Effect of Lonomia obliqua Venom on Human Neutrophils.
João Alfredo de MoraesGenilson RodriguesDaniel Guimarães-BastosVany Nascimento-SilvaErik SvensjöMariana Renovato-MartinsMarkus Berger OliveiraJorge GuimarãesThereza Christina Barja-FidalgoPublished in: Toxins (2021)
The significant incidence of deforestation in South America culminates in the contact of humans with typical forests species. Among these species, one may highlight Lonomia obliqua caterpillar, which, when touched by humans, can poison them through their bristles. Therefore, better acknowledging the mechanisms involved in envenomation caused by Lonomia obliqua caterpillar bristle extract (LOCBE) may contribute to further treatments. Recently, we demonstrated that LOCBE induces a pro-inflammatory profile in endothelial cells; thus, we decided to investigate the effects of LOCBE on human polymorphonuclear neutrophils (PMN), which are the first leukocytes that migrate to the inflammatory focus. Our results showed that treatment with LOCBE induced PMN chemotaxis together with alterations in actin cytoskeleton and focal adhesion kinase (FAK) activation, favoring migration. Concurrently, LOCBE induced PMN adhesion to matrix proteins, such as collagen IV, fibronectin, and fibrinogen. Moreover, we observed that LOCBE attenuated PMN apoptosis and increased reactive oxygen species (ROS) production together with nuclear factor kB (NF-κB) activation-a redox-sensitive transcription factor-as well as interleukin (IL)-1β and IL-8 release. We call attention to the ROS-dependent effect of LOCBE on increased cell migration once an antioxidant treatment reverted it. In summary, we report that LOCBE activates PMN, inducing pro-inflammatory responses modulated by ROS.
Keyphrases
- cell migration
- endothelial cells
- reactive oxygen species
- high glucose
- nuclear factor
- oxidative stress
- cell death
- diabetic rats
- dna damage
- transcription factor
- toll like receptor
- anti inflammatory
- signaling pathway
- biofilm formation
- risk factors
- cystic fibrosis
- pluripotent stem cells
- endoplasmic reticulum stress
- immune response
- cell cycle arrest
- combination therapy