Biochemical Mechanisms in Inflammation

Menkin, Valy

doi:10.1136/bmj.1.5185.1521

Cited by 69 publications

(42 citation statements)

References 2 publications

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“…For example, calcium is known to be released by injured and/or dying cells at sites of inflammation, producing calcium concentrations 1.5-to 3-fold higher than in serum. [63][64][65] Ca 2ϩ o levels may also rise near B cells when neighboring cells are activated (for example, T cells stimulated by antigen in a lymph node). When activated cells release Ca 2ϩ from their internal stores, they subsequently pump cytosolic calcium into the extracellular environment to restore homeostatic Ca 2ϩ i levels (20-100 nM).…”

Section: Discussionmentioning

confidence: 99%

Extracellular calcium sensing promotes human B-cell activation and function

Hammond

White

Tomić

et al. 2007

Blood

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Section: Discussionmentioning

confidence: 99%

Extracellular calcium sensing promotes human B-cell activation and function

Hammond

White

Tomić

et al. 2007

Blood

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“…Several investigators have previously claimed that pyrogenic substances may be extracted from various tissues. The first of these agents, "pyrexin" (17), derived from inflammatory exudates, appears almost certainly to have been contaminated by pyrogens of bacterial origin (3). Similarly, the endotoxic activity of the "tissue polysaccharides" of Landy and Shear has been traced to incidental contamination of these substances with Gram-negative bacteria during purification procedures (18).…”

Section: Discussionmentioning

confidence: 99%

The Presence of Endogenous Pyrogen in Normal Rabbit Tissues

Snell¹,

Atkins²

1965

The Journal of Experimental Medicine

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Saline extracts of homogenized, uninfected, rabbit tissues produced febrile responses when injected intravenously into rabbits. Extracts of muscle, lung, and heart evoked fevers that were similar to those induced by leucocyte pyrogen; extracts of spleen, liver, and kidney caused more sustained fevers. The minimal pyrogenic dose appeared to be between 1.5 and 3 gm wet weight of tissue. Evidence is presented that neither Gram-negative bacterial endotoxin nor polymorphonuclear leucocytes (circulating or sequestered in the tissues) can be implicated as the source of pyrogen in tissue extracts. It seems likely, therefore, that a pyrogenic material of truly endogenous origin is widely distributed in tissues. Tissue pyrogen appears to be a large molecule which is relatively resistant to treatment with acid but not with alkali. Possible pathological roles for this endogenous agent (or agents) are briefly indicated.

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“…The biologic activities of these toxins were originally attributed to an endogenous necrotizing factor called necrosin (7). The role that these substances play in infection, inflammation, or immunity is not currently appreciated but it seems reasonable to postulate that they are immunomodulators.…”

mentioning

confidence: 99%

Cellular receptor for 125I-labeled tumor necrosis factor: specific binding, affinity labeling, and relationship to sensitivity.

Kull¹,

Jacobs²,

Cuatrecasas³

1985

Proc. Natl. Acad. Sci. U.S.A.

245

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Tumor necrosis factor (TNF) is a proteinaceous toxin shed by stimulated myeloid cells. Murine TNF was radioiodinated to a specific activity of 1 mCi/nmol (1 Ci = 37 GBq) of monomer. 1351-labeled TNF (125I-TNF) retained complete cytotoxic activity and it was immunochemically identical to the native toxin in a quantitative immunoprecpitation assay.It could be shown by competition binding that '2-I-TNF bound to intact L929 cells with a specificity equal to that of native toxin. The conditions of time, temperature, and concentration involved in equilibrium specific binding to intact cells were studied in detail. When binding was carried out at 40C for 18 hr, four cell lines sensitive to 12BI-TNF cytotoxicity demonstrated high-affinity binding. The binding reached half-maximal level at 3 pM and saturated at 30 pM. These concentrations approximated those required for cell death. Scatchard analysis gave =1000 sites per cell. J774.1 cells, the source of the toxin, demonstrated similar binding but were not sensitive to 125I-TNF cytotoxicity. Other sensitive cell lines and freshly extracted tumor cells showed specific binding at 3 pM. Normal lymphoid organ cell suspensions and two human tumorigenic cell lines were not sensitive and failed to demonstrate specific binding. 1251-TNF, covalently cross-linked to its receptor on sensitive L-M cells with disucciniimidyl suberate, was isolated and analyzed by sodium dodecyl sulfate/polyacrylamide gel electrophoresis and autoradiograiphy. Two specific bands were identified. The most prominent band had a mobility corresponding to a molecular mass of 95 kDa and the second band had a molecular mass of 75 kfla. The presence of the binding site appears to be necessary but not sufficient to explain the sensitivity of cells to the cytotoxic action of TNF.

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Biochemical Mechanisms in Inflammation

Cited by 69 publications

References 2 publications

Extracellular calcium sensing promotes human B-cell activation and function

Extracellular calcium sensing promotes human B-cell activation and function

The Presence of Endogenous Pyrogen in Normal Rabbit Tissues

Cellular receptor for 125I-labeled tumor necrosis factor: specific binding, affinity labeling, and relationship to sensitivity.

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