**4. Conclusions**

Our study showed, for the first time, the pro-inflammatory effects of BaV and Kn-Ba upon THP-1 derived human macrophages. Both stimuli are responsible for the production of the cytokines TNF and the chemokines RANTES and IL-8. However, the significant production of these mediators occurred in response to Kn-Ba. Only Kn-Ba was able to induce the production of IL-6, MCP-1, and IP-10, whereas PGE2 was produced only in response to BaV. Finally, although both stimuli induced the production of IL-1β, suggesting that the inflammasomes may play a role in BaV envenomation, the highest production of this cytokine in response to BaV suggests the participation of other venom components in this process (Figure 8). These results together with previous data published by our group describing the biological actions of Kn-Ba and BaV-induced inflammation in vivo help us to better understand the inflammatory mechanisms involved in this envenomation, and to list important toxins for the future development of antivenoms.

**Figure 8.** Comparative overview of the inflammatory profiles induced by BaV and Kn-Ba in THP-1 macrophages. THP-1 macrophages were treated with BaV (left; blue) and Kn-Ba (right; red) resulting in the synthesis and secretion of the indicated cytokines, chemokines, and PGE2. The mediators highlighted in larger size were produced by both stimuli, but at higher levels at the evidenced side. Both stimuli induced the production and release of IL-1β, indicating the inflammasomes pathway activation during BaV envenomation. However, the highest production of this cytokine in response to BaV indicated the participation of other venom components in this process. The schematic art pieces used in this figure were provided by Servier Medical art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 4.0 Unported License.
