Mast Cell-Derived TNF-α Primes Sensory Nerve Endings in a Pulmonary Hypersensitivity Reaction

Houwelingen, Anneke H. van; Kool, Mirjam; Jager, Saskia C.A. de; Redegeld, Frank A.; Heuven-Nolsen, D. van; Kraneveld, Aletta D.; Nijkamp, Frans P.

doi:10.4049/jimmunol.168.10.5297

Cited by 63 publications

(30 citation statements)

References 45 publications

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“…Expression of TNF receptor subtypes occurs on cultured neonatal DRG cells (31,32), and TNF␣ can influence neuropathic pain via a p38 MAPKdependent mechanism (33). Furthermore, TNF␣ and TNF receptor 1 are suggested to play a prominent role in priming sensory nerve endings in mouse peripheral airways, leading to potentiation of a sensory nervemediated tracheal hyperpermeability response (34). The finding that TNF␣-induced knee swelling is greater in WT mice compared with TRPV1 Ϫ/Ϫ mice is consistent with the concept that TNF␣ can prime TRPV1 sensory nerve-mediated swelling in the knee joint, via as-yetuncharacterized mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Involvement of transient receptor potential vanilloid 1 in the vascular and hyperalgesic components of joint inflammation

Keeble¹,

Russell²,

Curtis³

et al. 2005

Arthritis & Rheumatism

154

117

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Objective. To investigate the endogenous involvement of transient receptor potential vanilloid 1 (TRPV1) in a model of knee joint inflammation in the mouse.Methods. Following characterization of wild-type (WT) and TRPV1-knockout mice, inflammation was induced via intraarticular (IA) injection of Freund's complete adjuvant (CFA). Knee swelling was assessed as diameter, and inflammatory heat hyperalgesia was determined using the Hargreaves technique, for up to 3 weeks. At 18 hours, acute hyperpermeability was measured with 125 I-albumin, and cytokines and myeloperoxidase activity, a marker of neutrophils, were assayed in synovial fluid extracts. The possibility that exogenous tumor necrosis factor ␣ (TNF␣) was involved in influencing TRPV1 activation was investigated in separate experiments.Results. Increased levels of knee swelling, hyperpermeability, leukocyte accumulation, and TNF␣ were found in WT mice 18 hours after IA CFA treatment compared with saline treatment. Significantly less knee swelling and hyperpermeability were found in TRPV1 ؊/؊ mice, but leukocyte accumulation and TNF␣ levels were similar in WT and TRPV1 ؊/؊ mice. Knee swelling in response to CFA remained significantly higher for a longer period in WT mice compared with TRPV1 ؊/؊ mice, with thermal hyperalgesic sensitivity observed at 24 hours and at 1 week in WT, but not TRPV1 ؊/؊ , mice. Knee swelling was attenuated (P < 0.05) in TRPV1 ؊/؊ compared with WT mice 4 hours after IA administration of TNF␣.Conclusion. Our findings indicate that TRPV1 has a role in acute and chronic inflammation in the mouse knee joint. Thus, selective antagonism of TRPV1 should be considered as a potential target for treatment of acute and chronic joint inflammation.

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Section: Discussionmentioning

confidence: 99%

Involvement of transient receptor potential vanilloid 1 in the vascular and hyperalgesic components of joint inflammation

Keeble¹,

Russell²,

Curtis³

et al. 2005

Arthritis & Rheumatism

154

117

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“…19 and A.D.K., M.K., and F.A.R., unpublished results). Mast cells also have been implicated in regulating the non-IgE immune response involved in skin and lung tissue inflammation (11,(25)(26)(27)(28). Specifically, these cells seemingly are involved in asthma pathogenesis (3)(4)(5), as evidenced by their increased number in the lungs of patients with nonatopic as well as atopic disease (6, 7).…”

