MCP-1 is selectively expressed in the late phase by cytokine-stimulated human neutrophils: TNF-α plays a role in maximal MCP-1 mRNA expression

Yamashiro, Shigeo; Kamohara, Hidenobu; Yoshimura, Teizo

doi:10.1002/jlb.65.5.671

Cited by 55 publications

(55 citation statements)

References 23 publications

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“…Following bacterial uptake, macrophages increased production of CCL2 in a Nod2-dependent manner. In contrast, we were unable to detect CCL2 production in neutrophils (49,50), the other professional phagocyte recruited in response to pneumococcal colonization. Lysozyme is also abundant within the lumen of the upper airway, raising the possibility that the epithelium could provide a source of LysM that could be important in Nod2-dependent sensing.…”

Section: Discussioncontrasting

confidence: 70%

Nod2 sensing of lysozyme-digested peptidoglycan promotes macrophage recruitment and clearance of S. pneumoniae colonization in mice

2011

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Streptococcus pneumoniae colonizes the mucosal surface of the human upper respiratory tract. A colonization event is gradually cleared through phagocytosis by monocytes/macrophages that are recruited to the airway lumen. Here, we sought to define the bacterial and host factors that promote monocyte/macrophage influx and S. pneumoniae clearance using intranasal bacterial challenge in mice. We found that the recruitment of monocytes/macrophages required their expression of the chemokine receptor CCR2 and correlated with expression of the CCR2 ligand CCL2. Production of CCL2 and monocyte/macrophage recruitment were deficient in mice lacking digestion of peptidoglycan by lysozyme (LysM) and cytosolic sensing of the products of digestion by Nod2. Ex vivo macrophages produced CCL2 following bacterial uptake, digestion by LysM, and sensing of peptidoglycan by Nod2. Sensing of digested peptidoglycan by Nod2 also required the pore-forming toxin pneumolysin. The generation of an adaptive immune response, as measured by anti-pneumococcal antibody titers, was also LysM-and Nod2-dependent. Together, our data suggest that bacterial uptake by professional phagocytes is followed by LysM-mediated digestion of S. pneumoniae-derived peptidoglycan, sensing of the resulting products by Nod2, release of the chemokine CCL2, and CCR2-dependent recruitment of the additional monocytes/macrophages required for the clearance of an S. pneumoniae colonization event.

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Section: Discussioncontrasting

confidence: 70%

Nod2 sensing of lysozyme-digested peptidoglycan promotes macrophage recruitment and clearance of S. pneumoniae colonization in mice

2011

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“…Alternatively, recruited polymorphonuclear leukocytes may also participate in the recruitment of monocytes through the production of CCL2, also reportedly enhanced by TNF. 62 The presence of this inflammatory infiltrate in the parenchyma leads to clinical disease.…”

Section: Discussionmentioning

confidence: 99%

A Tumor Necrosis Factor Receptor 1-Dependent Conversation between Central Nervous System-Specific T Cells and the Central Nervous System Is Required for Inflammatory Infiltration of the Spinal Cord

Gimenez

Sim

Archambault

et al. 2006

The American Journal of Pathology

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Experimental autoimmune encephalomyelitis (EAE) is an autoimmune demyelinating disease of the central nervous system (CNS). Because of similarities in clinical symptoms and CNS histology, 1-5 EAE serves as a model for multiple sclerosis and can be induced in mice by either immunization with myelin protein or peptides 6 or by adoptive transfer of myelin-specific Th1 CD4 ϩ T cells. 7,8As a result, inflammatory cells consisting mostly of CD4 ϩ T lymphocytes and macrophages infiltrate the CNS leading to demyelination and neuronal damage. 9Tumor necrosis factor receptor 1 (TNFR1), also known as the p55 kd TNF receptor, binds to two ligands, TNF and lymphotoxin-␣. 10 The dominant signaling pathway for TNFR1 promotes inflammation by up-regulating inflammatory cytokines, chemokines, and adhesion molecules 11-17 and also suppresses apoptosis by the induction of IAPs (inhibitors of apoptosis) through nuclear factor (NF)-B-dependent pathways.18 TNFR1 also has the ability to induce apoptosis through a death domain in its cytoplasmic region that initiates the FADD-dependent extrinsic apoptotic pathway. 19Our previous experiments have demonstrated that TNFR1 contributes to the pathogenesis of EAE mainly by promoting CNS inflammation, 20 and thereby, in the absence of TNFR1 expression, clinical disease is limited. Through our adoptive transfer experiments we have found a dramatic difference in the location of encephalitogenic T cells within the CNS of wild-type (WT) versus TNFR1-null mice. Although we observed equivalent numbers of T cells in the CNS of TNFR1-deficient mice compared to WT mice, we found that the T cells in the TNFR1-null animals were confined to the leptomeninges and perivascular spaces of the spinal cord, whereas in the

