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Qiu et al., Zhongguo Yao Li Xue Bao 1997 : Effects of dexamethasone and ibuprofen on LPS induced gene expression of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung
Riese et al., Zentralbl Chir 1999 : The presence of LPS resulted in a fourfold enhancement of this secretion ( MCP-1 : 13563 ( 1613 ), IL-8 : 9854 ( 1305 ) pg/ml ) and led to the production of MIP-1 alpha ( 1476 ( 240 ) pg/ml )
Jiang et al., J Periodontol 1999 (Dental Plaque) : In mononuclear cells, LPS induced high levels of MIP-1alpha and RANTES and moderate levels of MCP-1 ; in osteoblasts LPS only induced MCP-1
Olszyna et al., J Infect Dis 2000 (Endotoxemia) : Sixteen healthy subjects were intravenously injected with lipopolysaccharide (LPS), once with placebo and once with recombinant human interleukin (IL)-10 ( 25 microgram/kg ), to determine the effect of IL-10 on LPS induced production of macrophage inflammatory protein (MIP)-1alpha , MIP-1beta, and monocyte chemoattractant protein (MCP)-1 ... Pretreatment with IL-10 inhibited LPS induced release of MIP-1alpha , MIP-1beta, and MCP-1
Bukara et al., Alcohol 2000 (Acute Disease...) : Splenectomy significantly suppressed LPS induced RANTES release, but not MIP-1alpha and MCP-1
Drakes et al., Transpl Immunol 2000 : MIP-1alpha production by liver derived DC was stimulated by bacterial lipopolysaccharide (LPS) , and high levels were also detected in co-cultures of hepatic DC and allogeneic T cells
Sherry et al., Mol Med 2000 (HIV Infections) : LPS induced MIP-1alpha release is enhanced in HIV-1 infected, as compared to uninfected, monocyte/macrophage cultures, and this enhancing effect is partially blocked by the addition of inhibitors of NOS, and can be reproduced by chemical generators of NO even in the absence of HIV-1 infection
Aung et al., J Acquir Immune Defic Syndr 2001 (Disease Progression...) : Induction of MIP-1 alpha by lipopolysaccharide (LPS) in BAC of HIV-1 infected study subjects from the low CD4 group was less than BAC from healthy study subjects ( p < .001 ), and also was less than in BACs from the group with a high CD4 group ( p < .001 )
Zaitseva et al., Infect Immun 2001 : Both HBa and LPS-Ba stimulated high levels of MIP-1alpha and MIP-1beta production in elutriated monocytes and even higher levels in macrophages
Mariani et al., Exp Gerontol 2002 : We demonstrate that : ( a ) monocytes, T lymphocytes and NK cells spontaneously produced detectable amounts of chemokines, both in young and old subjects ; ( b ) monocyte dependent RANTES and MIP-1alpha production induced by LPS was up-regulated in nonagenarian subjects as anti-CD3 induced secretion from T cells ; ( c ) RANTES and MIP-1alpha production by IL-2 stimulated NK cells was reduced in elderly subjects ; ( d ) CCR1, CCR3 and CCR5 were widely expressed on monocytes, but less expressed on T lymphocytes and NK cells
Li et al., Anesth Analg 2003 : Furthermore, we found that adrenaline inhibited LPS induced MIP-1 alpha messenger RNA expression
Spek et al., J Clin Immunol 2003 : LPS induced MIP-1alpha , MIP-1beta, IL-8, IL-1beta, and IL-1Ra mRNA production, which was delayed by 1 hr and reduced twofold by IC14 treatment
Li et al., Anesth Analg 2003 : We conducted this study to investigate the effect of dobutamine on lipopolysaccharide (LPS) induced MIP-1alpha and IL-8 production by human monocytic THP-1 cells ... Dobutamine significantly inhibited LPS induced MIP-1alpha and IL-8 production by THP-1 cells in a dose dependent manner ... Salbutamol had a similar suppressive effect on LPS stimulated MIP-1alpha and IL-8 production
