HMC-1 human mast cells synthesize neurotensin (NT) precursor, secrete bioactive NT-like peptide(s) and express NT receptor NTS1

Cochrane, David E.; Carraway, Robert E.; Harrington, Kimberly Stacy; Laudano, Melissa; Rawlings, Stephen A.; Feldberg, Ross S.

doi:10.1007/s00011-011-0378-6

Cited by 15 publications

(11 citation statements)

References 53 publications

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“…Interestingly, the NTR antagonist reduced even basal VEGF release suggesting that mast cell-derived NT has a possible autocrine effect. This finding is supported by a recent report that the human leukemic mast cells (HMC-1) can synthesize NT precursor and release NT-like peptides [42]. Our present findings offer one possible explanation for our previous report that NT augments the ability of CRH to increase skin vascular permeability in rodents [11].…”

Section: Discussionsupporting

confidence: 91%

Neurotensin and CRH Interactions Augment Human Mast Cell Activation

et al. 2012

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Stress affects immunity, but the mechanism is not known. Neurotensin (NT) and corticotropin-releasing hormone (CRH) are secreted under stress in various tissues, and have immunomodulatory actions. We had previously shown that NT augments the ability of CRH to increase mast cell-dependent skin vascular permeability in rodents. Here we show that NT triggered human mast cell degranulation and significantly augmented CRH-induced vascular endothelial growth factor (VEGF) release. Investigation of various signaling molecules indicated that only NF-κB activation was involved. These effects were blocked by pretreatment with the NTR antagonist SR48692. NT induced expression of CRH receptor-1 (CRHR-1), as shown by Western blot and FACS analysis. Interestingly, CRH also induced NTR gene and protein expression. These results indicate unique interactions among NT, CRH, and mast cells that may contribute to auto-immune and inflammatory diseases that worsen with stress.

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Section: Discussionsupporting

confidence: 91%

Neurotensin and CRH Interactions Augment Human Mast Cell Activation

et al. 2012

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“…However, NT is also known for its interaction with immune cells such as lymphocytes and MCs . MCs produce NT on their own . Soon after the discovery of NT, it was reported that MCs bind NT .…”

Section: G‐protein‐coupled Receptors (Gpcrs)mentioning

confidence: 99%

Non‐IgE mediated mast cell activation

Redegeld

Kumari

et al. 2018

Immunological Reviews

160

105

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Mast cells (MCs) are innate immune cells that are scattered in tissues throughout the organism being particularly abundant at sites exposed to the environment such as the skin and mucosal surfaces. Generally known for their role in IgE-mediated allergies, they have also important functions in the maintenance of tissue integrity by constantly sensing their microenvironment for signals by inflammatory triggers that can comprise infectious agents, toxins, hormones, alarmins, metabolic states, etc. When triggered their main function is to release a whole set of inflammatory mediators, cytokines, chemokines, and lipid products. This allows them to organize the ensuing innate immune and inflammatory response in tight coordination with resident tissue cells, other rapidly recruited immune effector cells as well as the endocrine and exocrine systems of the body. To complete these tasks, MCs are endowed with a large repertoire of receptors allowing them to respond to multiple stimuli or directly interact with other cells. Here we review some of the receptors expressed on MCs (ie, receptors for Immunoglobulins, pattern recognition receptors, nuclear receptors, receptors for alarmins, and a variety of other receptors) and discuss their functional implication in the immune and inflammatory response focusing on non-IgE-mediated activation mechanisms.

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“…Activation of primary afferent nerves leads to the release of neurotensin from enteroendocrine cells of the epithelium [130,131]. Neurotensin is a potent activator of mast cells degranulation and can itself elicit fluid secretion [132,133]. While mast cell degranulation is a major contributor to the neurogenic inflammatory effects of toxin A, it is not essential because mast cell deficient mice have a reduced, but not abolished, inflammatory and secretory response to the toxin [134].…”

Section: The Gastrointestinal Tractmentioning

confidence: 99%

The Mast Cell-Nerve Functional Unit: A Key Component of Physiologic and Pathophysiologic Responses

Forsythe¹,

Bienenstock²

2012

Chemical Immunology and Allergy

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A key characteristic of mast cells appears to be an ability to span the division between nervous and immune system. Indeed, much of our understanding of the bi-directional relationship between the nervous and immune systems has come from the study of mast cell-nerve interaction. Although differences in species have been reported, morphologic as well as functional associations between mast cell and nerves are found in most tissues in many mammalian species, including humans. These interactions are involved in the regulation of physiologic homeostatic processes as well as in disease mechanisms. Here we discuss the influence of cholinergic and sensory neurons on mast cells as well as the importance of mast cell nerve interactions at specific tissue sites, including the brain.

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HMC-1 human mast cells synthesize neurotensin (NT) precursor, secrete bioactive NT-like peptide(s) and express NT receptor NTS1

Abstract: HMC-1 mast cells synthesize and secrete immunoreactive and bioactive NT-like peptide(s) and express the NT receptor, suggesting that NT from mast cells might serve autocrine and paracrine roles.

Cited by 15 publications

References 53 publications

Neurotensin and CRH Interactions Augment Human Mast Cell Activation

Neurotensin and CRH Interactions Augment Human Mast Cell Activation

Non‐IgE mediated mast cell activation

The Mast Cell-Nerve Functional Unit: A Key Component of Physiologic and Pathophysiologic Responses

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