Modulation of lectinophagocytosis of Escherichia coli by variation of pH and temperature

Rainho, C

doi:10.1016/s0928-8244(99)00012-7

Cited by 3 publications

(2 citation statements)

References 9 publications

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“…Moreover, the L-selectin-mediated binding of the human lymphocyte to the vascular endothelium is improved with the temperature in a febrile range, which favors the lymphocyte migration to the site of tissue inflammation. However, neutrophils and macrophages present a significant decrease in their functioning at temperatures of 41°C 96 . Finally, the increase in temperature causes acceleration of caspase-dependent apoptosis in human neutrophils, a process that plays a role in limiting inflammation and tissue damage during infection 97 .…”

Section: Immunological Consequences Of Fevermentioning

confidence: 99%

Fever and antipyretic therapy in the septic patient in the intensive care unit: an update

Donoso¹,

Arriaga²

2023

BMHIME

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Fever is a very common sign to observe in critically ill children during their Intensive Care Unit stay, which should be understood as an evolutionary biological response of normal adaptive character from the host to physiological stress. It is the result of a complex response to pyrogenic stimuli, resulting in the generation of cytokines and prostaglandins. The molecular mechanisms involved in the onset of fever are not yet fully specified. Therefore, difficulties in the knowledge of the exact pathophysiological processes involved are created, so it is necessary to elaborate an adequate and specific therapeutic strategy. Experimental studies conclude that fever and inflammation are beneficial to the host. However, antipyretic therapy is commonly employed, and human studies on the presence of fever and its treatment for the prognosis of critically ill septic patients are inconclusive. Up-to-date information on the physiology of human thermoregulation, the effect of temperature on the febrile range over multiple biological processes involved in host defense, and thermoregulatory interventions in the septic patient are essential to know by the critical care physician.

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Section: Immunological Consequences Of Fevermentioning

confidence: 99%

Fever and antipyretic therapy in the septic patient in the intensive care unit: an update

Donoso¹,

Arriaga²

2023

BMHIME

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“…Además, la unión mediada por L-selectina del linfocito humano al endotelio vascular se ve mejorada con la temperatura en rango febril, lo cual favorece la migración linfocitaria al sitio de inflamación tisular. Sin embargo, neutrófilos y macrófagos presentan una significativa disminución en su funcionamiento a temperaturas ≥ 41 °C 96 . Finalmente, el incremento de la temperatura ocasiona una aceleración de la apoptosis dependiente de la caspasa en neutrófilos humanos, proceso que desempeña un papel en limitar la inflamación y el daño tisular durante la infección 97 .…”

Section: Consecuencias Inmunitarias De La Fiebreunclassified

Fiebre y terapia antipirética en el paciente con sepsis en la unidad de cuidados intensivos: actualización

Donoso¹,

Arriagada²

2019

BMHIM

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Fever is a very common sign to observe in critically ill children during their intensive care unit stay. This should be understood as an evolutionary biological response, of normal adaptive character, from the host to the physiological stress. It is the result of a complex response to pyrogenic stimuli, resulting in the generation of cytokines and prostaglandins. The molecular mechanisms involved in the onset of fever are not yet fully specified, thus creating difficulties in the knowledge of the exact pathophysiological processes involved and, therefore, necessary to elaborate an adequate and specific therapeutic strategy. Experimental studies conclude that fever and inflammation are beneficial to the host. However, antipyretic therapy is commonly employed and human studies on the presence of fever and its treatment for the prognosis of critically ill septic patients are inconclusive. Up-to-date information on the physiology of human thermoregulation, the effect of temperature on febrile range over multiple biological processes involved in host defense, and thermoregulatory interventions in the septic patient are essential to know by the critical care physician.

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Alterations in Cell Surface Phosphatidylserine and Sugar Chains during Apoptosis and Their Time-Dependent Role in Phagocytosis by Macrophages.

Azuma

Inami

Matsumoto

2002

Biological & Pharmaceutical Bulletin

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Apoptosis, or programmed cell death, is a process crucial in organ development and homeostasis. Apoptotic cells are fragmented and form so-called apoptotic bodies that are engulfed and degraded by neighboring phagocytes. In order to engulf apoptotic cells, receptors on the phagocytes must recognize ligands expressed exclusively on apoptotic cells. Apoptosis induces several cellular changes, including membrane blebbing, condensation of chromatin along the nuclear membrane, and the generation of membrane-enclosed apoptotic bodies.1,2) In addition, specific changes in cell surface molecules have been observed during apoptosis, including the expression of phosphatidylserine (PS) and certain proteins, and changes in the sugar chains of glycoproteins and glycolipids. [3][4][5][6][7][8] These changes contribute to a number of different biological functions, in particular, phagocyte recognition and ingestion of apoptotic cells.Recently, many cell surface molecules, such as PS and sugar chains, have been reported to function in phagocyte recognition of apoptotic cells. [9][10][11][12][13][14] PS, which is normally restricted to the inner leaflet of the plasma membrane, becomes exposed on the outer leaflet of apoptotic cells, and changes in the pattern of glycosylation of cell surface glycoproteins and glycolipids also occur. Recognition of apoptotic cells is mediated by a variety of phagocytic receptors including lectins, scavenger receptor A (SR-A), and CD36 in conjunction with the vitronectin receptor. Ligands on apoptotic cells that are recognized by these receptors include sugars, PS, and surface-bound thrombospondin (TSP). However, this process is a cooperative interaction between several cell-recognizing molecules, not just a single molecule, and how these molecules work cooperatively during the process of phagocytosis remains uncertain. Thus, we estimated the changes in PS and sugar chains during apoptosis and studied several factors concerned with the phagocytosis of apoptotic cells in each of three phases, which were defined by changes in cell surface molecules. Although several researchers have studied this mechanism, most have been concerned with blood cells, such as lymphocytes; thus, the mechanism in epithelial cells has not been examined thoroughly. We used cells of the human colon adenocarcinoma cell line HT-29 as apoptotic cells and phorbol 12-myristate 13-acetate (PMA)-treated THP-1 cells as macrophages to study the mechanisms of phagocytosis of apoptotic cells. Apoptotic cells are effectively ingested and removed by phagocytes. This process is dependent on specific recognition by phagocytes of ligands expressed exclusively on apoptotic cells. These ligands, cell surface molecules such as phosphatidylserine (PS), altered sugar chains, and the thrombospondin-binding domain, are expressed following the induction of apoptosis. However, they are not expressed simultaneously, and each factor seems to have a respective role in different phases of apoptosis. In this paper, we classified the apoptotic process in...

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Modulation of lectinophagocytosis of Escherichia coli by variation of pH and temperature

Cited by 3 publications

References 9 publications

Fever and antipyretic therapy in the septic patient in the intensive care unit: an update

Fever and antipyretic therapy in the septic patient in the intensive care unit: an update

Fiebre y terapia antipirética en el paciente con sepsis en la unidad de cuidados intensivos: actualización

Alterations in Cell Surface Phosphatidylserine and Sugar Chains during Apoptosis and Their Time-Dependent Role in Phagocytosis by Macrophages.

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