Section: Discussionmentioning

confidence: 99%

Elicitation of allergic asthma by immunoglobulin free light chains

Kraneveld

Kool

Houwelingen

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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The observation that only 50% of patients with adult asthma manifest atopy indicates that other inflammatory mechanisms are likely involved in producing the characteristic features of this disorder; namely reversible airway obstruction, hyperresponsiveness, and pulmonary inflammation. Our recent discovery that antigen-specific Ig free light chains (LCs) mediate hypersensitivitylike responses suggests that these molecules may be of import in the pathophysiology of asthma. Using a murine experimental model of nonatopic asthma, we now have shown that an LC antagonist, the 9-mer peptide F991, can abrogate the development of airway obstruction, hyperresponsiveness, and pulmonary inflammation. Further, passive immunization with antigen-specific LCs and subsequent airway challenge can elicit a mast cell-dependent reaction leading to acute bronchoconstriction. These findings, and the demonstration that the concentration of free LCs in the sera of patients with adult asthma were significantly increased (as compared with age-matched nonasthmatic individuals), provide previously undescribed insight into the pathogenesis of asthma. In addition, the ability to inhibit pharmacologically LC-induced mast cell activation provides a therapeutic means to prevent or ameliorate the adverse bronchopulmonary manifestations of this incapacitating disorder.mast cells ͉ lung A sthma is a relatively common disorder manifested by airway inflammation that leads to bronchoconstriction and respiratory symptoms. Approximately 50% of adults with this disorder have atopic manifestations that involve IgE-mediated tissue sensitization with a T helper cell 2 response and eosinophilia (1, 2). However, that an equal percentage of patients with asthma are not atopic, as evidenced by negative skin-prick test as well as normal serum IgE levels and eosinophil counts (1, 2), indicates that other causative factors may be involved in the etiology of this disease. Furthermore, standardized comparisons across populations or time show only a weak and inconsistent association between the prevalence of adult asthma and the prevalence of atopy (1).Mast cells have been implicated as essential elements in the asthmatic process (3-5). Indeed, mast cell numbers are increased in the lungs of individuals with atopic as well as nonatopic variants of adult asthma, and the extent of degranulation of these cells is directly related to disease severity (6, 7). Although antigen-specific mast cell activation results from crosslinking of the high-affinity IgE receptor, FcRI, this effect can also occur in the absence of IgE antibodies (8-12); furthermore, anti-IgE antibody therapy has been of limited benefit in asthma (13-18).Our recent discovery that Ig free light chains (LCs) mediate antigen-specific mast cell-dependent hypersensitivity-like responses suggests that these molecules could be involved in the pathophysiology of adult asthma (19). We showed that mice, passively sensitized with antigen-specific LCs, when challenged by cutaneous exposure to the antigen, developed an...

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“…The fact that there is a close association between mast cells and peripheral nerves may help explain why allergic inflammation in particular is so adept at evoking such neuronal responses (1,2). It is rather well established that allergen-induced activation of tissue mast cells is associated with alterations in the phenotype or physiology of nearby primary afferent (sensory) nerves (3)(4)(5)(6)(7)(8)(9)(10). Some effect of mast cell activation on these nerves can be explained by defined mast cell mediators such as histamine, cys-leukotrienes, PGD2, and tryptase (3,4,10,11).…”

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confidence: 99%

Agonists of the Mas-Related Gene (Mrgs) Orphan Receptors as Novel Mediators of Mast Cell-Sensory Nerve Interactions

Lee

Dong

Liu

et al. 2008

The Journal of Immunology

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IgE-dependent activation of mast cell activation is often associated with symptoms attributed to activation of sensory nerves. Depending on the tissues involved such symptoms include itching, sneezing, irritation, vasodilation, and reflex secretions. In the present study, we hypothesize that sensory neuroactive mediators released from mast cells may include agonists of recently discovered orphan receptors referred to as sensory nerve specific receptors or products of mas related genes. HEK-293 cells expressing MrgC11 receptors and wild-type HEK-293 cells were loaded with the calcium indicator Fura-2. A known stimulant of MrgC11 receptors the RF-amide, neuropeptide FF, evoked a rapid increase in cytosolic calcium in the MrgC11 expressing cells but not in the wild-type HEK-293 cells. IgE-dependent stimulation of either rat basophilic leukemia-2H3 cells (RBL-2H3 cells) or mouse bone marrow-derived mast cells, released a substance(s) that stimulated increases in cytosolic calcium in the MrgC11 expressing cells that far exceeded that seen in control cells. RT-PCR revealed that both mouse mast cells and RBL-2H3 cells express the RF-amide precursor gene proneuropeptide FF (A). Immunohistochemical analysis demonstrated RF-amide immunoreactivity in mouse skin mast cells in situ and in mast cells isolated from mouse skin. These data support the hypothesis that agonists of certain sensory nerve specific receptors or mas related genes may participate in mast cell sensory nerve interactions.

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Mast Cell-Derived TNF-α Primes Sensory Nerve Endings in a Pulmonary Hypersensitivity Reaction

Cited by 63 publications

References 45 publications

Involvement of transient receptor potential vanilloid 1 in the vascular and hyperalgesic components of joint inflammation

Involvement of transient receptor potential vanilloid 1 in the vascular and hyperalgesic components of joint inflammation

Elicitation of allergic asthma by immunoglobulin free light chains

Agonists of the Mas-Related Gene (Mrgs) Orphan Receptors as Novel Mediators of Mast Cell-Sensory Nerve Interactions

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