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The following term was not found in PubMed: Lipopolysaccharide+macrophages+polarization+resveratrol+toll-like
Page 1
Interleukin-1 receptor-associated kinase 4 is essential for initial host control of Brucella abortus infection.
Oliveira FS, Carvalho NB, Brandão AP, Gomes MT, de Almeida LA, Oliveira SC. Oliveira FS, et al. Infect Immun. 2011 Nov;79(11):4688-95. doi: 10.1128/IAI.05289-11. Epub 2011 Aug 15. Infect Immun. 2011. PMID: 21844234 Free PMC article.
Therefore, we decided to study the role of the interleukin-1 receptor-associated kinase 4 (IRAK-4) in host innate immune response against B. abortus. ...Extracellular signal-regulated kinase 1 (ERK1) and ERK2 and p38 as well as p65 NF-kappaB phosphorylation w …
Therefore, we decided to study the role of the interleukin-1 receptor-associated kinase 4 (IRAK-4) in host innate immun …
Signaling of high mobility group box 1 (HMGB1) through toll-like receptor 4 in macrophages requires CD14.
Kim S, Kim SY, Pribis JP, Lotze M, Mollen KP, Shapiro R, Loughran P, Scott MJ, Billiar TR. Kim S, et al. Mol Med. 2013 May 20;19(1):88-98. doi: 10.2119/molmed.2012.00306. Mol Med. 2013. PMID: 23508573 Free PMC article.
Although HMGB1 interacts with multiple pattern recognition receptors (PRRs), many of its effects in injury models occur through an interaction with toll-like receptor 4 (TLR4). ...Furthermore, we show that HMGB1 stimulates tumor necrosis factor (TNF)-alpha re …
Although HMGB1 interacts with multiple pattern recognition receptors (PRRs), many of its effects in injury models occur through an in …
TLR4 acts as a death receptor for ultraviolet radiation (UVR) through IRAK-independent and FADD-dependent pathway in macrophages.
Zhou H, Harberts E, Fishelevich R, Gaspari AA. Zhou H, et al. Exp Dermatol. 2016 Dec;25(12):949-955. doi: 10.1111/exd.13222. Exp Dermatol. 2016. PMID: 27676214
UVR-induced migration of FADD to the cell membrane of WT macrophages, but not MyD88(-/-) macrophages, was observed (confocal microscopy). Co-immunoprecipitation using an epitope-tagged MyD88 revealed that FADD, but not TRADD, was recruited to MyD88 within 30 minutes …
UVR-induced migration of FADD to the cell membrane of WT macrophages, but not MyD88(-/-) macrophages, was observed (confocal m …
A MyD88-JAK1-STAT1 complex directly induces SOCS-1 expression in macrophages infected with Group A Streptococcus.
Wu J, Ma C, Wang H, Wu S, Xue G, Shi X, Song Z, Wei L. Wu J, et al. Cell Mol Immunol. 2015 May;12(3):373-83. doi: 10.1038/cmi.2014.107. Epub 2014 Nov 17. Cell Mol Immunol. 2015. PMID: 25399770 Free PMC article.
GAS-stimulated expression of STAT1 was severely impaired in MyD88(-/-) macrophages, whereas expression of JAK1 was unaffected, suggesting that MyD88 was involved in STAT1 expression and phosphorylation. ...
GAS-stimulated expression of STAT1 was severely impaired in MyD88(-/-) macrophages, whereas expression of JAK1 was unaffected, …
Toll-like receptor (TLR) signaling in response to Aspergillus fumigatus.
Mambula SS, Sau K, Henneke P, Golenbock DT, Levitz SM. Mambula SS, et al. J Biol Chem. 2002 Oct 18;277(42):39320-6. doi: 10.1074/jbc.M201683200. Epub 2002 Aug 8. J Biol Chem. 2002. PMID: 12171914 Free article.
Here, we examined the contribution of Toll-like receptor (TLR)-2, TLR4, the adapter protein MyD88, and CD14 to signaling in response to the three forms of A. fumigatus encountered during human disease: resting conidia (RC), swollen conidia (SC), and hyphae (H). Compared wi …
Here, we examined the contribution of Toll-like receptor (TLR)-2, TLR4, the adapter protein MyD88, and CD14 to signaling in response …
Heme induces programmed necrosis on macrophages through autocrine TNF and ROS production.
