Tumor Necrosis Factor (TNF) Is a Potent Rat Mast Cell Chemoattractant

Brzezińska‐Błaszczyk, Ewa; Pietrzak, Anna; Misiak-Tłoczek, Anna

doi:10.1089/jir.2006.0158

Cited by 36 publications

(42 citation statements)

References 64 publications

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“…These observations implicate that the increased tryptase in the airway tracts of COPD patients or CS rats is likely originated from mast cells situated in bronchial tissues, rather than in the cavity of airway tracts. Smoking-induced accumulation of mast cells in bronchial tissues has been found previously (Ekberg-Jansson et al 2005), which is mediated by histamine (Godot et al 2007) or TNF (Brzezińska-Błaszczyk et al 2007) related mechanism.…”

Section: Discussionmentioning

confidence: 87%

Tryptase Enzyme Activity Is Correlated with Severity of Chronic Obstructive Pulmonary Disease

Zhang

Zheng²,

et al. 2011

Tohoku J. Exp. Med.

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Tryptic enzymes, including tryptase, a signature enzyme in mast cells, are involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), a chronic inflammatory airway disease. However, the relationship between tryptase enzyme activity and COPD remains to be investigated. We therefore measured the enzyme activity and immunoreactivity of tryptase in the sputum and plasma of COPD patients in the present study. The results showed that tryptase enzyme activity in the sputum of severe COPD patients (FEV 1 s being recorded at ≤ 30% prediction values) was 3.4 times greater than that in patients with mild COPD (FEV 1 s being recorded at ≥ 80% of predicted values), whereas tryptic activity was 2.0 times higher in the severe COPD patients than in mild COPD patients. Moreover, tryptase enzyme activity, but not tryptic enzyme activity, was significantly elevated in the plasma of severe COPD patients compared with that of mild COPD patients. The level of immunoreactive tryptase was 1.9 times higher in the sputum of the severe COPD patients at admission than that at remission stage. We also employed a rat model of cigarette smoke-induced COPD. After 36 weeks of daily challenges with cigarette smoke, a well-established risk factor of COPD, tryptic and tryptase activities in the bronchoalveolar lavage fluid were elevated 1.5 and 2.6 times, respectively. These results indicate that smoking induces tryptase enzyme activity in the airway. In conclusion, tryptase enzyme activity is markedly increased in sputum and plasma of severe COPD patients. Enhanced tryptase enzyme activity may contribute to the pathogenesis of COPD.

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Section: Discussionmentioning

confidence: 87%

Tryptase Enzyme Activity Is Correlated with Severity of Chronic Obstructive Pulmonary Disease

Zhang

Zheng²,

et al. 2011

Tohoku J. Exp. Med.

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“…We did found that dihydrotestosterone treatment increased the mRNA of 2 purported TWIST11-responsive genes, CCL2 and TNF-a. TNF-a is also a potent chemoattractant for several cell lines (49). However, the effect of androgen on CCL2 and TNF-a mRNA appeared to be AR-dependent pathway but not TWIST1-dependent.…”

Section: Discussionmentioning

confidence: 94%

Indole-3-Carbinol and 3′,3′-Diindolylmethane Modulate Androgen's Effect on C-C Chemokine Ligand 2 and Monocyte Attraction to Prostate Cancer Cells

