scholarly journals Lymphocyte and mast cell counts are increased in the nasal mucosa in symptomatic natural colds

2003 ◽  
Vol 131 (1) ◽  
pp. 138-142 ◽  
Author(s):  
O.-P. ALHO ◽  
T. J. KARTTUNEN ◽  
R. KARTTUNEN ◽  
H. TUOKKO ◽  
M. KOSKELA ◽  
...  
Keyword(s):  
1996 ◽  
Vol 80 (4) ◽  
pp. 1322-1330 ◽  
Author(s):  
M. Longphre ◽  
L. Y. Zhang ◽  
J. R. Harkema ◽  
S. R. Kleeberger

Ozone (O3) exposure produces inflammation in the airways of humans and animal models. However, the mechanism by which O3 affects these changes is uncertain. Mast cells are strategically located below the epithelium of the airways and are capable of releasing a number of proinflammatory mediators. We tested the hypothesis that mast cells contribute to inflammation, epithelial sloughing, and epithelial proliferation in the nasal and terminal bronchiolar murine airways after O3 exposure. Mast cell-sufficient (+/+), mast cell-deficient (W/Wv), and mast cell-repleted [bone marrow-transplanted (BMT) W/Wv] mice were exposed to 2 ppm O3 or filtered air for 3 h. Nasal and bronchoalveolar lavage fluids were collected 6 and 24 h after exposure. Differential cell counts and protein content of the lavage fluids were used as indicators of inflammation and permeability changes in the airways. O3-induced epithelial injury was assessed by light microscopy, and O3-induced DNA synthesis in airway epithelium was estimated by using a 5-bromo-2′-deoxyuridine-labeling index in the nasal and terminal bronchiolar epithelia. Relative to air control mice, O3 caused significant increases in inflammation, epithelial injury, and epithelial DNA synthesis in +/+ mice. There was no significant effect of O3 exposure on any measured parameter in the W/Wv mice. To further assess the role of mast cells in O3-induced epithelial damage, mast cells were restored in W/Wv mice by BMT from +/+ congeners. Relative to sham-transplanted W/Wv mice, O3 caused significant increases in epithelial damage and DNA synthesis as well as inflammatory indicators in BMT W/Wv mice. These observations are consistent with the hypothesis that mast cells significantly modulate the inflammatory and proliferative responses of the murine airways to O3.


1970 ◽  
Vol 49 (3) ◽  
pp. 480-486
Author(s):  
F.M. Sorenson ◽  
J.S. Bennett ◽  
D. Fujita ◽  
F.R. Poindexter ◽  
W.B. Hall

Simple counts of mast cells per unit of human gingiva are often difficult to interpret because of the large numbers and varying sizes and shapes of the counted structures. The relatively simple photoelectric scanning method described herein eliminates tedious counting procedures while providing a measure of the relative quantity of stainable mast cell granules within the area scanned. Thus, the method may provide a better estimate of the total biologic activity than would simple mast cell counts.


1976 ◽  
Vol 24 (12) ◽  
pp. 1231-1238 ◽  
Author(s):  
L Enerbäck ◽  
G Berlin ◽  
I Svensson ◽  
I Rundquist

Mast cells can be automatically identified in a mixed cell population by flow cytofluorometry after Berberine sulphate staining. Volume specific counts of the total number of cells and number of mast cells, as well as frequency distributions of fluorescence intensities of mast cells, based on a large number of cells, can be rapidly obtained. Results obtained by microscope fluorometry of cells identified by phase contrast microscopy showviously published results it may be inferred that the fluorescence intensity of individual mast cells is proportional to mast cell heparin content. The automated cell counts correlated very well with manual hemocytometer counts. Both cell counts and the determination of mean mast cell fluorescence showed excellent reproducibility.


2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Zhikai Chi ◽  
Jing Xu ◽  
Romil Saxena

Objectives. Microscopic colitis (MC) is characterized by chronic diarrhea, normal colonoscopy findings, and mucosal inflammation in colonic biopsies and can be classified as collagenous colitis (CC) or lymphocytic colitis (LC). However, the pathogenesis of MC is largely unknown. In this study, we aimed to study mast cell counts and activation in MC. Methods. We investigated 64 biopsy samples from the surgical pathology database of Indiana University Health, which met the diagnostic criteria for CC or LC along with 20 control samples collected from 2014 to 2015. The specimens were used for the quantification of mast cells by examining the presence of intracellular and extracellular tryptase by immunohistochemistry. Results. In the lamina propria, the mast cell count was higher in both CC and LC groups than the control (mean highest count, 39/high-power field (HPF) vs. 30/HPF vs. 23/HPF; P<0.01). Extracellular tryptase was present in 10% of control subjects as compared to 41% of CC (P<0.05) and 60% of LC (P<0.001) patients. When LC patients were stratified into two groups with either <80% or >80% of fragments affected by inflammation, increased mast cell counts are only observed in the >80% involvement group compared with the control, but not the <80% involvement group. Conclusions. The increased mast cell count and degranulation are identified in MC, suggesting that mast cell activation might be involved in the pathogenesis of MC.


