Lourdes Arriaga‐Pizano

Centro Medico Nacional Siglo XXI

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Constantino López‐Macías

Mexican Social Security Institute

Eduardo Ferat‐Osorio

Mexican Social Security Institute

Armando Isibasi

Mexican Social Security Institute

Arturo Cérbulo‐Vázquez

Hospital General de México

Jessica L. Prieto‐Chávez

Mexican Social Security Institute

Héctor Mayani

Mexican Social Security Institute

Laura C. Bonifaz

Mexican Social Security Institute

Isabel Wong‐Baeza

Instituto Politécnico Nacional

Rodolfo Pastelin‐Palacios

Universidad Nacional Autónoma de México

Rosana Pelayo

Mexican Social Security Institute

Cooperative Institutions

Mexican Social Security Institute

256

Centro Medico Nacional Siglo XXI

179

Universidad Nacional Autónoma de México

171

Instituto Politécnico Nacional

141

Hospital de Especialidades

110

Center for Research and Advanced Studies of the National Polytechnic Institute

Hospital Infantil de México Federico Gómez

Hospital General de México

Secretaria de Salud

Instituto Nacional de Perinatología

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Adult, but not neonatal, human lymphoid progenitors respond to TLR9 ligation by producing functional NK-like cells

Experimental Hematology (2014)

Eduardo Vadillo Elisa Dorantes‐Acosta Lourdes Arriaga‐Pizano Antonieta Chávez‐González Elba Reyes‐Maldonado

TLR9

Innate lymphoid cell

10.1016/j.exphem.2014.03.008

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Citations (14)

Functional analysis of myelodysplastic syndromes-derived mesenchymal stem cells

Leukemia Research (2008)

Eugenia Flores‐Figueroa Juan José Montesinos Patricia Flores-Guzmán Guillermo Gutiérrez-Espı́ndola Rosa Marı́a Arana-Trejo

10.1016/j.leukres.2008.02.013

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Citations (98)

A Toll/IL-1R/resistance domain-containing thioredoxin regulates phagocytosis in Entamoeba histolytica

Parasites & Vectors (2012)

Ismael Mancilla‐Herrera Alfonso Méndez-Tenorio Isabel Wong‐Baeza Alexis Paulina Jiménez‐Uribe Marcela Alcántara‐Hernández

Abstract Background Entamoeba histolytica is a protozoan parasite that infects humans and causes amebiasis affecting developing countries. Phagocytosis of epithelial cells, erythrocytes, leucocytes, and commensal microbiota bacteria is a major pathogenic mechanism used by this parasite. A Toll/IL-1R/Resistance (TIR) domain-containing protein is required in phagocytosis in the social ameba Dictyostelium discoideum , an ameba closely related to Entamoeba histolytica in phylogeny. In insects and vertebrates, TIR domain-containing proteins regulate phagocytic and cell activation. Therefore, we investigated whether E. histolytica expresses TIR domain-containing molecules that may be involved in the phagocytosis of erythrocytes and bacteria. Methods Using in silico analysis we explored in Entamoeba histolytica databases for TIR domain containing sequences. After silencing TIR domain containing sequences in trophozoites by siRNA we evaluated phagocytosis of erythrocytes and bacteria. Results We identified an E. histolytica thioredoxin containing a TIR-like domain. The secondary and tertiary structure of this sequence exhibited structural similarity to TIR domain family. Thioredoxin transcripts silenced in E. histolytica trophozoites decreased erythrocytes and E. coli phagocytosis. Conclusion TIR domain-containing thioredoxin of E. histolytica could be an important element in erythrocytes and bacteria phagocytosis.

