Abstract
Bothrops jararaca venom (BjV) can induce mast cell degranulation. In order to investigate the role of mast cells and the interference of the host genetic background in the inflammation induced by BjV, we have used mouse strains selected for maximal (AIRmax) or minimal (AIRmin) acute inflammatory response (AIR). Mice were pretreated with an inhibitor of mast cell degranulation, cromolyn (CROM), and injected in footpads or intraperitoneally (i.p.) with BjV. Pain was measured with von Frey hairs, cell migration in the peritoneum by flow cytometry, and reactive oxygen species (ROS) production by chemiluminescence assays. The nociceptive response to BjV was higher in AIRmax than AIRmin mice; however, this difference was abolished by pretreatment with CROM. BjV induced peritoneal neutrophil (CD11b+ GR-1+) infiltration and ROS secretion in AIRmax mice only, which were partially inhibited by CROM. Our findings evidence a role for mast cells in pain, neutrophil migration, and ROS production triggered by BjV in AIRmax mice that are more susceptible to the action of BjV.
Highlights
The large majority of ophidic accidents in Brazil are caused by Bothrops jararaca (Bj) snakes [1]
To certify that CROM inhibits mast cell degranulation in our model, we analyzed the mesenteric tissue of AIRmax and AIRmin mice pretreated with CROM and injected with phosphate buffered saline (PBS), Bothrops jararaca venom (BjV), or C48/ 80, a compound known to degranulate mast cells
Despite the difference observed between PBS-injected AIRmax and AIRmin, the induction of mast cell degranulation by both C48/80 and BjV was similar in both strains
Summary
The large majority of ophidic accidents in Brazil are caused by Bothrops jararaca (Bj) snakes [1]. The inflammatory response resulting from tissue damage and the direct action of toxins is characterized by a local increase in blood flow, exudation of plasma proteins, and migration and activation of leukocytes from the vessels to the site of injury. At the end of the bidirectional selective process for the production of AIRmax and AIRmin lines, the gene alleles endowed with opposite effects in the regulation of the maximum and minimum acute inflammatory responses were considered to be accumulated in AIRmax and AIRmin mice, respectively [16]. These mouse lines are normal and represent the individuals who are situated at the extremes of high or low response that are found in heterogeneous populations
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