The Role of Human Mast Cell-Derived Cytokines in Eosinophil Biology

Shakoory, Bita; Fitzgerald, Steve; Lee, Steven A.; David, S.; Krishnaswamy, Guha

doi:10.1089/107999004323065057

Cited by 212 publications

(146 citation statements)

References 90 publications

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“…During this process, mast cells release several inflammatory mediators including histamine, 5-HT, plateletaggregating factor (PAF), leukotrienes, and a variety of cytokines which can elicit many events associated with allergic inflammation, such as edema formation and cellular infiltration (9). Eosinophil accumulation is the main feature of allergic inflammation, these being some of the most abundant leukocytes present at the site.…”

Section: Introductionmentioning

confidence: 99%

Pharmacological study of anti-allergic activity of Syzygium cumini (L.) Skeels

Brito

Lima

Ramos

et al. 2007

Braz J Med Biol Res

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Myrtaceae is a plant family widely used in folk medicine and Syzygium and Eugenia are among the most important genera. We investigated the anti-allergic properties of an aqueous leaf extract of Syzygium cumini (L.) Skeels (SC). HPLC analysis revealed that hydrolyzable tannins and flavonoids are the major components of the extract. Oral administration of SC (25-100 mg/kg) in Swiss mice (20-25 g; N = 7/group) inhibited paw edema induced by compound 48/80 (50% inhibition, 100 mg/kg; P ≤ 0.05) and, to a lesser extent, the allergic paw edema (23% inhibition, 100 mg/kg; P ≤ 0.05). SC treatment also inhibited the edema induced by histamine (58% inhibition; P ≤ 0.05) and 5-HT (52% inhibition; P ≤ 0.05) but had no effect on plateletaggregating factor-induced paw edema. SC prevented mast cell degranulation and the consequent histamine release in Wistar rat (180-200 g; N = 7/group) peritoneal mast cells (50% inhibition, 1 µg/mL; P ≤ 0.05) induced by compound 48/80. Pre-treatment of BALB/c mice (18-20 g; N = 7/group) with 100 mg/kg of the extract significantly inhibited eosinophil accumulation in allergic pleurisy (from 7.662 ± 1.524 to 1.89 ± 0.336 x 10 6 /cavity; P ≤ 0.001). This effect was related to the inhibition of IL-5 (from 70.9 ± 25.2 to 12.05 ± 7.165 pg/mL) and CCL11/eotaxin levels (from 60.4 ± 8.54 to 32.8 ± 8.4 ng/mL) in pleural lavage fluid, using ELISA. These findings demonstrate an anti-allergic effect of SC, and indicate that its anti-edematogenic effect is due to the inhibition of mast cell degranulation and of histamine and serotonin effects, whereas the inhibition of eosinophil accumulation in the allergic pleurisy model is probably due to an impairment of CCL11/eotaxin and IL-5 production.

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Section: Introductionmentioning

confidence: 99%

Pharmacological study of anti-allergic activity of Syzygium cumini (L.) Skeels

Brito

Lima

Ramos

et al. 2007

Braz J Med Biol Res

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“…Eosinophils and mast cells are known to be key cells in the early and late stages of allergic inflammation. In addition, activated mast cells can contribute to the eosinophil-mediated inflammatory response [24]. Eosinophil-derived mediators may also influence mast cell survival and activation.…”

Section: Discussionmentioning

confidence: 99%

Histamine Release and Inflammatory Cell Infiltration in Airway Mucosa in Methylene Diphenyl Diisocyanate (MDI)-Induced Occupational Asthma

et al. 2008

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Introduction Although methylene diphenyl diisocyanate (MDI) is widely used in industries, there have been few studies of the pathogenic mechanisms of MDI-induced occupational asthma (MDI-OA). Methods We performed immunohistochemical analyses, measured inflammatory mediators and cytokines, and quantified histamine release (HR) from peripheral basophils in MDI-OA patients. Thirteen MDI-exposed workers (five MDI-OA, two MDI-induced esoinophilic bronchitis, and six asymptomatic exposed controls, AEC) were enrolled. Results and Discussion Immunochemical analyses indicated significantly increased anti-eosinophilic cationic proteinstained cells in MDI-OA patients as compared with controls (P<0.05). Sputum eosinophil cationic protein levels were increased after MDI-specific inhalation challenge test in MDI-OA/EB patients (P<0.02). Sputum eosinophil counts were highly correlated with IL-8 and MMP-9 levels (P<0.05 and P<0.01, respectively). Basophil HR was significantly increased in MDI-OA patients after stimulations with anti-IgG4 and MDI-human serum albumin conjugates (both P<0.05). Eosinophil activation is a major feature of airway inflammation in MDI-OA patients. Increased HR by MDI may contribute to the pathogenic mechanisms of MDI-OA.

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“…Regulation of cytokine production is important in the pathogenesis of allergic diseases. Cytokines, including interleukin (IL)-6, IL-8 and monocyte chemotactic protein-1 (MCP-1)/CCL2, participate in the shift from acute to chronic phases of allergy and in the attraction of neutrophils and monocytes, culminating in allergic inflammation (6)(7)(8). The thymus and activation-regulated chemokine (TARC)/CCL17, which is a Th2 chemokine associated with allergy, specifically atopic dermatitis, is primarily produced in keratinocytes (9).…”

Section: Introductionmentioning

confidence: 99%

Arazyme inhibits cytokine expression and upregulates skin barrier protein expression

Kim

Shin³

et al. 2013

Molecular Medicine Reports

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Abstract. In the present study, the inhibitory effect of arazyme on allergic inflammation was investigated by evaluating the alteration of cytokine production and expression of skin barrier proteins in immune and HaCaT human keratinocyte cells. THP-1 human monocytic and EoL-1 human eosinophilic cells were treated with Dermatophagoides pteronissinus extract (DpE). Monocyte chemotactic protein-1 (MCP-1)/CCL2, interleukin (IL)-6 and IL-8 increased following DpE treatment and arazyme significantly blocked the increase of MCP-1, IL-6 and IL-8 expression in cell types. Secretion of MCP-1, IL-6 and IL-8 induced by lipopolysaccharide in THP-1 cells was also inhibited by arazyme treatment. Arazyme inhibited the secretion of IL-6 and IL-8 due to phorbol 12-myristate 13-acetate and calcium ionophores in human mast cells. Arazyme blocked the secretion of thymus and activation-regulated chemokine (TARC)/CCL17, MCP-1, IL-6 and IL-8 due to tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in HaCaT cells. TNF-α and IFN-γ suppressed the expression of skin barrier proteins, including filaggrin, involucrin and loricrin. By contrast, arazyme increased the expression of filaggrin, involucrin and loricrin. These results may contribute to the development of a therapeutic drug for the treatment of allergic diseases, including atopic dermatitis.

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The Role of Human Mast Cell-Derived Cytokines in Eosinophil Biology

Cited by 212 publications

References 90 publications

Pharmacological study of anti-allergic activity of Syzygium cumini (L.) Skeels

Pharmacological study of anti-allergic activity of Syzygium cumini (L.) Skeels

Histamine Release and Inflammatory Cell Infiltration in Airway Mucosa in Methylene Diphenyl Diisocyanate (MDI)-Induced Occupational Asthma

Arazyme inhibits cytokine expression and upregulates skin barrier protein expression

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