Human neutrophils exhibit disparate chemotactic factor gene expression

Strieter, Robert M.; Kasahara, Keita; Allen, Ron; Showell, Henry J.; Standiford, Theodore J.; Kunkel, Steven L.

doi:10.1016/s0006-291x(05)80095-6

Cited by 108 publications

(57 citation statements)

References 20 publications

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“…1B) are: 1) the complete lack of CXCL10 mRNA induction by ultra pure LPS in neutrophils in contrast to LPS-treated monocytes; 2) the very modest capacity of IFN-␥ to up-regulate CXCL10 mRNA in neutrophils, unlike its strong effect in monocytes (Fig. 1A) (12,13); 3) the synergistic induction of CXCL10 mRNA by ultra pure LPS and IFN-␥ in neutrophils (12, 13); 4) the potent effect of IFN-␥ on CD64 mRNA expression in neutrophils (37); 5) the biphasic effect of IFN-␥ on TNF-␣ and CCL4 (data not shown) mRNA expression in ultra pure LPS-treated neutrophils (38, 39); 6) the lack of induction of IL-6 and CCL2 (data not shown) mRNAs by ultra pure LPS in neutrophils that confirms earlier observations (8,40,41) and that also excludes any influence of possible contamination of monocyte RNA in our neutrophil preparations (8,42). Similar results were observed with a second ultra pure LPS, certified as being ineffective toward TLR4-deficient mouse cells by the supplier (Alexis).…”

Section: Effect Of Ultra Pure Lps On the Expression Of Cxcl10 And Othsupporting

confidence: 79%

“…A5060) Abs were from Sigma-Aldrich. Polyclonal Abs to NF-B-activating kinase-associated protein 1 (NAP1) were generated by immunization of mice with a synthetic peptide corresponding to the residues S 27 IYSGDESVASHFA 40 of human NAP1 (20) according to standard procedures. Anti-TLR4 and anti-TLR2 neutralizing Abs were provided, respectively, by Dr. Olsen (NovImmune) (21) and Dr. T. Musso (University of Turin, Turin, Italy) (22).…”

Section: Antibodiesmentioning

confidence: 99%

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The MYD88-Independent Pathway Is Not Mobilized in Human Neutrophils Stimulated via TLR4

Tamassia

Moigne

Calzetti

et al. 2007

The Journal of Immunology

104

112

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LPS activates both MyD88-dependent and -independent signaling via TLR4, but the extent to which each cascade is operative in different cell types remains unclear. This prompted us to revisit the intriguing issue of CXCL10 production, which we previously showed to be inducible in neutrophils stimulated with LPS and IFN-γ but not with either stimulus alone, contrary to other myeloid cells. We now report that in neutrophils the MyD88-independent pathway is not activated by LPS. Indeed, microarray and real-time PCR experiments showed that neither IFNβ nor IFNβ-dependent genes (including CXCL10) are inducible in LPS-treated neutrophils, in contrast to monocytes. Further investigation into the inability of LPS to promote IFNβ expression in neutrophils revealed that the transcription factors regulating the IFNβ enhanceosome, such as IFN-regulatory factor-3 and AP-1, are not activated in LPS-treated neutrophils as revealed by lack of dimerization, nuclear translocation, confocal microscopy, and inducible binding to DNA. Moreover, we show that the upstream TANK-binding kinase-1 is not activated by LPS in neutrophils. A lack of IFNβ/CXCL10 mRNA expression and IFN-regulatory factor 3 activation was also observed in myeloid leukemia HL60 cells differentiated to granulocytes and then stimulated with LPS, indicating that the inability of neutrophils to activate the MyD88-independent pathway represents a feature of their terminal maturation. These results identify a disconnected activation of the two signaling pathways downstream of TLR4 in key cellular components of the inflammatory and immune responses and help us to better understand the primordial role of neutrophils in host defense against nonviral infections.

