From the article: Pseudomonas aeruginosa is an extracellular Gram-negative, bacterial, opportunistic pathogen that exploits immunocompromised hosts. Although it is notorious for its ability to persist in the cystic fibrosis lung and establish chronic infection, P. aeruginosa is also a common cause of acute lower-respiratory-tract infections in critically ill patients. Indeed, P. aeruginosa was identified as the most common Gram-negative infection in a multicenter, international collaborative study of ICU infections in 75 countries (1), and P. aeruginosa infection is independently associated with increased ICU mortality (2). In this issue of the Journal, Amison and colleagues (pp. 331–340) provide compelling evidence that platelets are required in host defense against P. aeruginosa (3). This may be surprising because platelets are conventionally viewed as mediators of primary hemostasis; yet, platelets are increasingly being recognized as key players in the innate defense against infection (4). Amison and colleagues demonstrate that acute intrapulmonary P. aeruginosa infection induces peripheral thrombocytopenia with accumulation of activated platelets in lung tissue. Platelets found in the airspaces showed evidence of degranulation, with elevated platelet factor 4 levels in the BAL fluid of infected mice. They further show that the accumulation of activated platelets in the lungs is protective rather than deleterious during P. aeruginosa infection, as platelet depletion in mice results in enhanced pathogenicity of P. aeruginosa with a higher lung bacterial burden, increased weight loss, and increased mortality. Depletion of platelets also results in impaired leukocyte recruitment—most notably, neutrophils—in response to P. aeruginosa. Although the impaired neutrophil recruitment after infection may account for the worsened phenotype observed in platelet-depleted mice, the authors also suggest that platelets can limit bacterial growth in vitro. This finding invites the possibility that platelets serve an additional function of direct host defense against bacterial pathogens.
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