Eosinophils within the healthy or inflamed human intestine produce substance P and vasoactive intestinal peptide

Metwali, Ahmed; Blum, Arthur M.; Ferraris, L.; Klein, John S.; Fiocchi, Claudio; Weinstock, Joel V.

doi:10.1016/0165-5728(94)90164-3

Cited by 121 publications

(74 citation statements)

References 41 publications

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“…1A), which suggests that dental pulp inflammation is associated with the periodontal disease pathogen P. gingivalis and is modified by neuropeptides released in the dental pulp tissue. Neuropeptides are produced and released mainly by the nervous system (14,15) and also by cells other than neurocytes, e.g., macrophages (51) and eosinophils (52). CGRP and SP are abundantly copresent in nerve fibers and perivascular plexuses in the human dental pulp tissues (22,25).…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Release from Dental Pulp Cells by RgpB via Proteinase-Activated Receptor-2 Signaling

Tancharoen

Sarker

Imamura

et al. 2005

The Journal of Immunology

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Dental pulp inflammation often results from dissemination of periodontitis caused mostly by Porphyromonas gingivalis infection. Calcitonin gene-related peptide and substance P are proinflammatory neuropeptides that increase in inflamed pulp tissue. To study an involvement of the periodontitis pathogen and neuropeptides in pulp inflammation, we investigated human dental pulp cell neuropeptide release by arginine-specific cysteine protease (RgpB), a cysteine proteinase of P. gingivalis, and participating signaling pathways. RgpB induced neuropeptide release from cultured human pulp cells (HPCs) in a proteolytic activity-dependent manner at a range of 12.5–200 nM. HPCs expressed both mRNA and the products of calcitonin gene-related peptide, substance P, and proteinase-activated receptor-2 (PAR-2) that were also found in dental pulp fibroblast-like cells. The PAR-2 agonists, SLIGKV and trypsin, also induced neuropeptide release from HPCs, and HPC PAR-2 gene knockout by transfection of PAR-2 antisense oligonucleotides inhibited significantly the RgpB-elicited neuropeptide release. These results indicated that RgpB-induced neuropeptide release was dependent on PAR-2 activation. The kinase inhibitor profile on the RgpB-neuropeptide release from HPC revealed a new PAR-2 signaling pathway that was mediated by p38 MAPK and activated transcription factor-2 activation, in addition to the PAR-2-p44/42 p38MAPK and -AP-1 pathway. This new RgpB activity suggests a possible link between periodontitis and pulp inflammation, which may be modulated by neuropeptides released in the lesion.

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Section: Discussionmentioning

confidence: 99%

Neuropeptide Release from Dental Pulp Cells by RgpB via Proteinase-Activated Receptor-2 Signaling

Tancharoen

Sarker

Imamura

et al. 2005

The Journal of Immunology

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“…First, the discovery that disruption of the NK-1R gene protects against the injury induced by antigen-antibody complex formation in the airways has revealed that neurokinin amplification serves an essential rather than a cooperative role, at least in this type of injury (7). In addition, the detection of PPT-A mRNAs and substance P-like immunoreactivity in intrinsic airway neurons (8,9) and, more recently, in inflammatory cells (10)(11)(12)(13)(14)(15) has uncovered the existence of two cellular reservoirs of neurokinins in the lungs, one constitutive and the other migrant. Questioned when first reported, the now confirmed presence of substance P and other neurokinins in resident macrophages and circulating leukocytes is particularly intriguing because many of these cells also express neurokinin receptors (10,14).…”

Section: Introductionmentioning

confidence: 99%

Bone marrow transplantation reveals an essential synergy between neuronal and hemopoietic cell neurokinin production in pulmonary inflammation

Chavolla-Calderón¹,

Bayer²,

Fontan³

2003

J. Clin. Invest.

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Neurogenic inflammation is believed to originate with the antidromic release of substance P, and of other neurokinins encoded by the preprotachykinin A (PPT-A) gene, from unmyelinated nerve fibers (C-fibers) following noxious stimuli. Consistent with this concept, we show here that selective sensoryfiber denervation with capsaicin and targeted deletion of the PPT-A gene protect murine lungs against both immune complex-mediated and stretch-mediated injuries. Reconstitution of PPT-A gene-deleted mice with WT bone marrow does not abrogate this protection, demonstrating a critical role for PPT-A gene expression by sensory neurons in pulmonary inflammation. Surprisingly, reconstitution of WT mice with PPT-A gene-deficient bone marrow also confers protection against pulmonary injury, revealing that PPT-A gene expression in hemopoietic cells has a previously unanticipated essential role in tissue injury. Taken together, these findings demonstrate a critical synergy between capsaicin-sensitive sensory fibers and hemopoietic cells in neurokinin-mediated inflammation and suggest that such synergy may be the basis for a stereotypical mechanism of response to injury in the respiratory tract.This article was published online in advance of the print edition. The date of publication is available from the JCI website, http://www.jci.org.

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“…The role played by neuropeptides in inflammatory bowel disease is unclear, but vasoactive intestinal peptide (VIP) has potentially important immunomodulatory functions (13) and is produced by both nerve endings (14) and inflammatory cells in the lamina propria (15). In addition, eosinophils present in the normal mucosa may secrete VIP.…”

Section: Introductionmentioning

confidence: 99%

Regulation of proliferation of human colonic subepithelial myofibroblasts by mediators important in intestinal inflammation.

Jobson

Billington²,

Hall³

1998

J. Clin. Invest.

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An increase in myofibroblast number may be necessary for wound healing but may also lead to postinflammatory scarring. We have, therefore, studied the role of mediators important in inflammatory bowel disease in regulating proliferation of human colonic myofibroblasts. Using primary cultures of these cells, we have shown increases in [ 3 H]thymidine incorporation in response to platelet-derived growth factor (EC 50 ϭ 14 ng/ml), basic fibroblast growth factor (EC 50 ϭ 2.2 ng/ml), and epidermal growth factor (EC 50 ϭ 1.1 ng/ml). Coulter counting of cell suspensions demonstrated increases in cell number with these growth factors along with insulin-like growth factor-I and -II. In addition the proinflammatory cytokines IL-1 ␤ and TNF-␣ produced increases in

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Eosinophils within the healthy or inflamed human intestine produce substance P and vasoactive intestinal peptide

Cited by 121 publications

References 41 publications

Neuropeptide Release from Dental Pulp Cells by RgpB via Proteinase-Activated Receptor-2 Signaling

Neuropeptide Release from Dental Pulp Cells by RgpB via Proteinase-Activated Receptor-2 Signaling

Bone marrow transplantation reveals an essential synergy between neuronal and hemopoietic cell neurokinin production in pulmonary inflammation

Regulation of proliferation of human colonic subepithelial myofibroblasts by mediators important in intestinal inflammation.

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