Immunochemical detection of Lonomia obliqua caterpillar venom in rats

Abstract

Severe cases of human envenoming by caterpillars of the saturniid moth Lonomia obliqua in Brazil can result in renal damage, leading to renal failure, and intracerebral hemorrhaging. In this work, we used immunohistochemical staining with rabbit antiserum raised against L. obliqua venom to examine venom distribution in selected tissues of the brain (cerebellum and hippocampus), kidneys, and liver of male Wistar rats injected with a single dose of venom (200 microg/kg, i.v.) and sacrificed 6, 18, 24, and 72 hours later. The immunolabeling of GFAP was also examined to assess the venom effects on perivascular astrocytic end-feet in the microvasculature of the hippocampus and cerebellum. Venom was detected in the kidneys (6 and 18 hours) and in the liver (6 hours) but not in the brain at any of the time intervals examined. In contrast, immunolabeling for GFAP revealed astrogliosis in the cerebellum and enhanced expression of this protein in the glial processes of the cerebellum and hippocampus, with a maximum response from 24 hours onwards. The high immunoreactivity seen in the kidneys agreed with the renal damage and dysfunction reported for some patients. The lack of venom detection in the brain, despite the altered expression of GFAP in astrocytes, suggested either that the venom does not enter this organ or that its entrance is transient and fast. Alternatively, the circulating venom may induce the release of mediators that could serve as second messengers to provoke the late astrocytic reactivity and astrogliosis. It is possible that both of these mechanisms may contribute to the effects observed.

Mechanisms of acute kidney injury induced by experimental Lonomia obliqua envenomation

“…Previous studies are consistent with our observations. Using immunochemical and radio-labeling methods to analyze venom biodistribution in rats, the highest quantities of LOBE were detected in kidneys, blood and urine (Rocha-Campos et al , 2001; Da Silva et al , 2004). …”

Acute kidney injury due to tropical infectious diseases and animal venoms: a tale of 2 continents

“…246 The mechanisms of AKI are direct nephrotoxicity, intravascular hemolysis, systemic and endothelial inflammatory pathway activation, hypotension, increased renal tissue expression of proteins involved in cell stress, inflammation, heme-induced oxidative stress, coagulation, and complement system activation. [247][248][249] Renal histology has shown ATN, glomerular fibrin deposition, and ischemia and tubular atrophy. 243,244,249 Development of CKD following Lonomia venom-associated AKI was described in 5 patients.…”

Effects of Lonomia obliqua Venom on Vascular Smooth Muscle Cells: Contribution of NADPH Oxidase-Derived Reactive Oxygen Species

“…The VSMC dysfunction is characterized by an exacerbation of cell migration and proliferation, events that are amplified by the release of inflammatory mediators [ 18 , 23 , 24 , 25 , 26 ]. Although during the envenomation, the venom is primarily injected into the victim’s subcutaneous tissue, significant amounts of toxins are able to reach the vascular system, including the VSMC [ 11 , 15 ]. Then, we raised the hypothesis that L. obliqua venom could lead to VSMC dysfunction.…”

“…The venom can directly modulate the victim’s hemostatic system by the proteolytic activation of coagulation, fibrinolytic, and kinin cascades, generating high concentrations of intravascular thrombin, plasmin, and kallikrein [ 8 , 9 , 10 ]. Together, the factors released during the envenomation act on the vascular system, increasing vascular permeability, and inducing hypotension, as well as nociceptive and edematogenic responses [ 11 , 12 , 13 , 14 ].…”