Interleukin 8 and mast cell-generated tumor necrosis factor-? in neutrophil recruitment

Zhang, Y.; Ramos, Bernard F.; Jakschik, Barbara A.; Baganoff, Mark P.; Deppeler, Cindy L.; Meyer, Debra M.; Widomski, D. L.; Fretland, D. J.; Bolanowski, M A

doi:10.1007/bf01534385

Cited by 32 publications

(34 citation statements)

References 39 publications

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“…Following incubation, cells were transfected with 1-235TNF-EYFP and examined under a fluorescent microscope. At early stages post-transfection, similar reticular fluorescence patterns were observed in cells incubated with NH 4 Cl and control cells (data not shown), but after 16 h NH 4 Cl-treated cells, but not control cells, exhibited EYFP fluorescence in large vesicular structures located near the center of the cell. At the same time, there was no significant overlap between 1-235TNF-EYFP and TR-D, while the morphology of the structures containing TR-D (lysosomes and mast cell granules) was not seriously disturbed ( Fig.…”

Section: -235tnf-egfp Sorting To Mast Cell Granules Is Sensitive To supporting

confidence: 67%

“…In a model of bacteriainduced inflammation the lack of mast cell-derived TNFa was associated with drastically reduced neutrofil influx, and significantly higher mortality [1,2]. Similar data suggesting the critical role played by mast cellderived TNF-a in certain types of inflammatory response were obtained using reverse Arthus reaction as an animal model of inflammatory state [3,4]. The special role for mast cells as a source of TNF-a might be explained by the presence of preformed cytokine protein in cytoplasmic granules that allows for its immediate release upon stimulation [5].…”

Section: Introductionsupporting

confidence: 54%

“…RBL-2H3 cells were allowed to internalize TR-D overnight and were then incubated for 4 h with 10 mM NH 4 Cl, which is known to inhibit the MPRmediated transport. Following incubation, cells were transfected with 1-235TNF-EYFP and examined under a fluorescent microscope.…”

Section: -235tnf-egfp Sorting To Mast Cell Granules Is Sensitive To mentioning

confidence: 99%

“…5A-C). Thus, NH 4 Cl causes retention of the fusion protein in some compartment other than granules. To determine whether 1-235TNF-EYFP sorting to mast cell granules requires N-linked glycosylation, TR-D-fed RBL-2H3 cells were incubated with 2 lg/mL tunicamycin for 4 h prior to transfection with p1-235TNF-EYFP-N1.…”

Section: -235tnf-egfp Sorting To Mast Cell Granules Is Sensitive To mentioning

confidence: 99%

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Efficient sorting of TNF‐alpha to rodent mast cell granules is dependent on N‐linked glycosylation

et al. 2006

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Mast cells play an important role at the early stages of immunological response to bacterial infections and parasite infestations. One of the major mast cell proinflammatory mediators is TNF‐α. Mast cells are considered the only cells capable of storing TNF‐α in cytoplasmic granules and rapidly releasing it upon activation. To determine what pathway is utilized to direct TNF‐α to cytoplasmic granules and what motifs are responsible for the sorting process, we constructed a fusion protein covering the full sequence of TNF‐α, N‐terminally fused to enhanced green fluorescent protein (EGFP). In rodent mast cells, such protein was sorted to secretory granules, and this process was inhibited by both brefeldin A and monensin. Considering the relationship between lysosomes and secretory granules and following TNF‐α sequence analysis, it was determined whether TNF‐α is sorted through the mannose‐6‐phosphate receptor (MPR)‐dependent pathway. We observed that ammonium chloride and tunicamycin blocked TNF‐α‐EGFP fusion protein delivery to secretory granules. In situ mutagenesis experiments confirmed the necessity of N‐linked glycosylation for efficient sorting of TNF‐α into rodent mast cell granules. In this work we established that TNF‐α travels from the ER to mast cell granules via a brefeldin A‐ and monensin‐sensitive route, utilizing the MPR‐dependent pathway, although this dependency does not seem to be absolute.