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Section: Effect Of Ultra Pure Lps On the Expression Of Cxcl10 And Othsupporting

confidence: 79%

Section: Antibodiesmentioning

confidence: 99%

The MYD88-Independent Pathway Is Not Mobilized in Human Neutrophils Stimulated via TLR4

Tamassia

Moigne

Calzetti

et al. 2007

The Journal of Immunology

104

112

View full text Add to dashboard Cite

show abstract

“…[23][24][25][26] IL-8 is an inflammatory cytokine with a strong effect on neutrophil activation and chemotaxis. 27,28 Early evidence for the involvement of this chemokine in allergic inflammation was obtained from a study that demonstrated that cultured bronchial epithelial cells derived from asthmatic subjects released IL-8 into culture supernatant.…”

Section: Discussionmentioning

confidence: 99%

Enhanced Neutrophil Chemotactic Activity After Bronchial Challenge in Subjects with Grain Dust-Induced Asthma

Park

Jung

1998

Annals of Allergy, Asthma & Immunology

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“…Although many chemoattractants for human neutrophils have been described, there has been recent interest in the CXC chemokines, including IL-8, ENA-78, and growth-related oncogene ␣, ␤, and ␥ (17)(18)(19). Chemokines bind to glycosaminoglycan-containing proteoglycans, which are present on endothelial cells and in the extracellular matrix (20,21).…”

Section: P Lasminogen Activator Inhibitor-1 (Pai-1)mentioning

confidence: 99%

Regulation of Lipopolysaccharide-Induced Lung Inflammation by Plasminogen Activator Inhibitor-1 through a JNK-Mediated Pathway

Arndt

Young

Worthen

2005

The Journal of Immunology

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The neutrophil is of undoubted importance in lung inflammation after exposure to LPS. We have shown recently that systemic inhibition of JNK decreased neutrophil recruitment to the lung after exposure to LPS, although the mechanisms underlying this inhibition are incompletely understood. As plasminogen activator inhibitor-1 (PAI-1) accentuates cell migration, with JNK activation recently shown to up-regulate PAI-1 expression, this suggested that systemic JNK inhibition may down-regulate LPS-induced pulmonary neutrophil recruitment through a decrease in PAI-1 expression. We show in this study that exposure of mice to aerosolized LPS increased PAI-1 expression in the lung and alveolar compartment, which was decreased by pretreatment with the JNK inhibitor SP600125. Exogenous, intratracheally administered PAI-1 prevented the inhibition of pulmonary neutrophil recruitment in the setting of systemic JNK inhibition, thereby suggesting a role for PAI-1 in the JNK-mediated pathway regulating LPS-induced neutrophil recruitment. In addition, PAI-1−/− mice had a decrease in neutrophil recruitment to the alveolar compartment after exposure to LPS, compared with wild-type controls, further suggesting a role for PAI-1 in LPS-induced lung inflammation. An increase in the intravascular level of KC is a likely mechanism for the inhibition of pulmonary neutrophil recruitment after LPS exposure in the setting of decreased PAI-1 expression, as systemic KC levels after exposure to LPS were increased in PAI-1-deficient mice and in mice pretreated with SP600125, with augmentation of intravascular KC levels inhibiting neutrophil recruitment to the lung after exposure to LPS.

show abstract

Human neutrophils exhibit disparate chemotactic factor gene expression

Cited by 108 publications

References 20 publications

The MYD88-Independent Pathway Is Not Mobilized in Human Neutrophils Stimulated via TLR4

The MYD88-Independent Pathway Is Not Mobilized in Human Neutrophils Stimulated via TLR4

Enhanced Neutrophil Chemotactic Activity After Bronchial Challenge in Subjects with Grain Dust-Induced Asthma

Regulation of Lipopolysaccharide-Induced Lung Inflammation by Plasminogen Activator Inhibitor-1 through a JNK-Mediated Pathway

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