Expression and Secretion of CXCL8 (IL-8), Release of Tryptase and Transcription of Histidine Decarboxylase mRNA by Anti-IgE-Activated Human Umbilical Cord Blood-Derived Cultured Mast Cells

Castellani, M.L.; Shaik, Y.B.; Perrella, Alessandro; Frydas, S.; Simeonidou, Isaia; Salini, Vincenzo; Tetè, Stefano; Conti, Chiara; Vecchiet, Jacopo; Theoharides, Theoharides C.; Conti, Pio; Lutiis, Maria Anna De

doi:10.1159/000107425

Cited by 3 publications

(4 citation statements)

References 60 publications

(40 reference statements)

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“…In support of our observations with BMMC, Castellani et al [39,40] have recently reported that human umbilical cord blood-derived mast cells have increased levels of HDC transcript following IgE receptor cross-linking. One advantage of producing more histamine following activation may be to prepare for subsequent rounds of activation.…”

Section: Discussionsupporting

confidence: 91%

Activation-induced cellular accumulation of histamine in immature but not mature murine mast cells

Fitz

Brennan²,

Wood

et al. 2008

Cell. Mol. Life Sci.

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Mast cell activation involves the rapid release of inflammatory mediators, including histamine, from intracellular granules. The cells are capable of regranulation and multiple rounds of activation. The goal of this study was to determine if there are changes in the content of pre-formed mast cell mediators after a round of activation. After 24 h, the histamine content of bone marrow-derived mast cells (BMMC), but not that of peritoneal mast cells, exceeded the amount in resting cells. Accumulation of histamine in BMMC peaked at 72 h of activation, and returned toward preactivation levels by 96 h. The increase in histamine content was accompanied by an increase in the gene expression of histidine decarboxylase. No increases in beta hexosaminidase or murine mast cell protease-6 were observed. These findings indicate that BMMC respond to activation by increasing total cell-associated histamine content. This increase may be important to the response of these cells upon subsequent exposure to antigens.

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Section: Discussionsupporting

confidence: 91%

Activation-induced cellular accumulation of histamine in immature but not mature murine mast cells

Fitz

Brennan²,

Wood

et al. 2008

Cell. Mol. Life Sci.

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“…This death process results in the release of inflammatory mediators that serve a variety of roles, including mast cell and leukocyte recruitment. Chemokines such as IL-8 (CXCL8) attract neutrophils and eosinophils to inflammation sites (16). IL-8, in particular, is a proinflammatory cytokine that, when expressed in the airway epithelium, serves as an indicator of cellular inflammation (17).…”

mentioning

confidence: 99%

Postnatal Exposure History and Airways

Murphy

Schelegle

Edwards

et al. 2012

Am J Respir Cell Mol Biol

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Postnatally, the lung continues to grow and differentiate while interacting with the environment. Exposure to ozone (O(3)) and allergens during postnatal lung development alters structural elements of conducting airways, including innervation and neurokinin abundance. These changes have been linked with development of asthma in a rhesus monkey model. We hypothesized that O(3) exposure resets the ability of the airways to respond to oxidant stress and that this is mediated by changes in the neurokinin-1 receptor (NK-1R). Infant rhesus monkeys received episodic exposure to O(3) biweekly with or without house dust mite antigen (HDMA) from 6 to 12 months of age. Age-matched monkeys were exposed to filtered air (FA). Microdissected airway explants from midlevel airways (intrapulmonary generations 5-8) for four to six animals in each of four groups (FA, O(3), HDMA, and HDMA+O(3)) were tested for NK-1R gene responses to acute oxidant stress using exposure to hydrogen peroxide (1.2 mM), a lipid ozonide (10 μM), or sham treatment for 4 hours in vitro. Airway responses were measured using real-time quantitative RT-PCR of NK-1R and IL-8 gene expression. Basal NK-1R gene expression levels were not different between the exposure groups. Treatment with ozonide or hydrogen peroxide did not change NK-1R gene expression in animals exposed to FA, HDMA, or HDMA+O(3). However, treatment in vitro with lipid ozonide significantly increased NK-1R gene expression in explants from O(3)-exposed animals. We conclude that a history of prior O(3) exposure resets the steady state of the airways to increase the NK-1R response to subsequent acute oxidant stresses.

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“…Hemokines control mast cell infiltration in several inflammatory diseases, including stress and neurological dysfunctions (26)(27)(28).…”

mentioning

confidence: 99%

“…CXCL8 (IL-8) is a CXC chemokine with chemotactic and inflammatory properties. We recently found that SP is able to stimulate the release of IL-8 (CXCL8) in mast cells (26,(60)(61). Since CXCL8 is a member of the CXC chemokine subfamily with potent chemotactic activity on neutrophils (62), and is a primary inflammatory cytokine, we conclude that these observations, obtained from human derived cord blood mast cell cultures (HOCBMC), a good and valid model in vitro, support the concept that the neurogenic system modulates inflammatory events by substance P and chemokine CXCL8 release (26,(63)(64).…”

mentioning

confidence: 99%

Inflammatory Compounds: Neuropeptide Substance Pand Cytokines

et al. 2009

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Inflammatory diseases represent one of the major causes of morbidity and mortality throughout the world and they affect the functions of several tissues. The pathophysiology of these diseases involves release of many pro-inflammatory mediators such as cytokines/chemokines, histamine, C3a, C5a (complement components), bradykinin, leukotrienes (LTC4, LTD4, LTE4), PAF, and substance P, in addition to anti-inflammatory molecules. Recently, it has been demonstrated that neuroimmune interactions are important in the initiation and progress of inflammatory processes. Substance P is an 11-amino acid neuropeptide that is released from nerve endings in many tissues. It acts via membrane-bound NK1 receptors (NK1R). Inflammatory and neuropeptides such as substance P stimulate the release of chemokines, in particular IL-8, a potent neutrophil chemoattractant. Expression of IL-8 is regulated mainly by the transcription factors NF-kappaB, activating protein-1. Substance P plays an important role in immunological and inflammatory states, and it is a mediator of tissue injury, asthma, arthritis, allergy and autoimmune diseases. In this article, our studies revisited the interrelationship between these two powerful inflammatory compounds: substance P and cytokines. These observations suggest that these inflammatory molecules may represent a potential therapeutic target to treat several inflammatory states.

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Expression and Secretion of CXCL8 (IL-8), Release of Tryptase and Transcription of Histidine Decarboxylase mRNA by Anti-IgE-Activated Human Umbilical Cord Blood-Derived Cultured Mast Cells

Cited by 3 publications

References 60 publications

Activation-induced cellular accumulation of histamine in immature but not mature murine mast cells

Activation-induced cellular accumulation of histamine in immature but not mature murine mast cells

Postnatal Exposure History and Airways

Inflammatory Compounds: Neuropeptide Substance Pand Cytokines

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