Ultrastructural effects of intravascularly injected polyethylene glycol-hemoglobin in intestinal mucosa

1998 ◽  
Vol 275 (2) ◽  
pp. H615-H625 ◽  
Author(s):  
Ann L. Baldwin ◽  
Lisa M. Wilson ◽  
J. Edward Valeski
Keyword(s):  
Mast Cell ◽  
Polyethylene Glycol ◽  
Intestinal Mucosa ◽  
Time Course ◽  
Mast Cell Degranulation ◽  
Intestinal Lumen ◽  
Saline Control ◽  
Mucosal Mast Cell ◽  
Sprague Dawley ◽  
Cell Secretion

Polyethylene glycol (PEG)-conjugated Hb (PEG-Hb) is being considered as a blood substitute. Previously, we showed that PEG-Hb extravasates rapidly from the intestinal mucosa and causes transient epithelial sloughing, resulting in temporary unimpeded passage of material between the intestinal lumen and the microcirculation. The present study quantifies the time course of factors related to this disturbance. Anesthetized Sprague-Dawley rats (350–450 g) were injected with a bolus of PEG-Hb (10 mg/ml) in saline. Control animals received saline, alone or with Dextran 70 (5 mg/ml). After 2, 8, 15, 60, or 90 min, the small intestine was perfusion fixed for microscopy (4 animals for each time point). Epithelial cell detachment and mucosal mast cell degranulation peaked at 2 and 8–15 min, respectively, but by 90 min were back to normal. Goblet cell secretion increased with time up to 8–15 min, after which it leveled off. Mean interstitial width was significantly greater 8 min after injection than for controls and continued to increase with time. In capillaries, endothelial fenestral diaphragms were replaced by thick, amorphous structures. Mesenteric mast cell degranulation was significantly greater 60–90 min after injection compared with controls. We propose that these results are consistent with intravascular injection of PEG-Hb invoking a transient inflammatory response in the intestine.

Mucosal mast cells and developmental changes in gastric absorption

1995 ◽  
Vol 268 (1) ◽  
pp. G121-G127 ◽  
Author(s):  
A. G. Catto-Smith ◽  
J. L. Ripper
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Short Circuit ◽  
Mast Cell Degranulation ◽  
Mucosal Mast Cell ◽  
Sprague Dawley ◽  
Mucosal Permeability ◽  
Mucosal Mast Cells ◽  
Gastric Mucosal Mast Cell

We aimed to establish whether gastric mucosal mast cells undergo degranulation during normal postnatal development and to correlate this with gastric electrical parameters, paracellular permeability, and macromolecular absorption. Sprague-Dawley rats were studied between 10 and 30 days after birth. Gastric mucosal mast cell degranulation occurred and was maximal on days 15 and 17, measured by histology and gastric and serum levels of rat mast cell protease II. Short-circuit current, transepithelial conductance, and permeability of voltage-clamped glandular stomach were elevated in younger animals, falling with age except for a transient but significant increase in conductance and permeability at 17 days, closely correlated with maximal mast cell degranulation. Macromolecular uptake was significantly increased in animals aged 10-15 days. Concanavalin A and antigen-induced mast cell degranulation increased conductance and permeability in vitro in younger animals. We conclude that 1) gastric mucosal mast cells degranulate during development, 2) the neonatal stomach has increased permeability and uptake of macromolecules, and 3) gastric mucosal mast cell degranulation during development may affect mucosal permeability.

A laboratory demonstration for learning about mast cell degranulation.

1999 ◽  
Vol 276 (6) ◽  
pp. S19
Author(s):  
J Corado ◽  
A Eblen-Zajjur
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Experimental Model ◽  
Low Cost ◽  
Mast Cell Degranulation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

A simple experimental model of cell degranulation was implemented that exposed mast cells obtained from Sprague-Dawley rats to saponin. The model is flexible, asy, and low cost, is not very time-consuming to run, and needs a minimum of laboratory resources. It has been used for the last three years in our undergraduate medical physiology courses and has replaced the classic utilization of slides and drawings.

scholarly journals Expression Profiling Reveals Novel Innate and Inflammatory Responses in the Jejunal Epithelial Compartment during Infection with Trichinella spiralis

