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Disordered macrophage cytokine secretion underlies impaired acute inflammation and bacterial clearance in Crohn's disease.

Smith AM, Rahman FZ, Hayee B, Graham SJ, Marks DJ, Sewell GW, Palmer CD, Wilde J, Foxwell BM, Gloger IS, Sweeting T, Marsh M, Walker AP, Bloom SL, Segal AW.

J Exp Med. 2009 Aug 31;206(9):1883-97. doi: 10.1084/jem.20091233. Erratum in: J Exp Med. 2009 Sep 28;206(10):2301.


Optineurin deficiency in mice contributes to impaired cytokine secretion and neutrophil recruitment in bacteria-driven colitis.

Chew TS, O'Shea NR, Sewell GW, Oehlers SH, Mulvey CM, Crosier PS, Godovac-Zimmermann J, Bloom SL, Smith AM, Segal AW.

Dis Model Mech. 2015 Aug 1;8(8):817-29. doi: 10.1242/dmm.020362.


Monocyte-derived macrophages from Crohn's disease patients are impaired in the ability to control intracellular adherent-invasive Escherichia coli and exhibit disordered cytokine secretion profile.

Vazeille E, Buisson A, Bringer MA, Goutte M, Ouchchane L, Hugot JP, de Vallée A, Barnich N, Bommelaer G, Darfeuille-Michaud A.

J Crohns Colitis. 2015 May;9(5):410-20. doi: 10.1093/ecco-jcc/jjv053.


Defective tumor necrosis factor release from Crohn's disease macrophages in response to Toll-like receptor activation: relationship to phenotype and genome-wide association susceptibility loci.

Sewell GW, Rahman FZ, Levine AP, Jostins L, Smith PJ, Walker AP, Bloom SL, Segal AW, Smith AM.

Inflamm Bowel Dis. 2012 Nov;18(11):2120-7. doi: 10.1002/ibd.22952.


Macrophages from IBD patients exhibit defective tumour necrosis factor-α secretion but otherwise normal or augmented pro-inflammatory responses to infection.

Campos N, Magro F, Castro AR, Cabral J, Rodrigues P, Silva R, Appelberg R, Rodrigues S, Lopes S, Macedo G, Sarmento A.

Immunobiology. 2011 Aug;216(8):961-70. doi: 10.1016/j.imbio.2011.01.002.


Disruption of macrophage pro-inflammatory cytokine release in Crohn's disease is associated with reduced optineurin expression in a subset of patients.

Smith AM, Sewell GW, Levine AP, Chew TS, Dunne J, O'Shea NR, Smith PJ, Harrison PJ, Macdonald CM, Bloom SL, Segal AW.

Immunology. 2015 Jan;144(1):45-55. doi: 10.1111/imm.12338.


Defective macrophage handling of Escherichia coli in Crohn's disease.

Elliott TR, Hudspith BN, Rayment NB, Prescott NJ, Petrovska L, Hermon-Taylor J, Brostoff J, Boussioutas A, Mathew CG, Sanderson JD.

J Gastroenterol Hepatol. 2015 Aug;30(8):1265-74. doi: 10.1111/jgh.12955.


Lamina propria macrophage phenotypes in relation to Escherichia coli in Crohn's disease.

Elliott TR, Rayment NB, Hudspith BN, Hands RE, Taylor K, Parkes GC, Prescott NJ, Petrovska L, Hermon-Taylor J, Brostoff J, Boussioutas A, Mathew CG, Bustin SA, Sanderson JD.

BMC Gastroenterol. 2015 Jul 3;15:75. doi: 10.1186/s12876-015-0305-3.


Infliximab therapy increases the frequency of circulating CD16(+) monocytes and modifies macrophage cytokine response to bacterial infection.

Nazareth N, Magro F, Silva J, Duro M, Gracio D, Coelho R, Appelberg R, Macedo G, Sarmento A.

Clin Exp Immunol. 2014 Sep;177(3):703-11. doi: 10.1111/cei.12375.


Eating the enemy in Crohn's disease: an old theory revisited.

Caprilli R, Lapaquette P, Darfeuille-Michaud A.

J Crohns Colitis. 2010 Oct;4(4):377-83. doi: 10.1016/j.crohns.2010.05.007.


Enhanced secretion of tumour necrosis factor-alpha, IL-6, and IL-1 beta by isolated lamina propria mononuclear cells from patients with ulcerative colitis and Crohn's disease.

Reinecker HC, Steffen M, Witthoeft T, Pflueger I, Schreiber S, MacDermott RP, Raedler A.

Clin Exp Immunol. 1993 Oct;94(1):174-81.


What is wrong with granulocytes in inflammatory bowel diseases?

Levine AP, Segal AW.

Dig Dis. 2013;31(3-4):321-7. doi: 10.1159/000354686. Review.


Lipidomic profiling in Crohn's disease: abnormalities in phosphatidylinositols, with preservation of ceramide, phosphatidylcholine and phosphatidylserine composition.

Sewell GW, Hannun YA, Han X, Koster G, Bielawski J, Goss V, Smith PJ, Rahman FZ, Vega R, Bloom SL, Walker AP, Postle AD, Segal AW.

Int J Biochem Cell Biol. 2012 Nov;44(11):1839-46. doi: 10.1016/j.biocel.2012.06.016.


CARD15 variants determine a disturbed early response of monocytes to adherent-invasive Escherichia coli strain LF82 in Crohn's disease.

Peeters H, Bogaert S, Laukens D, Rottiers P, De Keyser F, Darfeuille-Michaud A, Glasser AL, Elewaut D, De Vos M.

Int J Immunogenet. 2007 Jun;34(3):181-91.


Lactoferrin prevents invasion and inflammatory response following E. coli strain LF82 infection in experimental model of Crohn's disease.

Bertuccini L, Costanzo M, Iosi F, Tinari A, Terruzzi F, Stronati L, Aloi M, Cucchiara S, Superti F.

Dig Liver Dis. 2014 Jun;46(6):496-504. doi: 10.1016/j.dld.2014.02.009.


Activity of Species-specific Antibiotics Against Crohn's Disease-Associated Adherent-invasive Escherichia coli.

Brown CL, Smith K, Wall DM, Walker D.

Inflamm Bowel Dis. 2015 Oct;21(10):2372-82. doi: 10.1097/MIB.0000000000000488.


Crohn's disease-associated Escherichia coli survive in macrophages by suppressing NFκB signaling.

Rahman K, Sasaki M, Nusrat A, Klapproth JM.

Inflamm Bowel Dis. 2014 Aug;20(8):1419-25. doi: 10.1097/MIB.0000000000000096.


Peripheral monocyte functions and activation in patients with quiescent Crohn's disease.

Schwarzmaier D, Foell D, Weinhage T, Varga G, Däbritz J.

PLoS One. 2013 Apr 26;8(4):e62761. doi: 10.1371/journal.pone.0062761.


Adherent invasive Escherichia coli strains from patients with Crohn's disease survive and replicate within macrophages without inducing host cell death.

Glasser AL, Boudeau J, Barnich N, Perruchot MH, Colombel JF, Darfeuille-Michaud A.

Infect Immun. 2001 Sep;69(9):5529-37.


A new transcription factor that regulates TNF-alpha gene expression, LITAF, is increased in intestinal tissues from patients with CD and UC.

Stucchi A, Reed K, O'Brien M, Cerda S, Andrews C, Gower A, Bushell K, Amar S, Leeman S, Becker J.

Inflamm Bowel Dis. 2006 Jul;12(7):581-7.

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