Chemotactic Factors Associated with Leukocyte Emigration in Immune Tissue Injury: Their Separation, Characterization, and Functional Specificity

Hayashi, Hideo; Honda, Mitsuo; Shimokawa, Y; Hirashima, Mitsuomi

doi:10.1016/s0074-7696(08)61304-2

Cited by 21 publications

(3 citation statements)

References 184 publications

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“…GRO1 and IL-8 are both chemotactic for neutrophils (21,50), which suggests that Act-mediated intestinal inflammation might involve infiltration of neutrophils in addition to monocytes. Although Act did not induce upregulation of GRO1 in polarized intestinal epithelial cells, IL-8 expression was induced (Tables 1 and 2) and would likely result in the same outcome (i.e., infiltration of neutrophils into the intestinal lumen during infection).…”

Section: Discussionmentioning

confidence: 99%

Microarray and Proteomics Analyses of Human Intestinal Epithelial Cells Treated with theAeromonas hydrophilaCytotoxic Enterotoxin

et al. 2005

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We performed microarray analyses on RNA from human intestinal epithelial (HT-29) cells treated with the cytotoxic enterotoxin (Act) of Aeromonas hydrophila to examine global cellular transcriptional responses. Based on three independent experiments, Act upregulated the expression of 34 genes involved in cell growth, adhesion, signaling, immune responses (including interleukin-8 [IL-8] production), and apoptosis. We verified the upregulation of 14 genes by real-time reverse transcriptase-PCR and confirmed Act-induced production of IL-8 by enzyme-linked immunosorbent assay on supernatants from nonpolarized and polarized HT-29 cells. Maximal production of IL-8 in response to Act required the presence of intracellular calcium, since chelation of calcium with BAPTA-AM significantly reduced Act-induced IL-8 production in HT-29 cells. We also examined activation of mitogen-activated protein kinases and, as demonstrated by Western blot analysis of apical side-treated polarized HT-29 cells, Act induced phosphorylation of p38, c-Jun NH2-terminal kinase, and extracellular signal-regulated kinase 1/2. In addition, KinetWorks proteomics screening of whole-cell lysates revealed Act-induced phosphorylation of cyclic AMP-response element binding protein (CREB), c-Jun, adducin, protein kinase C, and signal transducer and activator of transcription 3 (STAT3) and decreased phosphorylation of protein kinase Bα, v-raf-1 murine leukemia viral oncogene homolog 1 (i.e., Raf1), and STAT1. We verified activation of CREB and activator protein 1 in polarized cells by gel shift assay. This is the first description of human intestinal epithelial cell transcriptional alterations, phosphorylation or activation of signaling molecules, cytokine production, and calcium mobilization in response to this toxin

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Section: Discussionmentioning

confidence: 99%

Microarray and Proteomics Analyses of Human Intestinal Epithelial Cells Treated with theAeromonas hydrophilaCytotoxic Enterotoxin

et al. 2005

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“…Although much of the extracellular matrix between the fibroblasts within the inflamed connective tissue adjacent to the lymphoma cell transplants appeared well-organised and contained abundant collagen, in those locations where neutrophils were abundant the matrix was less organised and there was evidence of collagen degradation. Peptides generated through the actions of leukocyte-derived proteases on matrix glycoproteins may be chemotactic [19] and, along with EL4 lymphoma cell-derived chemotactic factors, could account for the influx of extravasated leukocytes into the site of transplantation of the lymphoma cells. The phagocytosis of degraded matrix molecules by macrophages would be one stimulus for 'priming' the macrophages.…”

Section: Histological Observations On the Inflammatory Response To Thmentioning

confidence: 99%

Macrophage-neoplastic cell interactions: implications for neoplastic cell growth

Pugh-Humphreys

1992

FEMS Microbiology Letters

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Subcutaneous transplantation of EL4 lymphoma cells within C57BL10 mice evoked an oedematous inflammatory responses involving increased leukopoiesis within the bone marrow, a blood leukocytosis, an influx of leukocytes into the transplant and surrounding host connective tissues, and extensive remodelling of sorrounding host connective tissues invloving fibroplasia and angiogenesis. Dexamethasone not only significantly reduced the numbers of circulating blood leukocytes within C57BL10 mice bearing the subcutaneous EL4 lymphoma transplants, but also reduced the oedematous inflammatory response to the transplants. The decreased influx of inflammatory leukocytes into a site of EL4 lymphoma cell transplantation within the dexamethasone‐treated mice, was accompanied by reduced growth of the transplants. Although the EL4 lymphoma cells produce factors with Colony Stimulating Factor activity and with chemotactic activity for cells of the monocyte‐macrophage lineage, they do not appear to produce fibroblast growth factors directly but can induce (or stimulate) macrophages to generate fibroblast growth factors in vitro. While not directly inhibiting the growth of subcutaneous fibroblast in vitro, dexamethasone does suppress the production and/or activity of fibroblast factors generated through macrophage‐EL4 cell interactions in vitro. The inhibitory effects of dexamethasone on macrophage influx, fibroplasia and angiogenesis within the connective tissue sorrounding the EL4 lymphoma transplants appear to be casually related events and would account for the inhibitory effect of dexamethasone on the growth of the lymphoma transplants.