1988 ◽  
Vol 65 (1) ◽  
pp. 445-451 ◽  
Author(s):  
C. R. Turner ◽  
J. Kolbe ◽  
E. W. Spannhake

In preliminary studies of antigen-induced airway inflammation, we noted an apparent increase in peribronchiolar mast cell number. Experiments were thus undertaken to investigate the nature of this migration of mast cells into the central and peripheral airway epithelium and to determine its time course. The tracheae and small airways of 10 anesthetized mongrel dogs were exposed via a bronchoscope to Ascaris suum antigen (Ag), fMet-Leu-Phe (fMLP), ovalbumin (OVA), and isotonic saline (SAL). In the central airways, all stimuli provoked a significant increase (P less than 0.05) in mast cell numbers at the base of the airway epithelium within 3 h. In the peripheral airways, only Ag aerosol stimulated a significant mast cell increase compared with unexposed tissue. In a second series of experiments, the trachea of seven dogs were exposed to 0.026, 0.26, and 2.6 micrograms of Ag. The tissue was collected at 1, 3, 6, and 10 h after exposure. In these experiments, there was a significant mast cell increase seen within 1 h but it was not dose dependent. By 6-10 h after exposure, mast cell counts were not significantly different from the unexposed condition, which is consistent with the idea that some of the cells either degranulated or migrated into the airway lumen. We conclude that mast cell migration is an acute response that can be demonstrated within 1 h of stimulation with Ag. The observation that nonimmunological stimuli may, in some cases, also stimulate mast cell movement affords the possibility that this process represents a generalized response to airway irritation.


1963 ◽  
Vol 41 (1) ◽  
pp. 1901-1906
Author(s):  
Frank C. Monkhouse ◽  
Donald G. Baker

Experiments were carried out to determine whether changes in endogenous heparin in rat tissues were related to changes in plasma levels of clearing factor lipase (CFL). Skin heparin levels, postheparin plasma CFL levels, and peritoneal mast cell counts were measured in normal, adrenalectomized, cortisone-treated, and X-irradiated rats. Total body X-irradiation in doses of 400 r to 600 r decreased skin heparin levels. The postheparin CFL levels of irradiated rats remained high while that of pair-fed controls dropped significantly. Cortisone treatment for 6 days caused an increase in plasma CFL levels in both intact and adrenalectomized rats but no significant change in skin heparin levels or mast cell count. Adrenalectomy caused no significant change in either postheparin CFL or skin heparin levels.


2020 ◽  
Vol 12 (02) ◽  
pp. 141-146
Author(s):  
Bhavya P. Mohan ◽  
K.P. Aravindan

Abstract Background and Objective Serotonin levels are increased in acute appendicitis. We investigated the possible source of this increase. The aim of this study was to compare the distribution and density of epithelial and nonepithelial enterochromaffin (EC) cells as well as numbers of degranulated and nondegranulated mast cells in different layers of normal appendices and acute appendicitis. Methods Sections from 15 cases of acute appendicitis and 10 cases where the appendix was morphologically normal were stained with Hematoxylin & Eosin, Toluidine blue, and immunohistochemically for chromogranin and CD-117. EC cells stained by chromogranin were counted per crypt and extraepithelial EC cells counted and expressed as cells per unit area (mm2). Mast cells stained by Toluidine blue and CD-117 were counted in lamina propria, submucosa, and muscle layers. The difference between Toluidine blue and CD117 stained mast cells was taken to be an estimate of degranulated cells. The cell counts were expressed per unit area (mm2) as well as per cross-sectional area of the appendix. Results There was no statistically significant difference in epithelial and extraepithelial EC cells between acute appendicitis and normal appendix. Estimated mast cell degranulation as indicated by mast cell counts per cross-sectional area is greatly increased in acute appendicitis when compared with normal. Conclusion Degranulated mast cells rather than EC cells may be the main source of raised serotonin in acute appendicitis.


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