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Increased TNF-α production in response to IL-6 in patients with systemic inflammation without infection.
Cabrera-Rivera, Graciela L; Madera-Sandoval, Ruth L; León-Pedroza, José Israel; Ferat-Osorio, Eduardo; Salazar-Rios, Enrique; Hernández-Aceves, Juan A; Guadarrama-Aranda, Uriel; López-Macías, Constantino; Wong-Baeza, Isabel; Arriaga-Pizano, Lourdes A.
Afiliação
  • Cabrera-Rivera GL; Unidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
  • Madera-Sandoval RL; Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Mexico City, Mexico.
  • León-Pedroza JI; Unidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
  • Ferat-Osorio E; Coordinación de Investigación, Unidad 401-C, Urgencias Médicas, Hospital General de México "Dr. Eduardo Liceaga", Mexico City, Mexico.
  • Salazar-Rios E; Coordinación de Ciclos Básicos, Universidad Anáhuac, Mexico City, Mexico.
  • Hernández-Aceves JA; Unidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
  • Guadarrama-Aranda U; División de Investigación en Salud, UMAE Hospital de Especialidades "Dr. Bernardo Sepúlveda Gutiérrez", Centro Médico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
  • López-Macías C; Unidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
  • Wong-Baeza I; Facultad de Medicina, Universidad Autónoma del Estado de Morelos, Mexico City, Mexico.
  • Arriaga-Pizano LA; Unidad de Investigación Médica en Inmunoquímica, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social, Mexico City, Mexico.
Clin Exp Immunol ; 209(2): 225-235, 2022 08 19.
Article em En | MEDLINE | ID: mdl-35647912
Acute systemic inflammation can lead to life-threatening organ dysfunction. In patients with sepsis, systemic inflammation is triggered in response to infection, but in other patients, a systemic inflammatory response syndrome (SIRS) is triggered by non-infectious events. IL-6 is a major mediator of inflammation, including systemic inflammatory responses. In homeostatic conditions, when IL-6 engages its membrane-bound receptor on myeloid cells, it promotes pro-inflammatory cytokine production, phagocytosis, and cell migration. However, under non-physiologic conditions, such as SIRS and sepsis, leucocyte dysfunction could modify the response of these cells to IL-6. So, our aim was to evaluate the response to IL-6 of monocytes from patients diagnosed with SIRS or sepsis. We observed that monocytes from patients with SIRS, but not from patients with sepsis, produced significantly more TNF-α than monocytes from healthy volunteers, after stimulation with IL-6. Monocytes from SIRS patients had a significantly increased baseline phosphorylation of the p65 subunit of NF-κB, with no differences in STAT3 phosphorylation or SOCS3 levels, compared with monocytes from septic patients, and this increased phosphorylation was maintained during the IL-6 activation. We found no significant differences in the expression levels of the membrane-bound IL-6 receptor, or the serum levels of IL-6, soluble IL-6 receptor, or soluble gp130, between patients with SIRS and patients with sepsis. Our results suggest that, during systemic inflammation in the absence of infection, IL-6 promotes TNF-α production by activating NF-κB, and not the canonical STAT3 pathway.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Interleucina-6 / Fator de Necrose Tumoral alfa / Síndrome de Resposta Inflamatória Sistêmica / Sepse Limite: Humans Idioma: En Revista: Clin Exp Immunol Ano de publicação: 2022 Tipo de documento: Article País de afiliação: México

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Interleucina-6 / Fator de Necrose Tumoral alfa / Síndrome de Resposta Inflamatória Sistêmica / Sepse Limite: Humans Idioma: En Revista: Clin Exp Immunol Ano de publicação: 2022 Tipo de documento: Article País de afiliação: México