We observed that the TNFa i.p. injection triggered a fast recruitment of neutrophils, later followed by monocytes, into the peritoneal cavity. Vascular Delamanid permeability was also observed: when we i.v. injected Evans blue prior to TNFa i.p. injection, we could observe a continued influx of the dye into the peritoneum. However, in mice pretreated with the siRNAPLD1, there was a significant reduction in the TNFa-triggered neutrophil and monocyte infiltration, as well as a marked reduction in the Evans blue influx. We also show here that the i.p. administration of TNFa caused an increase in CAMs and cytokine/chemokine levels in the peritoneal cavity, and that this increase was substantially inhibited in mice pretreated with the siRNA-PLD1. It is well-established that phagocytic cell infiltration and proinflammatory cytokine production are universal components of a wide range of inflammatory conditions and diseases, such as nephritis, arthritis, and acute graft rejection. Thus, agents that can inhibit phagocyte infiltration and/or the production of cytokines and chemokines may have wide therapeutic applications in the prevention and treatment of inflammatory diseases. The present study indicates that genetic silencing of PLD1, leading to the knockdown of PLD1 expression, very effectively blocked the cytokine/chemokine production, vascular permeability and leukocyte recruitment triggered by TNFa in vivo. Interestingly, at the cellular level, it has been reported that upregulation in the expression of ICAM-1, VCAM1, IL-6 and MIP1a/b is mediated by ERK1/2 and NFkB activities. This is in agreement with our Entrectinib (RXDX-101) earlier finding that TNFa-triggered ERK1/2 and NFkB activities and proinflammatory cytokine/chemokine production are downstream of PLD1 activation. Taken together, these observations suggest a potential role for PLD1 in the TNFa-triggered proinflammatory responses in vivo. However, it is possible that the knockdown of PLD1 has an effect not only on the TNFa-mediated signaling, but also on other receptors that may be stimulated as secondary events, following TNFa-triggered responses.