About this Research Topic
Background: It has been more than 60 years since Dr. Gasser and Dr. Gianantonio have described the Hemolytic uremic syndrome (HUS), an unknown new pathology that affected mainly children. HUS is an illness characterized by a triad of events including non-immune haemolytic anaemia, thrombocytopenia, and acute renal failure caused by Shiga toxin (Stx) expressed by enterohemorrhagic Escherichia coli (EHEC). Patients may initially develop bloody diarrhea when EHEC succeeds to colonize the gastrointestinal tract.
Once Stx reaches the bloodstream it may target endothelial, kidney, and/or brain cells through the Stx globotriaosylceramide receptor (Gb3), causing cytotoxicity. Neurological impairment frequently occurs and is associated with a worse prognosis. In addition to Stx2 pathogenicity, lipopolysaccharide (LPS) is another virulence factor that is also released from EHEC, enhancing the deleterious effects of Stx in different cells and organs.
New reports have shown that in addition to children, different etiological populations suffer from HUS and related encephalopathies including the elderly and immunosuppressed people in sporadic outbreaks or individual cases.
Goal: In recent years, interest has arisen in unravelling the pathophysiological mechanisms that occur in different organs and tissues during a Shiga Toxin-producing Escherichia coli (STEC)- infection. Different forms of circulating Stx have been described: either alone as Stx2in microvesicles in blood cells, or as Stx phages. In addition to this, alternative non canonical receptors to Stx have been proposed whereby the toxin can bind to a host cell. The cytotoxic response is usually accompanied by an inflammatory condition in the host, define the severity of the injury. Another explored field has been the influence of diet and microbiota on the severity of gastrointestinal tract diseases, and how this condition may affect the health of organs.
There is also currently great interest in the study of drugs capable of neutralizing or alleviating STEC infection. One of the most successful research to date was the development of antibodies. However, there is still no effective and protocolized treatment for this condition, nor an effective diagnostic to detect earlier this disease for preventive purposes.
Understanding the pathophysiological mechanisms of STEC infections from the molecular and cellular level to integrate the involved organs to clinical and behavioral consequences by which STEC triggers is a current challenge that has yet to be fulfilled. Studies and development of novel therapeutic strategies are fundamental to prevent or palliate this affection. Pursuing novel clinical and experimental findings are essential to shed light on the comprehension of these pathological mechanisms. This Research Topic therefore aims to explore these mechanisms further.
Scope: In this Research Topic we welcome manuscripts on, but not limited to the following sub-themes:
• Pathophysiological mechanisms produced by STEC: clinical studies and experimental research.
• Research on STEC serotypes and virulence factors.
• Investigation of how Stx circulates in the bloodstream including its entrance or exit in different organs.
• Alternative non-canonical receptors for Stx.
• Inflammation studies associated with clinical and experimental STEC infection.
• Multidisciplinary research regarding STEC infection.
• Novel therapeutic approaches against STEC infection.
Once Stx reaches the bloodstream it may target endothelial, kidney, and/or brain cells through the Stx globotriaosylceramide receptor (Gb3), causing cytotoxicity. Neurological impairment frequently occurs and is associated with a worse prognosis. In addition to Stx2 pathogenicity, lipopolysaccharide (LPS) is another virulence factor that is also released from EHEC, enhancing the deleterious effects of Stx in different cells and organs.
New reports have shown that in addition to children, different etiological populations suffer from HUS and related encephalopathies including the elderly and immunosuppressed people in sporadic outbreaks or individual cases.
Goal: In recent years, interest has arisen in unravelling the pathophysiological mechanisms that occur in different organs and tissues during a Shiga Toxin-producing Escherichia coli (STEC)- infection. Different forms of circulating Stx have been described: either alone as Stx2in microvesicles in blood cells, or as Stx phages. In addition to this, alternative non canonical receptors to Stx have been proposed whereby the toxin can bind to a host cell. The cytotoxic response is usually accompanied by an inflammatory condition in the host, define the severity of the injury. Another explored field has been the influence of diet and microbiota on the severity of gastrointestinal tract diseases, and how this condition may affect the health of organs.
There is also currently great interest in the study of drugs capable of neutralizing or alleviating STEC infection. One of the most successful research to date was the development of antibodies. However, there is still no effective and protocolized treatment for this condition, nor an effective diagnostic to detect earlier this disease for preventive purposes.
Understanding the pathophysiological mechanisms of STEC infections from the molecular and cellular level to integrate the involved organs to clinical and behavioral consequences by which STEC triggers is a current challenge that has yet to be fulfilled. Studies and development of novel therapeutic strategies are fundamental to prevent or palliate this affection. Pursuing novel clinical and experimental findings are essential to shed light on the comprehension of these pathological mechanisms. This Research Topic therefore aims to explore these mechanisms further.
Scope: In this Research Topic we welcome manuscripts on, but not limited to the following sub-themes:
• Pathophysiological mechanisms produced by STEC: clinical studies and experimental research.
• Research on STEC serotypes and virulence factors.
• Investigation of how Stx circulates in the bloodstream including its entrance or exit in different organs.
• Alternative non-canonical receptors for Stx.
• Inflammation studies associated with clinical and experimental STEC infection.
• Multidisciplinary research regarding STEC infection.
• Novel therapeutic approaches against STEC infection.
Keywords: STEC, EHEC, Stx, LPS, Virulence Factor, Inflammation, Pathophysiological Mechanisms, Phages, Microvesicles, Neutrophils Experimental Models, Blood Brain Barrier, Blood Gut Barrier, Stx Non-Canonical Receptors
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