Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of CD3+ T lymphocytes and the expression of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNF alpha) by macrophages in canine lymph nodes with mineral-associated lymph-adenopathy, granulomatous lymphadenitis or reactive hyperplasia was examined immunohistochemically. In areas of preserved lymph node architecture, CD3+ T lymphocytes were located in the paracortex, with scattered cells in the follicular mantle and germinal centre, and small aggregates in the medullary cords. T cells were prominent within areas of diffuse granulomatous inflammation and formed a peripheral rim around microgranulomas. TNF alpha expression was demonstrated in macrophages from seven of 11 dogs with mineral-associated lymphadenopathy, one of five dogs with granulomatous lymphadenitis and three of five with reactive hyperplasia. Positive macrophage staining for IL-1 beta and IL-6 was seen in two lymph nodes with reactive hyperplasia. Lymph nodes from control (clinically normal) dogs showed no evidence of cytokine expression. Neutrophils expressing IL-1 beta were observed within the medullary sinuses of two lymph nodes with mineral-associated lymphadenopathy and one with reactive hyperplasia, and in the inflammatory infiltrate in one lymph node with granulomatous lymph-adenitis. The sensitivity of immunohistochemical examination as a means of detecting cytokines in abnormal tissue is discussed.
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PMID:Expression of interleukin-1 beta, interleukin-6 and tumour necrosis factor alpha by macrophages in canine lymph nodes with mineral-associated lymphadenopathy, granulomatous lymphadenitis or reactive hyperplasia. 872 78

We investigated serum levels of interferon alpha, interferon gamma, tumour necrosis factor alpha, interleukin-2 (IL-2) and interleukin-6 (IL-6) in patients with necrotizing lymphadenitis (Kikuchi's disease) (NL). Four male patients, diagnosed as having NL following biopsy of the affected lymph nodes and by the clinical course, were included in this study. All four patients had higher than normal serum interferon gamma and IL-6 levels during the acute phase, which returned to normal levels during the convalescent phase. Interferon alpha, tumour necrosis factor alpha and IL-2 were, however, within the normal ranges. Our findings indicate the possibility that interferon gamma and IL-6 may play an important role in the pathogenesis of NL.
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PMID:Elevated serum interferon gamma and interleukin-6 in patients with necrotizing lymphadenitis (Kikuchi's disease). 898 35

Dendritic cells (DC) orchestrate innate and adaptive immune responses to bacteria. How Haemophilus ducreyi, which causes genital ulcers and regional lymphadenitis, interacts with DC is unknown. H. ducreyi evades uptake by polymorphonuclear leukocyte and macrophage-like cell lines by secreting LspA1 and LspA2. Many H. ducreyi strains express cytolethal distending toxin (CDT), and recombinant CDT causes apoptosis of DC in vitro. Here, we examined interactions between DC and H. ducreyi 35000HP, which produces LspA1, LspA2, and CDT. In human volunteers infected with 35000HP, the ratio of myeloid DC to plasmacytoid DC was 2.8:1 in lesions, compared to a ratio of 1:1 in peripheral blood. Using myeloid DC derived from monocytes as surrogates for lesional DC, we found that DC infected with 35000HP remained as viable as uninfected DC for up to 48 h. Gentamicin protection and confocal microscopy assays demonstrated that DC ingested and killed 35000HP, but killing was incomplete at 48 h. The expression of LspA1 and LspA2 did not inhibit the uptake of H. ducreyi, despite inactivating Src kinases. Infection of DC with live 35000HP caused less cell surface marker activation than infection with heat-killed 35000HP and lipopolysaccharide (LPS) and inhibited maturation by LPS. However, infection of DC with live bacteria caused the secretion of significantly higher levels of interleukin-6 and tumor necrosis factor alpha than infection with heat-killed bacteria and LPS. The survival of H. ducreyi in DC may provide a mechanism by which the organism traffics to lymph nodes. Partial activation of DC may abrogate the establishment of a full Th1 response and an environment that promotes phagocytosis.
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PMID:Haemophilus ducreyi partially activates human myeloid dendritic cells. 1792 25