Entamoeba

10.1186/1756-3305-5-224

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Citations (3)

Human Mesenchymal Stem/Stromal Cells from Umbilical Cord Blood and Placenta Exhibit Similar Capacities to Promote Expansion of Hematopoietic Progenitor Cells In Vitro

Stem Cells International (2017)

Guadalupe R. Fajardo-Orduña Héctor Mayani Patricia Flores-Guzmán Eugenia Flores‐Figueroa Érika Hernández-Estévez

Mesenchymal stem/stromal cells (MSCs) from bone marrow (BM) have been used in coculture systems as a feeder layer for promoting the expansion of hematopoietic progenitor cells (HPCs) for hematopoietic cell transplantation. Because BM has some drawbacks, umbilical cord blood (UCB) and placenta (PL) have been proposed as possible alternative sources of MSCs. However, MSCs from UCB and PL sources have not been compared to determine which of these cell populations has the best capacity of promoting hematopoietic expansion. In this study, MSCs from UCB and PL were cultured under the same conditions to compare their capacities to support the expansion of HPCs in vitro. MSCs were cocultured with CD34+CD38-Lin- HPCs in the presence or absence of early acting cytokines. HPC expansion was analyzed through quantification of colony-forming cells (CFCs), long-term culture-initiating cells (LTC-ICs), and CD34+CD38-Lin- cells. MSCs from UCB and PL have similar capacities to increase HPC expansion, and this capacity is similar to that presented by BM-MSCs. Here, we are the first to determine that MSCs from UCB and PL have similar capacities to promote HPC expansion; however, PL is a better alternative source because MSCs can be obtained from a higher proportion of samples.

Cord blood

Cord lining

10.1155/2017/6061729

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Citations (14)

Activated endothelial cells limit inflammatory response, but increase chemoattractant potential and bacterial clearance by human monocytes

Cell Biology International (2015)

Ismael Mancilla‐Herrera José Antonio Alvarado‐Moreno Arturo Cérbulo‐Vázquez Jessica L. Prieto‐Chávez Eduardo Ferat‐Osorio

Inflammation is the normal immune response of vascularized tissues to damage and bacterial products, for which leukocyte transendothelial migration (TEM) is critical. The effects of cell-to-cell contact seen in both leukocyte and endothelial cells include cytoskeleton rearrangement, and dynamic expression of adhesion molecules and metalloproteinases. TEM induces expression of anti-apoptotic molecules, costimulatory molecules associated with antigen presentation, and pattern recognition receptors (PRR), such as TLR-4, in monocytes. However, little is known about how TLR-4 increment operates in monocytes during an inflammatory response. To understand it better, we used an in vitro model in which monocytes crossed a layer of IL-1β stimulated Human Umbilical Vein Endothelial Cells (HUVEC). After TEM, monocytes were tested for the secretion of inflammatory cytokines and chemokines, their phenotype (CD14, CD16, TLR-4 expression), and TLR-4 canonical [Nuclear Factor kappa B, (NF-κB) pathway] and non-canonical [p38, extracellular signal-regulated kinases (ERK) 1/2 pathway] signal transduction induced by lipopolysaccharide (LPS). Phagocytosis and bacterial clearance were also measured. There was diminished secretion of LPS-induced inflammatory cytokines (IL-1β, IL-6, and TNF-α) and higher secretion of chemokines (CXCL8/IL-8 and CCL2/MCP-1) in supernatant of TEM monocytes. These changes were accompanied by increases in TLR-4, CD14 (surfaces expression), p38, and ERK1/2 phosphorylated cytoplasmic forms, without affecting NF-κB activation. It also increased bacterial clearance after TEM by an O2 -independent mechanism. The data suggest that interaction between endothelial cells and monocytes fine-tunes the inflammatory response and promotes bacterial elimination.

