CV Lattes
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Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB) (Institutional affiliation from the last research proposal) Birthplace: Brazil
Dr. Steiner did his undergraduate and graduate training at the University of Sao Paulo (Brazil), having obtained his PharmD in 1999 and his PhD in Physiology in 2002. He did his postdoctoral training at Joseph?s Hospital & Medical Center (Phoenix, AZ, USA) from 2002 to 2007. His first faculty appointment was as an Assistant Professor at the Albany College of Pharmacy & Health Sciences (Albany, NY, USA), where he stayed until 2012. Since then, Dr. Steiner has been a faculty member in Immunology at the Institute of Biomedical Sciences of the University of Sao Paulo, where he currently occupies an Associate Professor position. The Steiner laboratory studies the multilateral interactions among immune system and physiological systems in life-threatening infections (sepsis) and systemic inflammation. The overall goal is to identify the mechanisms by which these systems cooperate or compete with each other under different contexts. Many, but certainly not all, of the cooperative mechanisms rely on the central nervous system as an integrator of immune, physiological and environmental clues. Currently, Dr. Steiner?s research projects fall in one of three lines of investigation: (i) Tissue-specific functions of resident macrophages, their crosstalk, and their neuroendocrine modulation; (ii) Cost-benefit relationship of fever versus hypothermia in bacterial sepsis and fungal infections; (iii) Hemodynamics of septic shock. E-mail: asteiner@usp.br. (Source: Lattes Curriculum)
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Infectious diseases continue to be of major cause of morbidity and mortality worldwide. It is recognized that therapies that target the immune system have the potential to improve outcome in infectious diseases, but the development of effective immunomodulatory therapies has proven to be quite challenging. One reason underscoring the challenge is that the immune response is a double-edged…
By monitoring systemic hemodynamics with the highest temporal resolution in unanesthetized rats, in combination with ex-vivo assessment of vascular function, we found that early development of hypotension following injection of bacterial lipopolysaccharide (LPS) is brought about by a fall in vascular resistance when arterioles are still fully responsive to vasoactive agents. This approach…
Sepsis (systemic inflammation in the setting of infection) is a leading cause of mortality in Brazil and worldwide. A switch in thermal state from fever to hypothermia occurs in the most severe cases of sepsis, which has led to the perception that hypothermia reflects organ failure and is detrimental. We argue that this perception may be premature and incorrect, since there is evidence in…
Sepsis (systemic inflammation in the setting of infection) is a leading cause of mortality in Brazil and worldwide. A switch in thermal state from fever to hypothermia occurs in the most severe cases of Sepsis, which has led to the perception that hypothermia reflects organ failure and is detrimental. We argue that this perception may be premature and incorrect, since there is evidence in…
Septic shock is seen as a condition in which decreases in systemic vascular resistance (SVR) compromise tissue perfusion pressure. In this project, unexpected preliminary results have led us to question the applicability of this model to the most terminal phase of septic shock. We hypothesize that this terminal phase is associated with a switch in hemodynamic profile, with SVR transitioni…
(Only some records are available in English at this moment)
Context: Survival from sepsis depends on a delicate balance between pathogen elimination and containment of host tissue damage. Among the mediators involved, tumor necrosis factor (TNF) plays a central role in this balance. Although the spleen has traditionally been considered the primary source of TNF, recent evidence demonstrates that its removal, followed by systemic inflammatory stimu…
By monitoring systemic hemodynamics with the highest temporal resolution in unanesthetized rats, in combination with ex-vivo assessment of vascular function, we found that early development of hypotension following injection of bacterial lipopolysaccharide (LPS) is brought about by a fall in vascular resistance when arterioles are still fully responsive to vasoactive agents. This approach…
In this project, we aim to investigate the activity mechanisms of NADPH oxidase (NOX), which has the primary function of catalyzing the production of reactive oxygen species (ROS), by exploring the overexpression of protein subunits in macrophages. We hypothesize that thermal stimulation regulates the enzymatic activity mechanisms of the gp47-phox, gp91-phox, and gp22-phox subunits. When …
The inflammatory response to a widespread infection is an immune response mechanism capable of protecting the body against pathogen infections, but if unregulated, it can also lead to sepsis. The inflammatory reflex pathway has been described as capable of generating the necessary regulation for the acute inflammatory response.The increased predisposition to bacterial infections due to vi…
Previous results in our laboratory demonstrated a spleen-liver axis regulates TNF production in the bacterial lipopolysaccharide (LPS) induced systemic inflammation model in rats. Our proposal is that humoral signals released by spleen macrophages (which may include leukotriene B4) reach the liver via the bloodstream, where they interact with the liver's resident macrophages (Kupffer cell…
(Only some records are available in English at this moment)
Resident macrophages are sentinel immune cells that sense microbes and the tissue microenvironment, being essential for host defense. They are highly heterogeneous, with each subpopulation playing tissue-specific roles. However, the cellular mechanisms underlying such heterogeneity are not understood, and neither are the mechanisms by which macrophages from distinct organs communicate wit…
As presented in the activity report, the results obtained so far not only question the prematurely accepted pro-inflammatory role of leptin, but, on the contrary, demonstrate that physiological concentrations of leptin exert anti-inflammatory effects. Our results further show that such anti-inflammatory effect does not result from a direct action of leptin on peripheral macrophages. Lepti…