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“…Os mecanismos imunológicos envolvem mediadores inflamatórios, diferentes tipos celulares e cascatas de sinalização que interagem entre si na tentativa de proteger e garantir a homeostase do organismo. Na AR, observase a participação de citocinas e quimioxinas (POBER et al, 1990;OPPENHEIM et al, 1991;KOCH et al, 1992) ;PONDER 1927;PABER et al, 2001;HONG et al, 2002 (HOLMES et al, 1967;QUIE et al, 1967 (COCHRANE et al, 1966;TILL et al, 1982;OHTSU et al, 2000;LALLY, 2005 (KELLER et al, 1983;HAYASHI et al, 1984;SHERRY et al, 1988;KOOPMAN, 2001 (HUIZINGA et al, 1989;ANDERSON et al, 1990 (CAMPBELL et al, 2000;BRAND et al, 2003;KANNAN et al, 2005 A expressão de CR1 em leucócitos de pacientes com AR têm sido avaliada (YEN et al, 1990;KUMAR et al, 1994;GOODFELLOW et al, 2000). FUORTES et al, 1993).…”

Section: Lista De Abreviaturasunclassified

Avaliação do metabolismo oxidativo de polimordonucleares mediado por receptores para IgG e para o complemento em pacientes com artrite reumatóide em diferentes estágios da doença

Paschoalato¹

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Que sempre me apoiaram, que vibram com minhas conquistas, que dividem as minhas dores para que eu possa suportá-las. Por me acolherem como filha do coração. Agradeço profundamente... AOS MEUS PADRINHOS E PRIMOS RUBENS (in memorian) E TEREZINHA COELHO, pela presença amorosa e constante, me ensinando a valorizar os "pequenos" ensinamentos que a vida nos proporciona. À MINHA AMIGA E "IRMÃ" CRISTINA ANTONIALLI SILVA, que a distância e o tempo jamais irão separar! Por acompanhar minha formação profissional desde o início com imenso carinho e atenção. AOS AMIGOS ETERNOS SRA. NILVA E SR. JOSÉ, pela amizade verdadeira e, pelo incansável apoio. Despertando em mim a necessidade de trabalhar, primeiramente, meu crescimento espiritual que refletirá no progresso da minha existência. À MINHA AMIGA LUCIENE CAMACHO, que cuidou do meu lar e da minha família com dedicação e carinho como se fosse sua. À MINHA AMIGA MARIA LUÍZA ROSA, que acreditou em mim e abriu as "primeiras portas" para que eu pudesse aplicar meu aprendizado na formação acadêmica e científica dos alunos do curso de Medicina da UNIFIPA, em Catanduva. Amigo não é aquele que diz "vá em frente", mas aquele que diz "vou contigo". Aos "amigos incansáveis" e colegas do Laboratório de Bioquímica da FCFRP-USP À Mirian R. Moreira, pela amizade, pelo carinho, pela solidariedade e pelos inúmeros momentos de aprendizado e crescimento compartilhados. À Daiani C.O. Andrade pela amizade, pelo companheirismo "nas frentes" de trabalho e pela alegria constante que aliviou nossas dificuldades. À Luciana Mariko Kabeya pela amizade incondicional e sincera, pelo incentivo constante e pelo respeito às minhas imperfeições. Ao Alexandre Kanashiro pela amizade, atenção e apoio sempre presentes todos estes anos. À Denise P.S. Leitão, pela amizade, pelas reflexões e pelos inúmeros momentos de alegria. À Livia M.C.S. Ambrosio pela preciosa amizade e carinho sempre presentes. À Cleni M.M.Marzocchi-Machado pela amizade, convivência e pelas valiosas contribuições ao longo deste estudo, com atenção especial no entendimento e aproveitamento dos resultados, que me permitiu valorizar este trabalho. À Elisa M.S. Russo-Carbolante pela amizade, generosidade e companheirismo durante estes anos. À Ana Paula L. Librandi pela amizade preciosa, pela delicadeza e apoio constante. À Cláudia S. Bitencourt pela amizade e pela cooperação valiosas para o meu aprendizado. À Fabiana S. Paula pela amizade e pela convivência importante para o crescimento de um grupo de pesquisa. À Andrea S.G. Figueiredo pela bondade e amizade, transparentes no sorriso. Ao Joel G. Souza pela alegria e pelo companheirismo. Ao Amarildo A. Cavenaghi pela realização dos experimentos sobre o complemento, por sua alegria e bom humor constantes. Ao Gustavo Martelli pela amizade preciosa, pelos momentos de riso compartilhados e pelo apoio constante. À Marlene Rodrigues da Silva por seu carinho e por sempre ter acreditado em mim. À Maria Angélica dos Santos Cunha Chellegatti por sua amizade e por sua intensa alegria de viver.

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Chemotactic Factors Associated with Leukocyte Emigration in Immune Tissue Injury: Their Separation, Characterization, and Functional Specificity

Cited by 21 publications

References 184 publications

Microarray and Proteomics Analyses of Human Intestinal Epithelial Cells Treated with theAeromonas hydrophilaCytotoxic Enterotoxin

Microarray and Proteomics Analyses of Human Intestinal Epithelial Cells Treated with theAeromonas hydrophilaCytotoxic Enterotoxin

Macrophage-neoplastic cell interactions: implications for neoplastic cell growth

Avaliação do metabolismo oxidativo de polimordonucleares mediado por receptores para IgG e para o complemento em pacientes com artrite reumatóide em diferentes estágios da doença

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