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showed direct, in vivo evidence that GPVI is a central mediator of LPS-induced pulmonary thrombo-inflammationpromoting PNC formation, neutrophil recruitment, and NETosiswhile its inhibition protects mice from LPS-induced acute lung injury and respiratory failure (164).There has been extensive debate about the in vitro effects of LPS on plateletsspecifically, whether it activates them, primes them, or has no effect (150153, 160, 162, 165167)

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