Monocyte

Interleukin 8

CD16

Proinflammatory cytokine

10.1002/cbin.10440

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Citations (8)

Prolactin down-regulates CD4+CD25hiCD127low/− regulatory T cell function in humans

Journal of Molecular Endocrinology (2011)

María Victoria Legorreta-Haquet Adriana Karina Chávez-Rueda Eduardo Montoya-Díaz Lourdes Arriaga‐Pizano Raúl Silva‐García

Among its many functions, prolactin (PRL) participates in immune responses and promotes the activation, differentiation and proliferation of T cells. However, the mechanisms by which PRL regulates regulatory T (T(reg)) cells are still unknown. Our goal was to determine whether PRL plays a role in T(reg) function. We measured the expression of PRL and its receptor in T(reg) and effector T (T(eff)) cells from 15 healthy individuals. We also evaluated the functional activity of T(reg) cells by examining proliferation and cytokine secretion in cells activated with anti-CD3/CD28 in the presence or absence of PRL. We report that T(reg) cells constitutively expressed PRL receptor, whereas T(eff) cells required stimulation with anti-CD3/CD28 to induce PRL receptor expression. Expression of PRL was constitutive in both populations. We found that the addition of PRL inhibited the suppressor effect (proliferation) mediated by T(reg) cells in vitro, reducing suppression from 37.4 to 13% when PRL was added to co-cultures of T(reg) and T(eff) cells (P<0.05). Cultures treated with PRL favoured a Th1 cytokine profile, with increased production of TNF and IFNγ. We report for the first time that PRL receptor expression was constitutive in T(reg) cells but not in T(eff) cells, which require stimulation to induce PRL receptor expression. PRL inhibited the suppressive function of T(reg) cells, apparently through the induced secretion of Th1 cytokines.

10.1530/jme-11-0040

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Citations (25)

Report of the First National Consensus Meeting for Acute Leukemias Immunophenotyping

Gaceta Médica de México (2019)

Lourdes Arriaga‐Pizano Dalia Ramírez-Ramírez Jessica L. Prieto‐Chávez Rosana Pelayo Alejandro Ruı́z-Argüelles

En 2005 se publicaron recomendaciones para la tipificación de hemopatías malignas en Latinoamérica.Se consideró necesario realizar una reunión nacional para actualizarlas.Se convocaron y reunieron 95 profesionales expertos en el tema para analizar y contrastar alternativas y llegar a un consenso.Se alcanzaron opiniones de consenso en lo relativo a indicaciones, tipos y manejo de muestras, anticuerpos, nomenclatura e informe de resultados para el diagnóstico y seguimiento de las leucemias agudas.Las recomendaciones se describen en este artículo y se hace hincapié en la necesidad de que los laboratorios nacionales se apeguen a ellas.

Immunophenotyping

Consensus conference

10.24875/gmm.m19000226

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Citations (2)

Triggering receptor expressed on myeloid cells (TREM-1) is regulated post-transcriptionally and its ligand is present in the sera of some septic patients

Clinical & Experimental Immunology (2006)

Isabel Wong‐Baeza Nestor González-Roldán Eduardo Ferat‐Osorio Noemí Esquivel-Callejas Rosalía Aduna-Vicente

Summary Inflammation is necessary for survival, but it is also an important cause of human morbidity and mortality, as exemplified by sepsis. During inflammation, cells of the innate immune system are recruited and activated in response to infection, trauma or injury. These cells are activated through receptors, such as Toll-like receptors (TLRs), which recognize microbial ligands such as lipopolysaccharide (LPS). Triggering receptor expressed on myeloid cells (TREM)-1 amplifies the inflammatory response initiated by TLRs, and its expression on the surface of monocytes increases in the presence of TLR ligands. Here we have shown that in monocytes TREM-1 mRNA levels, measured by reverse transcription–polymerase chain reaction (RT–PCR), remained unchanged and TREM-1 protein levels, measured by flow cytometry, increased, indicating that LPS increases TREM-1 expression by a post-transcriptional mechanism. We also showed that TREM-1/Fc fusion protein decreased the ability of the sera of some patients with sepsis to activate monocytes, indicating that the TREM-1 ligand, whose identity is unknown, may be present in the sera of some of these patients. We describe a mechanism for the regulation of TREM-1 expression on monocytes and the possible presence of its ligand in serum; these findings help to explain the contribution of TREM-1 during systemic inflammation.