2004 ◽  
Vol 72 (10) ◽  
pp. 6076-6086 ◽  
Author(s):  
Pamela A. Knight ◽  
Alan D. Pemberton ◽  
Kevin A. Robertson ◽  
Douglas J. Roy ◽  
Steven H. Wright ◽  
...  
Keyword(s):  
Mast Cell ◽  
Goblet Cell ◽  
Expression Profiling ◽  
Time Course ◽  
Inflammatory Responses ◽  
Trichinella Spiralis ◽  
Mucosal Mast Cell ◽  
Screening Process ◽  
Mucin Gene ◽  
Enhanced Production

ABSTRACT Infection with intestinal nematodes induces profound pathological changes to the gut that are associated with eventual parasite expulsion. We have applied expression profiling as an initial screening process with oligonucleotide microarrays (Affymetrix MG-U74AV2 gene chips) and time course kinetics to investigate gene transcription triggered by the intraepithelial nematode Trichinella spiralis in jejunal epithelium from BALB/c mice. Of the 4,114 genes detected, 2,617 were present in all uninfected and T. spiralis-infected replicates, 8% of which were notably upregulated, whereas 12% were downregulated at the time of worm expulsion (day 14 postinfection). Upregulation of goblet cell mucin gene transcripts intestinal mucin gene 3 (MUC3), calcium chloride channel 5 (CLCA5), and goblet cell gene 4 (GOB4) is consistent with enhanced production and alteration of mucus, whereas a 60- to 70-fold upregulation of transcripts for mast cell proteases 1 and 2 (MCPT-1 and -2) is consistent with intraepithelial mucosal mast cell recruitment. Importantly, there was novel expression of sialyltransferase 4C (SIAT4C), small proline-rich protein 2A (SPRR2A), and resistin-like molecule β (RELMβ) on day 14 postinfection. In contrast, DNase I and regenerating protein 3 (REG3) transcripts were substantially downregulated. Time course analyses revealed early (within 48 h of infection) induction of Siat4c, Sprr2A, and Relmβ and later (within 120 h) induction of Mcpt-1 and -2. The findings demonstrate early innate responses and later inflammatory changes within the epithelium. The early epithelial responses may be associated both with repair (Sprr2A) and with the development of innate immunity (Siat4c and Relmβ).

Substance P enhances electrical field stimulation-induced mast cell degranulation in rat trachea

1996 ◽  
Vol 270 (6) ◽  
pp. L985-L991 ◽  
Author(s):  
X. Y. Hua ◽  
S. M. Back ◽  
E. K. Tam
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Substance P ◽  
Electrical Field Stimulation ◽  
Mast Cell Degranulation ◽  
Facilitatory Effect ◽  
Neurokinin A ◽  
Field Stimulation ◽  
Cell Secretion ◽  
Electrical Field

We previously demonstrated in an ex vivo rat tracheal model that chymotryptic activity is an index of mast cell degranulation and that substance P (SP) and electrical field stimulation (EFS) synergistically degranulate mucosal and connective tissue mast cells. In the current study, we found that the facilitatory effect of SP was apparent at concentrations as low as 10(-9) M. This effect was mimicked by 10(-7) M neurokinin A or by 10(-6) M capsaicin and was blocked by the NK1 receptor antagonist CP-96,345. SP + EFS-induced mast cell secretion was significantly attenuated by 10(-6) M tetrodotoxin. The response was also attenuated in tracheas from rats in which sensory nerves had been depleted by systemic pretreatment with capsaicin or in which sympathetic nerves had been depleted by systemic pretreatment with 6-hydroxy-dopamine. Atropine (10(-6) M) or indomethacin (10(-5) M) also attenuated SP + EFS-induced mast cell secretion. Our findings suggest the importance of a sensitizing rather than a direct stimulating effect of SP on mast cell degranulation. SP may increase the sensitivity of mast cells to EFS-discharged mediators or facilitate the release of mast cell-stimulating mediators from autonomic nerves.

scholarly journals Delayed Expulsion of the Nematode Trichinella spiralisIn Mice Lacking the Mucosal Mast Cell–Specific Granule Chymase, Mouse Mast Cell Protease-1

