Browsing by Autor "Henry Montes"

Now showing 1 - 2 of 2

MECHANISMS OF NEUTROPHIL DEATH IN HIV INFECTED PATIENTS: ROLE OF ROS, CASPASES AND MAP KINASES PATHWAYS (46.14)
(American Association of Immunologists, 2007) Siham Salmen; Henry Montes; Andrés Sóyano; Dimas Hernández; Lisbeth Berrueta
Abstract Neutrophils from HIV+ patients have an increased susceptibility to undergo programmed cell death (PCD), which could explain neutropenia during advanced disease. In this work, key steps of PCD have been evaluated in neutrophils from HIV+ patients. The role of caspase-3, caspase-8, MAPK and ROS, were analyzed. Spontaneous neutrophil death is caspase-3 but no caspase-8 dependent, suggesting that the intrinsic pathway is involved as a pathogenic mechanism of PCD. Inhibition of ROS decreased spontaneous PCD and caspase-3 hydrolysis, connecting oxidative stress and Caspase-3 within neutrophils PCD in HIV infected patients. An increased constitutive phosphorylation of p38 MAPK, associated to increased neutrophils death in HIV+ patients, following inhibition of this kinase, was observed, suggesting a role for p38 MAPK in cell survival during the disease. We conclude that oxidative stress secondary to HIV infection can accelerate neutrophil death.
[Role of human immunodeficiency virus in leukocytes apoptosis from infected patients].
(National Institutes of Health, 2005) Siham Salmen; Carolina Guillermo; Melisa Colmenares; Luisa Barboza; Loredana Goncalves; Guillermo Terán; Nacarid Alfonso; Henry Montes; Lisbeth Berrueta
The hallmark of the immunodeficiency virus infection is a progressive detriment of the immune response which has been associated to a gradual loss of its responsible components, in particularly, CD4 positive T cells. Although this cell population is considered the main target of the virus, there is a recent deal of interest in studying other components that may not be targets of the virus, but are important elements to control infectious microorganisms and that have been demonstrated to be altered during HIV infection. Neutrophils (PMN) are innate immune components that play a fundamental role against HIV infection and these cells have been described as functionally altered during AIDS. It has been suggested that such a dysfunction could be attributed to an increased susceptibility of these cells to accelerated spontaneous apoptosis. However, the underlying mechanisms that induce programmed cell death of neutrophils remain unknown. In previous works we have explored some events involved during cell death of neutrophils from HIV infected patients. It is the purpose of this work to review the current knowledge of apoptosis signals in neutrophils and to discuss our own data about some mechanisms involved in spontaneous and Fas mediated apoptosis, which may contribute to understand neutrophils dysfunction during HIV infection.