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onsdag 15 oktober 2014

After Ebola virion budding, the membrane is shedding microvesicles containing microparticles with PtdSer, TF. (Sic! DIC)

Med Mal Infect. 2012 Aug;42(8):335-43. doi: 10.1016/j.medmal.2012.05.011. Epub 2012 Jul 4.

Microparticles and infectious diseases.


Membrane shedding with microvesicle (MV) release after membrane budding due to cell stimulation is a highly conserved intercellular interplay. MV can be released by micro-organisms or by host cells in the course of infectious diseases.
 Host MVs are divided according to cell compartment origin in microparticles (MPs) from plasma membrane and exosomes from intracellular membranes.
MPs are cell fragments resulting from plasma membrane reorganization characterized by phosphatidylserine (PhtdSer) content and parental cell antigens on membrane.
 The role of MPs in physiology and pathophysiology is not yet well elucidated; they are a pool of bioactive molecules able to transmit a pro-inflammatory message to neighboring or target cells.
 The first acknowledged function of MP was the dissemination of a procoagulant potential via PhtdSer and it is now obvious than MPs bear tissue factor (TF).
Such MPs have been implicated in the coagulation disorders observed during sepsis and septic shock.
 MPs have been implicated in the regulation of vascular tone and cardiac dysfunction in experimental sepsis. Beside a non-specific role, pathogens such as Neisseria meningitidis and Ebola Virus can specifically activate blood coagulation after TF-bearing MPs release in the bloodstream with disseminated intravascular coagulopathy (DIC)  and Purpura fulminans.
 The role of MPs in host-pathogen interactions is also fundamental in Chagas disease, where MPs could allow immune evasion by inhibiting C3 convertase.
During cerebral malaria, MPs play a complex role facilitating the activation of brain endothelium that contributes to amplify vascular obstruction by parasitized erythrocytes.
Phagocytosis of HIV induced MPs expressing PhtdSer by monocytes/macrophages results in cellular infection and non-inflammatory response via up-regulation of TGF-β.

 After an incubation period of about 8 days (range 3-21 days), patients typically present with the abrupt onset of non-specific signs and symptoms including fever, malaise, headache, chest pain, and myalgia/arthralgia, followed rapidly by gastrointestinal symptoms (vomiting, diarrhea, abdominal pain) and, in some cases, a maculopapular skin rash. Severe cases develop bleeding (sub-conjunctival hemorrhage, epistaxis, bleeding from the mouth and rectum, oozing from venipuncture sites), neurologic involvement (disorientation, convulsions, coma), shock, and multi-organ system failure. Mild-to-moderate leukopenia and thrombocytopenia are often present and disseminated intravascular coagulation (DIC) commonly develops, best indicated by the presence of D-dimers.

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