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“…PMNs were derived from heparinized blood obtained from healthy donors at the National Institutes of Health Blood Bank (Bethesda, MD) or from SAIC-Frederick (Frederick, MD) as previously described (14). Leukocyte-rich plasma was overlaid onto Accu-prep (Accurate, Westbury, NY) and centrifuged at 800g for 20 minutes.…”

Section: Methodsmentioning

confidence: 99%

Up‐regulated expression and activation of the orphan chemokine receptor, CCRL2, in rheumatoid arthritis

Galligan¹,

Matsuyama²,

Matsukawa³

et al. 2004

Arthritis & Rheumatism

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Objective. Rheumatoid arthritis (RA) is a chronic inflammatory condition characterized by a cellular influx and destruction of the joint architecture. Chemokines characteristically regulate leukocyte recruitment and activation. Chemokine (CC motif) receptor-like 2 (CCRL2) is an orphan receptor with homology to other CC chemokine receptors. We undertook this study to examine CCRL2 expression in RA, cytokine regulation of expression, and the source of a putative ligand in an attempt to determine the role of this receptor during inflammation.Methods. Expression of CCRL2 on joint-infiltrating leukocytes was examined by immunocytochemistry. In vitro studies evaluated CCRL2 expression in primary neutrophils using Northern and Western blotting and reverse transcriptase-polymerase chain reaction. HEK 293 cells expressing two splice variants of CCRL2 (HEK/CCRL2A or HEK/CCRL2B) were generated with a retroviral expression system, and their migration in response to fractions of synovial fluid (SF) from RA patients was examined using a 48-well chamber.Results. CCRL2 expression was observed on all infiltrating neutrophils and on some macrophages obtained from the SF of 5 RA patients. In vitro studies of primary neutrophils revealed that CCRL2 messenger RNA (mRNA) was rapidly up-regulated following stimulation with lipopolysaccharide (1 g/ml) or tumor necrosis factor (5 ng/ml). The mRNA for both CCRL2A and CCRL2B were expressed in cytokinestimulated neutrophils. Cells expressing either of these splice variants migrated in response to a fraction of RA SF.Conclusion. CCRL2 expression is up-regulated on synovial neutrophils of RA patients. Inflammatory products present in the SF activate this receptor, indicating that CCRL2 is a functional receptor that may be involved in the pathogenesis of RA.

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MCP-1 is selectively expressed in the late phase by cytokine-stimulated human neutrophils: TNF-α plays a role in maximal MCP-1 mRNA expression

Cited by 55 publications

References 23 publications

Nod2 sensing of lysozyme-digested peptidoglycan promotes macrophage recruitment and clearance of S. pneumoniae colonization in mice

Nod2 sensing of lysozyme-digested peptidoglycan promotes macrophage recruitment and clearance of S. pneumoniae colonization in mice

A Tumor Necrosis Factor Receptor 1-Dependent Conversation between Central Nervous System-Specific T Cells and the Central Nervous System Is Required for Inflammatory Infiltration of the Spinal Cord

Up‐regulated expression and activation of the orphan chemokine receptor, CCRL2, in rheumatoid arthritis

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