Opinion Article - (2015) Volume 1, Issue 1
Lizziane Kretli Winkelstroter*
University of Western São Paulo (UNOESTE), José Bongiovani St. 700 19050-920 - Presidente Prudente, SP, Brazil
Corresponding Author:
Lizziane Kretli Winkelstroter
Lizziane Kretli Winkelstroter, University of Western São Paulo (UNOESTE), José Bongiovani St. 700 19050-920 - Presidente Prudente, SP, Brazil
Tel: 5518 32291000, 08007715533
E-mail: lizzianekretli@gmail.com
Received date: October 02, 2015 Accepted date: October 07, 2015 Published date: October 30, 2015
Citation: Kretli L, Dietary W. Microbial Biofilms: The Challenge of Food Industry. Biochem Mol Biol J. 2016, 1:1.
Failure in the cleaning process may form a conditioned film on the food processing surfaces which allows bacterial adherence. After the initial adhesion the microorganism start to multiplicate and results in a cell mass embedded in a complex exopolysaccharide matrix known as biofilm. Microorganisms in biofilm are more resistant to antimicrobial compounds than planktonic cells. That behavior allows them to persist and to survive even after sanitization processes. Biofilms is a relevant public health problem and represents potential source of contamination. Moreover, the food industry can face serious consequences by the presence of biofilms which results in economic losses. To guarantee the quality and the safety of food product, efforts are needed to improve the cleaning and sanitizing program used to inactivate microorganisms and prevent the biofilms formation. Thus, understanding the concept of microbial biofilms, the aspects inherent to their structure and composition, as well as its mechanism of formation, are fundamental for the development of effective strategies to control and prevent them.
Keywords
Purinergic signaling; Purinoceptors; Ectonucleotidases; Hypertension disease; Neurotransmitters
Introduction
The purinergic signaling concept was firstly proposed by Burnstock in the early 1970s [1]. At that time, the idea that ATP could act as a neurotransmitter besides its well established role as energy source for several metabolic processes faced intense resistance. Nowadays, the nucleotides’ signaling is widely accepted as a primitive and highly conserved system and distinct roles for nucleotides (e.g. ATP, ADP) and nucleosides (e.g. adenosine) as extracellular transmitters are now extensively described in a range of tissues [2]. It is remarkable that nucleotides and nucleosides must reach the extracellular space in order to function as cellular messengers. This may either occur by cellular lysis or under mechanical stimulus (shear stress, hypoxia) as well as release from nerve terminals together with other neurotransmitters [3]. Once they get the extracellular space, nucleotides will bind purinergic P2 receptors (P2X, ion channels exclusive responsive to ATP or P2Y, G-coupled receptors that may respond to ATP, ADP, UTP, UDP and UDP-glucose) while adenosine will be recognized by a class of purinoceptors named P1 [4].
After passing their message inside the cell, these molecules must be metabolized to finish purinergic signaling. The hydrolysis of nucleotides and nucleosides is guaranteed by a cascade of ectonucleotidases, which are ectoenzymes able to regulate the agonist availability as well as the purinoceptors activation [5]. Among all ectonucleotidases already described, the families ecto-nucleotide-triphosphate diphosphohydrolase (E-NTPDase1-8) and ecto-5’-nucleotidase (CD73, E-5’-N) seem to be the most important. Acting in concert, both E-NTPDase and CD73 may at the same time finish with ATP signaling and promote adenosine signaling activation. The role of purinergic signaling in the regulation of cardiovascular system has becoming more and more important. Importantly, the activation of endothelial P2 receptors induces a local vasorelaxation by the release of nitric oxide (NO), prostacyclin (PGI2) and endothelium-derived hyperpolarizing factor (EDHF) [6]. In an opposite way, the VSMC purinoceptors activation promotes a vasoconstriction via P2 and P2Y [7]. A broad range of studies has showing the importance of purines in the cardiovascular regulation. Our group has focused in the investigation of ectonucleotidases, mainly NTPDase1 and ecto-5’- nucleotidase, in distinct pathophysiological scenarios of vascular biology. In this regard, we have already kinetically characterized the presence of soluble NTPDases in serum fraction, as well as in circulating platelets [8,9]. Ultimately, we have putting a big effort to clarify the role of these enzymes in the development and progression of hypertension disease. From the literature, we know that NTPDase1, expressed in both VSMC and EC, is the main ectonucleotidase in the vasculature that is able to modulate the availability of nucleotides and the activation of specific purinergic receptors, controlling the vascular tone and blood pressure [10]. Presently, we are investigating if there is a “standard behavior” for ectonucleotidases activities in response to different hypertension models (chemical, genetic and diet-induced). Purinergic signaling components are expressed in all animal biological systems. More than this, some of purinergic elements are being already manipulated in clinics as is the case for thienopyridines that are selective irreversible P2Y12 platelet antagonists, used as anti-platelet drugs. Also, the importance of this signaling pathway has been compared to other classical regulators of cardiovascular processes, such as sympathetic and renin-angiotensin systems. The scarcity of selective agonists and antagonists to purinergic receptors as well as the lack of specific inhibitors to ectonucleotidases still restricts the use of purinergic therapies. Nonetheless, this paucity also strengths the purinergic signaling studies as a very fertile ground of investigation to be used as a new approach in the understanding and treatment of cardiovascular processes and pathologies.