Fortes GB, Alves LS, de Oliveira R, Dutra FF, Rodrigues D, Fernandez PL, Souto-Padron T, De Rosa MJ, Kelliher M, Golenbock D, Chan FK, Bozza MT. Fortes GB, et al. Blood. 2012 Mar 8;119(10):2368-75. doi: 10.1182/blood-2011-08-375303. Epub 2012 Jan 18. Blood. 2012. PMID: 22262768 Free PMC article.
Heme-induced cell death required TNFR1 and TLR4/MyD88-dependent TNF production. Addition of TNF to Tlr4(-/-) or to Myd88(-/-) macrophages restored heme-induced cell death. The use of necrostatin-1, a selective inhibitor of receptor-interacting protein 1 (RIP1 …
Heme-induced cell death required TNFR1 and TLR4/MyD88-dependent TNF production. Addition of TNF to Tlr4(-/-) or to Myd88(-/-) macr …
Fatal Mycobacterium tuberculosis infection despite adaptive immune response in the absence of MyD88.
Fremond CM, Yeremeev V, Nicolle DM, Jacobs M, Quesniaux VF, Ryffel B. Fremond CM, et al. J Clin Invest. 2004 Dec;114(12):1790-9. doi: 10.1172/JCI21027. J Clin Invest. 2004. PMID: 15599404 Free PMC article.
Toll-like receptors (TLRs) such as TLR2 and TLR4 have been implicated in host response to mycobacterial infection. Here, mice deficient in the TLR adaptor molecule myeloid differentiation factor 88 (MyD88) were infected with Mycobacterium tuberculosis (MTB). While primary …
Toll-like receptors (TLRs) such as TLR2 and TLR4 have been implicated in host response to mycobacterial infection. Here, mice deficie …
Critical role of TLR2 and MyD88 for functional response of macrophages to a group IIA-secreted phospholipase A2 from snake venom.
Leiguez E, Giannotti KC, Moreira V, Matsubara MH, Gutiérrez JM, Lomonte B, Rodríguez JP, Balsinde J, Teixeira C. Leiguez E, et al. PLoS One. 2014 Apr 9;9(4):e93741. doi: 10.1371/journal.pone.0093741. eCollection 2014. PLoS One. 2014. PMID: 24718259 Free PMC article.
In MT-III-stimulated TLR2-/- macrophages, formation of LDs and release of eicosanoids and cytokines were abrogated. In MyD88-/- macrophages, MT-III-induced release of PGE2, IL-1beta and IL-10 was abrogated, but release of PGD2 and PGJ2 was maintained. ...
In MT-III-stimulated TLR2-/- macrophages, formation of LDs and release of eicosanoids and cytokines were abrogated. In MyD88-/- ma …
MyD88-dependent signaling contributes to protection following Bacillus anthracis spore challenge of mice: implications for Toll-like receptor signaling.
Hughes MA, Green CS, Lowchyj L, Lee GM, Grippe VK, Smith MF Jr, Huang LY, Harvill ET, Merkel TJ. Hughes MA, et al. Infect Immun. 2005 Nov;73(11):7535-40. doi: 10.1128/IAI.73.11.7535-7540.2005. Infect Immun. 2005. PMID: 16239556 Free PMC article.
The ability of heat-killed B. anthracis to induce a TNF-alpha response was preserved in TLR2-/- but not in MyD88-/- macrophages. In vivo studies revealed that TLR2-/- mice and TLR4-deficient mice were resistant to challenge with aerosolized Sterne strain spores but …
The ability of heat-killed B. anthracis to induce a TNF-alpha response was preserved in TLR2-/- but not in MyD88-/- macrophages …
The matrix component biglycan is proinflammatory and signals through Toll-like receptors 4 and 2 in macrophages.
Schaefer L, Babelova A, Kiss E, Hausser HJ, Baliova M, Krzyzankova M, Marsche G, Young MF, Mihalik D, Götte M, Malle E, Schaefer RM, Gröne HJ. Schaefer L, et al. J Clin Invest. 2005 Aug;115(8):2223-33. doi: 10.1172/JCI23755. Epub 2005 Jul 14. J Clin Invest. 2005. PMID: 16025156 Free PMC article.
In agreement, the stimulatory effects of biglycan are significantly reduced in TLR4-mutant (TLR4-M), TLR2-/-, and myeloid differentiation factor 88-/- (MyD88-/-) macrophages and completely abolished in TLR2-/-/TLR4-M macrophages. Biglycan-null mice have a considerab …
In agreement, the stimulatory effects of biglycan are significantly reduced in TLR4-mutant (TLR4-M), TLR2-/-, and myeloid differentiation fa …
14 results