Kim

Milner

et al. 2013

Cancer Prevention Research

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Inflammation has a role in prostate tumorigenesis. Recruitment of inflammatory monocytes to the tumor site is mediated by C-C chemokine ligand 2 (CCL2) through binding to its receptor CCR2. We hypothesized that androgen could modulate CCL2 expression in hormone-responsive prostate cancer cells and thereby promote recruitment of monocytes. Given the inhibitory effect of broccoli-derived compounds indole-3-carbinol (I3C) and 3,3 0 -diindolylmethane (DIM) on androgen-dependent pathways, we also reasoned that I3C and DIM could modulate the effect of androgen on CCL2-mediated pathways. Dihydrotestosterone was found to induce a time-dependent (0-72 hours) and concentration-dependent (0-1 nmol/L) increase in CCL2 mRNA levels in androgen-responsive human prostate cancer cells (LNCaP). This increase in CCL2 mRNA corresponded with increased secretion of CCL2 protein. The effect of dihydrotestosterone was mediated through an androgen receptor (AR)-dependent pathway as small inhibitor RNA against AR negated the induction of CCL2. Although dihydrotestosterone also induced TWIST1 mRNA, an epithelialmesenchymal transition-related factor, and purported inducer of CCL2, blocking its expression with small inhibitor RNA did not inhibit dihydrotestosterone induction of CCL2 mRNA. Moreover, conditioned media from androgen-treated cells promoted human monocyte THP-1 cell migration and this effect was blocked by antibody against CCL-2. Both I3C and DIM inhibited promotional effects of dihydrotestosterone on CCL2 and migration. These results show that androgen may regulate CCL2 and promote inflammatory microenvironment in prostate tumors and that this process can be blocked by broccoli-derived compounds.Cancer Prev Res; 6(6); 519-29. Ó2013 AACR.

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“…Stimulate migration of MC [107] ; promote cellular differentiation, survival, and production of inflammatory cytokines and chemokines [156] .…”

Section: Indution Of Eos and Neu Accumulationmentioning

confidence: 99%

“…For example, the interactions of eotaxin, RANTES and MCP-1 with CCR3 (CD193) are responsible for the recruitment of basophils, eosinophils and mast cells [104] . While IL-6 [105] , IL-8 [106] , and TNF [107] stimulate mast cells migration [108] , and IL-29 induces mast cell infiltration via CD18-and intercellular adhesion molecule-1 (ICAM-1)-dependent mechanisms [101] .…”

Section: Wwwchinapharcom He Sh Et Almentioning

confidence: 99%

Mast cells and basophils are essential for allergies: mechanisms of allergic inflammation and a proposed procedure for diagnosis

Zhang

Zeng

et al. 2013

Acta Pharmacol Sin

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The current definition of allergy is a group of IgE-mediated diseases. However, a large portion of patients with clinical manifestations of allergies do not exhibit elevated serum levels of IgE (sIgEs). In this article, three key factors, ie soluble allergens, sIgEs and mast cells or basophils, representing the causative factors, messengers and primary effector cells in allergic inflammation, respectively, were discussed. Based on current knowledge on allergic diseases, we propose that allergic diseases are a group of diseases mediated through activated mast cells and/or basophils in sensitive individuals, and allergic diseases include four subgroups: (1) IgE dependent; (2) other immunoglobulin dependent; (3) non-immunoglobulin mediated; (4) mixture of the first three subgroups. According to our proposed definition, pseudo-allergic-reactions, in which mast cell or basophil activation is not mediated via IgE, or to a lesser extent via IgG or IgM, should be non-IgE-mediated allergic diseases. Specific allergen challenge tests (SACTs) are gold standard tests for diagnosing allergies in vivo, but risky. The identification of surface membrane activation markers of mast cells and basophils (CD203c, CCR3, CD63, etc) has led to development of the basophil activation test (BAT), an in vitro specific allergen challenge test (SACT). Based on currently available laboratory allergy tests, we here propose a laboratory examination procedure for allergy.

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Tumor Necrosis Factor (TNF) Is a Potent Rat Mast Cell Chemoattractant

Cited by 36 publications

References 64 publications

Tryptase Enzyme Activity Is Correlated with Severity of Chronic Obstructive Pulmonary Disease

Tryptase Enzyme Activity Is Correlated with Severity of Chronic Obstructive Pulmonary Disease

Indole-3-Carbinol and 3′,3′-Diindolylmethane Modulate Androgen's Effect on C-C Chemokine Ligand 2 and Monocyte Attraction to Prostate Cancer Cells

Mast cells and basophils are essential for allergies: mechanisms of allergic inflammation and a proposed procedure for diagnosis

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