratones
INFLAMACIÓN: reparar tejidos dañados: el papel de madre hematopoyéticas / células progenitoras
Las células madre hematopoyéticas (HSC), y las células progenitoras hematopoyéticas (HPCs) son la fuente de células circulating in the blood. Also been suggested to play a role in tissue repair at sites of inflammation. Using two mouse models of sterile inflammation, Israel Charo and colleagues at the Gladstone Institute of Cardiovascular Diseases, San Francisco, have found that HSCs / HPCs are recruited to sites of inflammation, where they promote tissue repair, and protein expression of CCR2 is crucial for their ability to be hired.
In the study, an observation of particular interest, given that the most common acute liver failure in the developed world is acute acetaminophen (paracetamol) overdose, administration of normal HSCs / HPCs, but not those lacking CCR2, accelerated repair liver damage induced by paracetamol in mice. The authors hope that further define the molecular mechanisms that control the recruitment of HSCs / HPCs to sites of inflammation provide a framework for the development of therapies based on cells DAMAGE or organs.
TITLE: CCR2 mediates hematopoietic stem cells and progenitor cells trafficking to sites of inflammation in mice
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