Blood platelets in the liver of mice team up to defend the body against pathogenic bacteria according to a report published online this week in Nature Immunology.Thus these findings demonstrate platelets contribute to innate immune defenses.
Paul Kubes and colleagues imaged of the liver of live mice to discover a patrolling role for blood platelets and their interaction with Kupffer cells (KCs)-specialized immune cells that reside within liver sinusoids. The mechanism of the immune surveillance is reportedly transient platelet interactions with two KC surface proteins, glycoprotein Ib (GP1b) and von Willebrand factor (vWF), in the liver. When a KC catches a bacterium, it activates vWF and immediately induces adhesion of platelets via GP1b and another surface protein GPIIbIIIa. This triggers extensive platelet adherence with KCs as well as platelet release of antimicrobial factors. This interaction was critical in the clearance of blood-borne bacteria, such as methicillin-resistant Staphylococcus aureus.
The authors show platelet-depleted mice die within four hours post-infection, whereas most untreated mice survive. Bacteria were entrapped by Kupffer cells in the liver, reflected by the absence of bacteremia in replete mice but profound bacteremia is found in platelet-depleted mice.