Abstract
Sepsis induces a severe systemic inflammatory response that may result in multiple organ dysfunction and death. Studies using a protein derived from natural Hevea brasiliensis (rubber tree) latex, denominated Hev b 13, have demonstrated important anti-inflammatory effects, but no data have been published regarding its effects on sepsis. The aim of this study was to investigate the effects of Hev b 13 on the inflammatory response and lung lesions of septal rats. Male Wistar rats were submitted to cecal ligation and puncture (CLP), randomized into groups and treated with subcutaneously administered doses of 0.5/2.0/3.0 mg/Kg of Hev b 13. Next, animals were subdivided into three different points in time (1, 6 and 24 hours after treatments) for collection of blood samples and euthanasia accompanied by organ removal. Total and differential leukocyte counts, cytokine dosage and histological assessment were analyzed. Treatment with Hev b 13 resulted in a significant decline in total and differential leukocytes as well as suppression of TNF-α and IL-6 production, associated with the increase in IL-10 and IL-4 in plasma and lung tissue. Moreover, it reduced morphological and pathological changes found in the lungs, including neutrophil infiltration, edema and alveolar thickening. The present study concluded that Hev b 13 exerts anti-inflammatory effects and attenuates lung lesions in septal rats, showing potential for clinical application.
Highlights
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection (Shankar-Hari et al, 2016)
The animals submitted to cecal ligation and puncture (CLP) (CLP control) exhibited progressive leukocytosis in accordance with sepsis evolution
The increase in total, mature and basophil leukocytes in the groups treated with Hev b 13 at all doses (0.5/2.0/3.0mg/kg) was significantly lower than in the CLP control group after 1 hour of treatment (p
Summary
Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection (Shankar-Hari et al, 2016). During the development of sepsis, bacterial components activate transmembrane recognition proteins, called toll like receptors (TLRs), which recognize pathogen-associated molecular patterns (PAMPs). These initiate an immunological cascade resulting in the release of pro-inflammatory interleukins, including the tumor necrosis factor (TNF-α), interleukin (IL) 1, IL-2, IL-6, IL-8, and IL-12, among others (Cai et al, 2016). Overproduction of these inflammatory mediators (cytokine storm) induces vasodilation, increased capillary permeability, hypotension, hemoconcentration, macromolecular leakage and edema, and may lead to multiple organ dysfunction syndrome (MODS), where the lungs are the most frequently affected (Matsuda and Hattori, 2006; Stearns-Kurosawa et al, 2011; Ates et al, 2015)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