Jing et al., J Leukoc Biol 2003 : Intraperitoneal administration of PGE2 together with LPS results in a reduction in the levels of CCL3 and CCL4 released in the peritoneal fluid, a reduction in the number of dendritic cells accumulating in the peritoneal cavity, and a reduction in CCL3 amount per cell in the peritoneal cell population
Olszyna et al., Eur Cytokine Netw 2003 (Endotoxemia) : IC14 attenuated the LPS induced release of MIP-1beta, but not of MIP-1alpha
Uchiyama et al., Clin Exp Pharmacol Physiol 2004 (Respiratory Distress Syndrome, Adult) : Furthermore, TMG attenuated the LPS induced increase in pulmonary expression of KC, MIP-1alpha and MCP-1 at both the transcriptional and translational levels
Sprong et al., Infect Immun 2004 (Inflammation...) : Interleukin-1beta (IL-1beta), tumor necrosis factor alpha, and macrophage inflammatory protein 1alpha production was predominantly dependent on LPS , in contrast to IL-8 production, which was also markedly induced by the LPS- meningococci
Chintalacharuvu et al., Clin Exp Rheumatol 2005 (Arthritis, Experimental...) : LY309886 and LY329201 also inhibited LPS induced TNF alpha and MIP1 alpha in these cells and in primary macrophages
Inoue et al., FASEB J 2006 (Inflammation...) : In both genotypes of mice, LPS enhanced protein expression of interleukin (IL)-1beta, IL-6, granulocyte/macrophage-colony stimulating factor, macrophage inflammatory protein (MIP)-1alpha , MIP-2, macrophage chemoattractant protein-1, and keratinocyte chemoattractant in the lung, kidney, and liver and circulatory levels of IL-1beta, IL-6, MIP-2, and KC
Lucchi et al., J Reprod Immunol 2007 : LPS induced time dependent expression and secretion of IL-8, macrophage inflammatory protein (MIP)-1alpha and MIP-1beta from ST cells and an upregulation of ICAM-1
Fan et al., Immunology 2007 : In contrast to the role of G ( i ) proteins as a positive regulator of mediators, LPS induced production of MIP-1alpha and granulocyte-macrophage colony stimulating factor ( GM-CSF ) were increased in macrophages from Galpha ( i1/3 ) ( -/- ) mice, and SA-induced MIP-1alpha production was increased in both groups of Galpha ( i ) protein depleted mice
Ryu et al., J Periodontol 2007 (Gingivitis...) : MIP-1alpha expression in PMNs and gingival epithelial cells was induced by IL-1beta and LPS , but neither induced MIP-1alpha expression in gingival fibroblasts or osteoblastic cells
Stockmann-Juvala et al., Food Chem Toxicol 2008 : Moreover, FB ( 1 ) inhibited the LPS induced expression of IL-6, IL-1beta, CCL3 and CCL5
Bhavsar et al., Thorax 2008 (Asthma) : The inhibition of LPS induced interleukin (IL)1beta, IL6, IL8, monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-1alpha release by dexamethasone ( 10 ( -6 ) M ) was significantly less in macrophages from patients with severe asthma than in macrophages from patients with non-severe asthma
Martin et al., Cell Immunol 1991 : In contrast, PGE1 inhibits LPS induced JE, MIP-1 alpha , and MIP-1 beta mRNA expression and this inhibition is partially dependent on a cAMP mediated pathway of signal transduction
Reale et al., Brain Behav Immun 2009 (Parkinson Disease) : Basal and LPS induced levels of MCP-1, RANTES, MIP-1alpha , IL-8, IFNgamma, IL-1beta and TNFalpha were significantly higher in PD patients than in HC subjects ( p < 0.001 ), as determined by RT-PCR and Elisa methods
Kim et al., Mol Cells 2008 : Rosmarinic acid down-regulates the LPS induced production of monocyte chemoattractant protein-1 ( MCP-1 ) and macrophage inflammatory protein-1alpha ( MIP-1alpha ) via the MAPK pathway in bone-marrow derived dendritic cells