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Section: -235tnf-egfp Sorting To Mast Cell Granules Is Sensitive To supporting

confidence: 67%

Section: Introductionsupporting

confidence: 54%

Section: -235tnf-egfp Sorting To Mast Cell Granules Is Sensitive To mentioning

confidence: 99%

Section: -235tnf-egfp Sorting To Mast Cell Granules Is Sensitive To mentioning

confidence: 99%

See 2 more Smart Citations

Efficient sorting of TNF‐alpha to rodent mast cell granules is dependent on N‐linked glycosylation

et al. 2006

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“…Thus, following initiation of the cutaneous Arthus reaction, in agreement with others (30) we also consider TNF-␣ as a marker of the inflammatory response. From previous studies of both the peritoneal (27,43) and dermal Arthus reaction (44), it is known that the release (from MCs) of TNF-␣, which chemoattracts neutrophils, is C dependent. In accordance, we observed raised levels of TNF-␣ and MPO in the dermal RPAR and a subsequent reduction of both parameters on inhibition of C for each animal.…”

Section: Discussionmentioning

confidence: 99%

A Peptide Derived from the Parasite Receptor, Complement C2 Receptor Inhibitor Trispanning, Suppresses Immune Complex-Mediated Inflammation in Mice

Inal

Schneider

Armanini³

et al. 2003

The Journal of Immunology

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Complement C2 receptor inhibitor trispanning (CRIT) is a Schistosoma protein that binds the human complement protein, C2. We recently showed that peptides based on the ligand binding region of CRIT inhibit the classical pathway (CP) of complement activation in human serum, using hemolytic assays and so speculated that on the parasite surface CRIT has the function of evading human complement. We now show that in vitro the C2-binding 11-aa C terminus of the first extracellular domain of CRIT, a 1.3-kDa peptide termed CRIT-H17, inhibits CP activation in a species-specific manner, inhibiting mouse and rat complement but not that from guinea pig. Hitherto, the ability of CRIT to regulate complement in vivo has not been assessed. In this study we show that by inhibiting the CP, CRIT-H17 is able to reduce immune complex-mediated inflammation (dermal reversed passive Arthus reaction) in BALB/c mice. Upon intradermal injection of CRIT-H17, and similarly with recombinant soluble complement receptor type 1, there was a 41% reduction in edema and hemorrhage, a 72% reduction in neutrophil influx, and a reduced C3 deposition. Furthermore, when H17 was administered i.v. at a 1 mg/kg dose, inflammation was reduced by 31%. We propose that CRIT-H17 is a potential therapeutic agent against CP complement-mediated inflammatory tissue destruction.

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Regulation of early peritoneal neutrophil migration by macrophage inflammatory protein-2 and mast cells in experimental peritonitis

Mercer-Jones

Shrotri

Heinzelmann

et al. 1999

Journal of Leukocyte Biology

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Neutrophil (PMN) migration into the peritoneal cavity in response to fecal peritonitis is an important mechanism of host defense against bacterial invasion. We show that the murine C-X-C (PMN-specific) chemokine, macrophage inflammatory protein-2 (MIP-2), on intraperitoneal injection in mice, causes PMN migration into the peritoneum. MIP-2 mRNA and protein were expressed by peritoneal leukocytes after cecal ligation and puncture (CLP) in mice and neutralization of MIP-2 reduced peritoneal PMN migration. A prerequisite for neutrophil-endothelial adhesion and subsequent migration from the circulation is selectin-mediated rolling. Pretreatment of mice with an anti-P-selectin antibody before intraperitoneal injection of MIP-2 significantly reduced peritoneal PMN migration. However, there are no reports that a C-X-C chemokine can up-regulate endothelial selectins. We postulated that MIP-2, when injected intraperitoneally, interacts with a cell that is known to release factors that up-regulate endothelial selectins. A likely candidate is the mast cell, which contains histamine and tumor necrosis factor alpha (TNF-alpha), and both of these factors induce selectins. Intraperitoneally injected MIP-2 caused an early significant increase in peritoneal TNF-alpha, whereas histamine levels were unaffected. In a subsequent experiment, mast cell-deficient mice and their normal controls were then injected intraperitoneally with MIP-2 or underwent CLP. Significantly fewer PMNs migrated into the peritoneal cavity in the mast cell-deficient mice after MIP-2 injection or CLP. Thus, our findings indicate that mast cells and MIP-2 are necessary for PMN migration into the peritoneum in response to intra-abdominal infection, and that MIP-2 appears to facilitate this through an increase in TNF-alpha release.

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Interleukin 8 and mast cell-generated tumor necrosis factor-? in neutrophil recruitment

Cited by 32 publications

References 39 publications

Efficient sorting of TNF‐alpha to rodent mast cell granules is dependent on N‐linked glycosylation

Efficient sorting of TNF‐alpha to rodent mast cell granules is dependent on N‐linked glycosylation

A Peptide Derived from the Parasite Receptor, Complement C2 Receptor Inhibitor Trispanning, Suppresses Immune Complex-Mediated Inflammation in Mice

Regulation of early peritoneal neutrophil migration by macrophage inflammatory protein-2 and mast cells in experimental peritonitis

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