Abstract
Thalassophryne nattereri (niquim) is a venomous fish found off North and Northeast coast of Brazil, where it is known by the severity of the accidents involving humans. This review article is divided into four topics. The first one provides a brief description of the animal biology and its distribution off Brazilian coastal waters, the venom apparatus, signs and symptoms observed in envenomated humans and also describes envenomation in mice. The second topic describes the use of modern genetic approach and mass spectrometry for identification of highly expressed genes in its venom glands and the sequence of major toxins. The third chapter offers a detailed study of tissue injury induced by the venom and reveals the role of toxins that impair inflammation reduction. Finally, the fourth section expands the understanding of many extrinsic and intrinsic essential factors in maintaining survival of memory B cell compartment. Our results demonstrate the wide possibilities for research in the area of toxinology, also the necessity of interconnection among biochemistry, pharmacology and immunology areas for the expansion of knowledge and for generation of innovation.
Highlights
The Immunoregulation Unit has been developing research at the Butantan Institute since 1996 and began its work trying to clarify the pathophysiology of envenomation caused by the venomous fish Thalassophryne nattereri, common in the waters of the North and Northeast Brazilian coast
We confirmed that the antagonist effect of natterins is mediated by the activation of serine/threonine phosphatases and by the key signaling PI3K molecule
We describe a transcriptome analysis of 775 expressed sequence tags (ESTs) which represents a general panorama of the transcripts responsible for the physiological events that take place in the venom gland, since those data were generated from a non-normalized cDNA library
Summary
These works started asking how the main toxins of the T. nattereri venom contribute to the deficient influx of inflammatory leukocytes, which leads to the delayed inflammatory response in injured tissue By their end, we demonstrated that natterins may control the leukocyte-endothelial wall interactions in a mechanism dependent on negative signals derived from TLR2TLR4/Myd signaling cascade. We confirmed in an in vitro model the existence of a hierarchical process in which CD19-positive Bmem become CD138-positive IgG producing-ASC by a mechanism directly dependent on B-cell receptor (BCR) stimulation by venom, which could be potentiated by IL-17A [30] These studies shed new light on survival factors involved in the differentiation and maintenance of ASC in inflamed tissue and demonstrated that these cells require signals derived from antigen and IL-17A for the secretion of venom-specific antibodies for long periods of time. We showed that the longevity of ASC B220neg into inflamed peritoneal cavity induced by natterins is strong supported by up-regulated CXCR4 expression dependent on SP1R signals in B lymphocytes
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