Anti IL-1 β  

Immunofluorescence microscopy after staining of mouse carotid artery tissue with anti-Mouse IL-1s antiserum (p/n 110-401-319, less purified form of 210-401-319) diluted 1:50. Tissue sections were prepared after cryofixation. Reaction occurred at room temperature for 60' followed by washes and reaction with Rhodamine conjugated Gt-a-Rabbit IgG (p/n 611-100-122). Tissue was counterstained with bis-benzimide solution at 0.5 mg/ml in PBS for 15 min at room temperature. Panel A) shows no antibody staining of WT uninjured mouse carotid tissue. Panel B) shows anti-IL-1s staining of cells after surgical injury of tissue. Panel C) shows no antibody staining of injured carotid tissue from an IL-1s KO mouse.

This antibody will recognize 10% of the non-denatured (native) precursor 31,000 MW mouse IL-1s containing samples but will primarily detect all of the 17,000 MW mature molecule. However, in western blot analysis, the usual procedure of heating the sample in SDS with or without reducing agents will facilitate denaturing of the 31,000 MW IL- 1s precursor molecule. Denatured IL-1s will have a 18 kDa band.

Immunohistochemistry of Rabbit anti-IL1Beta Antibody in Mouse Embryonic Kidney Tissue: Mouse Embryonic Kidney Fixation: FFPE buffered formalin 10% conc Ag Retrieval: Heat, Citrate pH 6.2. Pressure Cooker Primary antibody: 2ug/ml 1.5 hour @ room T Secondary Ab: MACH 1 HRP POLYMER 1:50 45” RT

(h) Expression of IL-6 (upper panel, magenta) and IL-1β (lower panel, magenta) by GFAP+ astrocytes (green, arrows) in CRND8 mice at 9 months. (i) Western blot analysis of overall increases in IL-6 and IL-1β expression (mature form at 17？kDa, arrowhead) in the cortex of transgenic mice at 1, 4 and 9 months (with n？=？3 for control and Tg+ at 1 month, n？=？4 for control and n？=？3 for Tg+ at 4 months, and n=4 for control and n？=？4 for Tg+ at 9 months). (j) IL-1β clusters (green) are closely juxtaposed to hyperphosphorylated Tau granules (AT8; magenta) in CRND8 mice. Scale bars: 20？μm (a,e？h), 5？μm (j). Fig 5. PMID:？27090093

Treatment with niacin does not alter expression of IL-1β within lesions from middle-aged mice. a.？Representative images depicting lesions immunostained for CD45 (white) and IL-1β (red) at 3 days post-demyelination from middle-aged demyelinated mice receiving either saline vehicle or niacin once a day for 3 days at a dose of 100 mg/kg IP.？b.？There is no difference in the percentage of IL-1β associated with CD45+ cells in lesions from both groups.？c.？Normalized mean fluorescence intensity (MFI) of IL-1β between lesions from vehicle- and niacin-treated mice 3 days post-demyelination did not differ. Values are represented as mean with the standard error of the mean. Results were analyzed with a 1-tail student’s t-test and each data point represents 1 mouse (n.s. = not significant). Scale bar equals 100 μm. SF9. PMID:？32030468

(a？c) RGN astrocytes in AD tissue express the pro-inflammatory cytokines IL-6 and IL-1β and the IL-1β processing enzyme Caspase 1. (a) 3D projection showing IL-6-expressing GFAP+ astrocytes near an Aβ plaque in AD cortex (male, 87 years old). Overlay shows IL-6 (magenta), GFAP (green), and Thiazine red (cyan). (b) 3D projection showing IL-1β expression (magenta) in GFAP+ astrocytes (green) around an Thiazine red-labeled Aβ plaque (cyan). (c) Reactive astrocytes (magenta) close to Aβ plaques (blue; dotted ellipse) also express the IL-1β processing enzyme Caspase 1 (green; arrowhead) in the same AD patient. (d,e) Astrocyte are sources of pro-inflammatory cytokines inside and outside RGNs: Examples of astrocytic IL-6 (d, magenta) and IL-1β (e, magenta) expression inside and outside RGNs with the local astrocyte network (GFAP+, green) in AD cortex. Scale bars: 20？μm (a,b,d,e), 10？μm (c). Fig 6. PMID:？27090093