10.1111/j.1365-2249.2006.03158.x

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Citations (62)

Electrical Stimulation at the ST36 Acupoint Protects against Sepsis Lethality and Reduces Serum TNF Levels through Vagus Nerve‐ and Catecholamine‐Dependent Mechanisms

Evidence-based Complementary and Alternative Medicine (2014)

Albino Villegas-Bastida Rafael Torres‐Rosas Lourdes Arriaga‐Pizano Javier Flores‐Estrada Altamirano Gustavo-Acosta

Electrical vagus nerve (VN) stimulation during sepsis attenuates tumor necrosis factor (TNF) production through the cholinergic anti-inflammatory pathway, which depends on the integrity of the VN and catecholamine production. To characterize the effect of electroacupuncture at ST36 (EA-ST36) on serum TNF, IL-6, nitrite, and HMGB1 levels and survival rates, based on VN integrity and catecholamine production, a sepsis model was induced in rats using cecal ligation and puncture (CLP). The septic rats were subsequently treated with EA-ST36 (CLP+ST36), and serum samples were collected and analyzed for cytokines levels. The serum TNF, IL-6, nitrite, and HMGB1 levels in the CLP+ST36 group were significantly lower compared with the group without treatment, the survival rates were significantly higher (P < 0.05), and the acute organ injury induced by CLP was mitigated by EA-ST36; however, when subdiaphragmatic vagotomy was performed, the serum levels of TNF in the CLP+ST36 group did not show a significant difference compared with the group without electrostimulation, and, similarly, no significant difference in serum TNF levels was found under the pharmacological blockade of catecholamines. These results suggest that in rats with CLP sepsis models EA-ST36 reduces serum TNF levels through VN- and atecholamine-dependent mechanisms.

Lethality

Vagus Nerve Stimulation

10.1155/2014/451674

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Citations (39)

Innate Lymphoid Cells Have Decreased HLA-DR Expression but Retain Their Responsiveness to TLR Ligands during Sepsis

The Journal of Immunology (2018)

David Cruz‐Zárate Graciela Libier Cabrera‐Rivera Bibiana Patricia Ruiz‐Sánchez Jeanet Serafín‐López Rommel Chacón‐Salinas

Sepsis, one of the leading causes of death in intensive care units, is caused by a dysregulated host response to infection that leads to life-threatening organ dysfunction. The proinflammatory and anti-inflammatory responses activated by the infecting microorganism become systemic, and the sustained anti-inflammatory response induces a state of immunosuppression that is characterized by decreased expression of HLA-DR on monocytes, T cell apoptosis, and reduced production of TNF-α by monocytes and macrophages in response to TLR ligands. Innate lymphoid cells (ILCs) are lymphocytes that lack Ag-specific receptors and lineage-specific markers; they express HLA-DR and are activated by cytokines and by direct recognition of microbial molecules. In this study, we evaluated if ILCs are affected by the anti-inflammatory response during sepsis. We found that the number of peripheral blood ILCs was decreased in septic patients compared with healthy volunteers; this decrease was caused by a reduction in ILC1 and ILC3 and is associated with apoptosis, because ILCs from septic patients expressed active caspase 3. ILCs from septic patients had decreased HLA-DR expression but increased expression of the activating receptors NKp46 and NKp44; they also showed a sustained expression of CD127 (IL-7R α-chain) and retained their capacity to produce TNF-α in response to TLR ligands. These results indicate that during sepsis, ILCs have decreased HLA-DR expression and die via apoptosis, similar to monocytes and T cells, respectively. However, other effector functions of ILCs (activation through NKp46 and NKp44, TNF-α production) may remain unaffected by the immunosuppressive environment prevailing in septic patients.

Innate lymphoid cell

Proinflammatory cytokine

10.4049/jimmunol.1800735

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Citations (19)