Rosenson et al., Obesity (Silver Spring) 2009 (Metabolic Syndrome X) : In multivariate models including age, gender, and waist circumference, there were inverse correlations between changes in adiponectin and vascular cell adhesion molecule-1 ( VCAM-1 ) ( r = -0.54, P < 0.0001 ) and intercellular adhesion molecule-1 ( ICAM-1 ) ( r = -0.57, P < 0.0001 ), and C-reactive protein (CRP) ( r = -0.40, P = 0.0041 ) ; lipopolysaccharide (LPS) stimulated production of tumor necrosis factor-alpha (TNF-alpha) ( r = -0.30, P = 0.035 ), interleukin (IL)-1beta ( r = -0.44, P = 0.0016 ), monocyte chemotactic protein-1 (MCP-1) ( r = -0.46, P = 0.001 ), and macrophage inflammatory protein-1alpha ( MIP-1alpha ) ( r = -0.45, P = 0.0012 )
Chung et al., Mol Cells 2009 : These results indicate that A. actinomycetemcomitans LPS stimulates the several chemokines expressions ( MIP-1alpha , MIP-1beta, MIP-1gamma, RANTES, MIP-2, and IP 10 ) in Raw 264.7 cells ... Microarray results showed that the induction of monocyte chemoattractant protein-1alpha ( MCP-1alpha ) and macrophage inflammatory protein-1alpha ( MIP-1alpha ), MIP-1beta, MIP-1gamma, regulated upon activation, normal T-cell expressed and secreted ( RANTES ), macrophage inflammatory protein-2 ( MIP-2 ), and interferon-gamma inducible protein 10 ( IP 10 ) by A. actinomycetemcomitans LPS was increased to 12.5, 1.53, 9.09, 17.3, 2.82, 16.1, and 18.1 folds at 18 h, respectively
Marpegan et al., Chronobiol Int 2009 (Shock, Septic) : We found that LPS induced levels of interleukin (IL)-1beta, IL-6, JE ( MCP-1 ), and MIP1alpha were significantly higher at zeitgeber time ( ZT ) 11 ( time of increased mortality ) than at ZT19 ( ZT12 = time of lights-off in the animal quarters for the 12L : 12D condition )
Kang et al., J Immunol 2011 (Arthritis, Experimental...) : Compared to the wild-type cells, TTP ( -/- ) macrophages produced higher levels of LPS induced CCL3
Buenestado et al., Br J Pharmacol 2012 : Roflumilast and roflumilast N-oxide concentration-dependently reduced the LPS stimulated release of CCL2, CCL3 , CCL4, CXCL10 and TNF-a from human lung macrophages, whereas that of CXCL1 or CXCL8 was not altered
Tannheimer et al., Pulm Pharmacol Ther 2012 (Inflammation) : Addition of roflumilast ( 10 nM ) in the presence of dexamethasone increased the inhibition of LPS induced TNFa and CCL3
Berkman et al., J Immunol 1995 : Both LPS ( 1 micrograms/ml ) and IL-1 beta ( 10 ng/ml ) induced the expression of MIP-1 alpha mRNA and the release of MIP-1 alpha protein from these cells ... In the presence of an anti-human IL-10 neutralizing Ab, the release of MIP-1 alpha induced by LPS and IL-1 beta was further enhanced in monocytes but unchanged in alveolar macrophages
Standiford et al., J Immunol 1995 (Inflammation...) : Finally, the pretreatment of animals with sTNFR : Fc ( soluble TNF receptor : Ig construct ) resulted in a 60 % reduction in LPS induced MIP-1 alpha mRNA expression within lung homogenates at 4 h post-LPS
Kasama et al., J Exp Med 1993 : These findings support the notion that PMNs are capable of producing MIP-1 alpha in the presence of LPS , and that GM-CSF can influence this production through prolongation of MIP-1 alpha mRNA t1/2
Berkman et al., Am J Respir Cell Mol Biol 1996 : In AM, IL-13 reduced LPS induced MIP-1 alpha protein release of 2,030 +/- 242 pM by 32 +/- 8 % ( P < 0.05 ) and MIP-1 alpha mRNA by 27 +/- 1 % ( NS )
