NADPH‐d‐Positive Mast Cells in the Canine Paranal Sinus

Abstract

This study aimed to investigate the enzyme histochemical expression of NADPH-d in mast cells in the wall of the paranal sinus in male and female dogs. NADPH-d-positive cells with weak, medium and strong enzyme histochemical expression were observed in the stroma of the sinus near the blood vessels of the microcirculatory bed and around the apocrine and sebaceous glands. In the same areas, mast cells with similar dimensions and morphology were demonstrated by metachromasia on paraffin and cryostat cross-sections and stained with 0.1% toluidine blue in McIlvane's buffer (pH 3). These findings suggest that the mast cells that are located in the stroma near the blood vessels, the lining epithelium and the glands correspond with the cells with marked NADPH-d activity. The possibility of mast cells having nitric oxide activity could be used in the regulation of mast cells function when treating paranal sinus tumours and inflammations.

Pulmonary Protein Oxidation and Oxidative Stress Modulation by Lemna minor L. in Progressive Bleomycin-Induced Idiopathic Pulmonary Fibrosis

“…Therefore, the L. minor addition has a beneficial effect on BLM-induced inflammation and fibrotic processes, possibly participating in the Th1/Th2 immune response modulation and the subsequent decrease in the MCs and eosinophils set. Our results are supported by reports from a number of authors on the crucial role of mast cells and the Th2 immune response in IPF progression [16][17][18][21][22][23]69]. The accumulation of collagen together with increased MCs number in the interalveolar septa in BLM treated group detected in the current study correlates with the findings of several authors suggested that the MCs mediators tryptase, chymase and histamine induce lung fibroblast proliferation and collagen production [23,[70][71][72][73] recently demonstrated that stretch-induced degranulating MCs activate the pro-fibrotic cytokine TGF-β1.…”

“…It is well-known that lung MCs synthesize mediators involved in the contraction of airway and lung smooth muscle cells, such as serotonin and ghrelin [16]. Inhibitory non-adrenergic non-cholinergic airway smooth muscle response is mediated by nitric oxide (NO) [17], and mast cells are a secondary source of NO-dependent relaxation of smooth muscle cells [18,19]. MCs accumulation in the lungs of patients with various forms of pulmonary fibrosis has been reported in a number of studies [20][21][22].…”