Lung Immunoreactivity and Airway Inflammation: Their Assessment After Scorpion Envenomation

Abstract

Release and activation of pro-inflammatory mediators are among the most important induced factors that are involved in the scorpion envenomation pathogenesis. Inflammatory response and lung reactivity were studied in mice following subcutaneous injection with Androctonus australis hector (Aah) venom. Venom immunodetection in lungs and sequestered cell population in the airways were determined. Cytokines, cellular peroxidase activities (eosinophil peroxidase, myeloperoxydase), and IgE antibodies were also assessed. Immunohistochemical study revealed a positive detection of the Aah venom in the alveolar wall, venule lumens, and inside inflammatory cells. Severe lung edema associated with rapid inflammatory response was observed after animal envenomation. Lung neutrophilia and eosinophilia were accompanied with IL-4, IL-5 release, and IgE synthesis. In conclusion, high cytokine levels, recruitment of inflammatory cells (eosinophils and neutrophils), and increased IgE concentration may contribute to the exacerbation and maintenance of the induced inflammatory response in lungs by scorpion venom. These results lead to the better understanding of this induced pathogenesis and could help the physicians to take care of envenomed patients.

Systemic Responses following Brain Injuries and Inflammatory Process Activation Induced by a Neurotoxin of <b><i>Androctonus</i></b> Scorpion Venom

“…The activation of inflammatory response induced by KTX 2 contributes probably to the increase in the production of proinflammatory cytokines such as TNF-α and IL-6, leading to an immunological imbalance and migration of leukocytes into the peripheral blood and into the inflammatory sites. Neutrophil and eosinophil recruitment at the site of injury (brain, pancreas and liver) leads to the release of oxygen free radicals and cytotoxic leukocyte-derived products (such as EPO and MPO), which can induce alterations of endothelial cells and subendothelial matrix proteins resulting in tissue injuries [13,29]. …”

Neuropathophysiological Effect and Immuno-Inflammatory Response Induced by Kaliotoxin of <b><i>Androctonus</i></b> Scorpion Venom

“…Eosinophil accumulation and activation were measured by evaluating EPO activity in brain, heart, and lung homogenates and in sera as previously described [17]. Samples were mixed with Tris-HCl buffer containing OPD (10 m m ) and H 2 O 2 (0.4 m m ).…”

“…The pathogenesis of these disturbances is multifactorial. In previous studies, it has been reported that A. australis Hector venom and its toxins are able to induce an inflammatory response characterized by high serum levels of cytokines, nitric oxide (NO), cellular peroxidase activities [eosinophil peroxidase (EPO), myeloperoxidase (MPO)], and tissue leucocytosis [14,15,17,18]. …”

Mesobuthus tamulus venom induces acute respiratory distress syndrome in rats involving additional mechanisms as compared to oleic acid model

“…Pulmonary edema can be attributed to both cardiogenic and non-cardiogenic factors (Isbister and Bawaskar, 2014;Sofer and Gueron, 1988;Bahloul et al, 2013;Amaral et al, 1994;Deshpande and Akella, 2012). The non cardiogenic factors include pulmonary edema producing toxin (PO-Tx) isolated from Mesobuthus tamulus venom, inflammatory mediators, direct toxicity etc (Abdoon et al, 2006;Adi-Bessalem et al, 2012;Deshpande et al, 1999Deshpande et al, , 2005Dutta and Deshpande, 2011;Kanoo et al, 2009a;Saidi et al, 2013;Pandey and Deshpande, 2004;Petricevich, 2010). In addition, ventilatory changes have also been reported in mice after scorpion envenomation (Paneque-Peres et al, 2009).…”