Cassatella et al., Immunol Lett 1996 : Lipopolysaccharide (LPS) is a potent inducer of macrophage inflammatory protein-1 alpha ( MIP-1 alpha ) production in human polymorphonuclear leukocytes ( PMN ), and it was recently shown that Interferon- gamma (IFN gamma) transiently inhibits MIP-1 alpha mRNA accumulation in LPS stimulated PMN ... IFN gamma did not affect MIP-1 alpha mRNA stability in LPS treated PMN, indicating that the cytokine does not regulate the LPS induced MIP-1 alpha gene expression through post-transcriptional events
Mühl et al., J Immunol 1997 : To ascertain the importance of the L-arginine/nitric oxide ( NO ) pathway in LPS induced MIP-1 alpha release, we stimulated human adherent PBMC with LPS in the presence of the NO synthase inhibitor N ( G ) -monomethyl-L-arginine ( L-NMMA ) ... L-NMMA decreased LPS induced MIP-1 alpha protein release ( 45.5 % inhibition ) and steady state levels of mRNA ( 48 % inhibition ) in adherent PBMC ... Most of the MIP-1 alpha release was attributed to the activity of IL-1 and TNF, since coincubation of LPS stimulated PBMC with IL-1R antagonist and TNF binding protein abrogated LPS induced MIP-1 alpha release ( by 76.8 % ) ... In the presence of exogenous NO provided by NO donors, LPS induced MIP-1 alpha release was enhanced
Shi et al., Inflammation 1998 (Inflammation) : The rat alveolar macrophage cell line ( NR8383 ) also showed increased MIP-1 alpha mRNA levels in response to LPS ( 10 micrograms/ml ) with a maximal increase after 6-8 h ... The induction of MIP-1 alpha mRNA expression by LPS in NR8383 cells was attenuated by cotreatment with the antioxidants N-acetylcysteine and dimethylsulfoxide, suggesting that the induction of MIP-1 alpha mRNA by LPS is mediated via the generation of reactive oxygen species
Ishii et al., J Neurooncol 1998 (Astrocytoma...) : However, MIP-1alpha production was increased in three cell lines by stimulation with lipopolysaccharide (LPS) and 5 cell lines by stimulation with phorbol-12myristate-13-acetate ( PMA )
McManus et al., J Immunol 1998 : In response to LPS , TNF-alpha, or IL-1 beta, both MIP-1 alpha and MIP-1 beta were induced at the mRNA and protein levels in a dose- and time dependent manner
Kimata et al., Pharmacology 1998 : Pharmacological modulation of LPS induced MIP-1 alpha production by peripheral blood mononuclear cells ... MIP-1 alpha production was induced by LPS in a concentration dependent fashion and reached the maximum at 10 micrograms/ml LPS ( 27.5 +/- 2.3 ng MIP-1 alpha/10 ( 6 ) PBMC )
Sherry et al., Mol Med 1998 : Further studies have revealed that several immunomodulatory cytokines known to be up-regulated in vivo as a consequence of exposure to an invasive stimulus ( gamma-IFN, IL-10, IL-4, and transforming growth factor [ TGF ] -beta ) down-regulated the LPS induced release of MIP-1 alpha by macrophages in vitro, but spared the MIP-1 beta response
Haskó et al., Br J Pharmacol 1998 : Northern blot analysis demonstrated that NA ( 100 nM-10 microM ), Ad, isoproterenol, as well as rolipram ( 100 nM-10 microM ) decreased LPS induced MIP-1alpha mRNA accumulation ... Pretreatment of mice with either isoproterenol ( 10 mg kg ( -1 ), i.p. ) or rolipram ( 25 mg kg ( -1 ), i.p. ) decreased LPS induced plasma levels of MIP-1alpha , while propranolol ( 10 mg kg ( -1 ), i.p. ) augmented the production of this chemokine, confirming the role of a beta-adrenoceptor mediated endogenous catecholamine action in the regulation of MIP-1alpha production in vivo
Faggioni et al., Am J Physiol 1999 (Obesity) : No differences were detected in LPS induced serum levels of interleukin (IL)-1beta, tumor necrosis factor, macrophage inflammatory protein-1alpha , and interferon-gamma in ob/ob mice compared with their own littermates