2000 ◽  
Vol 192 (12) ◽  
pp. 1849-1856 ◽  
Author(s):  
Pamela A. Knight ◽  
Steven H. Wright ◽  
Catherine E. Lawrence ◽  
Yvonne Y.W. Paterson ◽  
Hugh R.P. Miller
Keyword(s):  
Mast Cell ◽  
Serine Proteases ◽  
Trichinella Spiralis ◽  
Gastrointestinal Nematodes ◽  
Intestinal Lumen ◽  
Mucosal Mast Cell ◽  
Mast Cell Protease ◽  
Muscle Larvae ◽  
Mouse Mast Cell

Expulsion of gastrointestinal nematodes is associated with pronounced mucosal mast cell (MMC) hyperplasia, differentiation, and activation, accompanied by the systemic release of MMC granule chymases (chymotrypsin-like serine proteases). The β-chymase mouse mast cell protease-1 (mMCP-1) is expressed predominantly by intraepithelial MMCs, and levels in the bloodstream and intestinal lumen are maximal at the time of worm expulsion in parasitized mice. To address the in vivo functions of MMC-specific β-chymases, we have generated transgenic mice that lack the mMCP-1 gene. They were backcrossed onto a congenic BALB/c background to investigate the response to nematode infection. The deletion of the mMCP-1 gene is associated with significantly delayed expulsion of Trichinella spiralis and increased deposition of muscle larvae in BALB/c mice despite the presence of normal and sometimes increased numbers of MMCs. Neither worm fecundity nor worm burdens were altered in Nippostrongylus-infected mMCP-1−/− BALB/c mice. These data demonstrate, for the first time, that the ablation of an MMC-derived effector molecule compromises the expulsion process.

In vitro activation of murine DRG neurons by CGRP-mediated mucosal mast cell degranulation

2004 ◽  
Vol 287 (1) ◽  
pp. G178-G191 ◽  
Author(s):  
F. De Jonge ◽  
A. De Laet ◽  
L. Van Nassauw ◽  
J. K. Brown ◽  
H. R. P. Miller ◽  
...  
Keyword(s):  
Mast Cell ◽  
Nerve Fibers ◽  
Mast Cell Degranulation ◽  
Mucosal Mast Cell ◽  
Close Apposition ◽  
Drg Neurons ◽  
Nodose Ganglia ◽  
Mouse Mast Cell

Upregulation of CGRP-immunoreactive (IR) primary afferent nerve fibers accompanied by mastocytosis is characteristic for the Schistosoma mansoni-infected murine ileum. These mucosal mast cells (MMC) and CGRP-IR fibers, which originate from dorsal root (DRG) and nodose ganglia, are found in close apposition. We examined interactions between primary cultured MMC and CGRP-IR DRG neurons in vitro by confocal recording of intracellular Ca2+concentration ([Ca2+]i). The degranulatory EC50for the mast cell secretagogue compound 48/80 (C48/80; 10 μg/ml) and the neuropeptides CGRP (2.10−8M) and substance P (SP; 3.10−8M) were determined by measurement of extracellular release of the granule chymase, mouse mast cell protease-1. Application of C48/80 (10 μg/ml) and CGRP and SP (both 10−7M) to Fluo-4-loaded MMC induced a transient rise in [Ca2+]iafter a lag time, indicative of mast cell degranulation and/or secretion. The CGRP response could be completely blocked by pertussis toxin (2 μg/ml), indicating involvement of Giproteins. Application of MMC juice, obtained by C48/80 degranulation of MMC, to Fluo-4-loaded DRG neurons induced in all neurons a rise in [Ca2+]i, indicative of activation. Degranulation of MMC by C48/80 in culture dishes containing Fluo-4-loaded DRG neurons also caused activation of the DRG neurons. In conclusion, these results demonstrate a bidirectional cross-talk between cultured MMC and CGRP-IR DRG neurons in vitro. This indicates that such a communication may be the functional relevance for the close apposition between MMC and CGRP-IR nerve fibers in vivo.

Endothelin-1 induces mucosal mast cell degranulation and tissue injury via ETA receptors

2002 ◽  
Vol 103 (s2002) ◽  
pp. 31S-34S ◽  
Author(s):  
Mihály BOROS ◽  
László SZALAY ◽  
József KASZAKI
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Receptor Antagonist ◽  
Mast Cell Degranulation ◽  
Tissue Response ◽  
Mucosal Mast Cell ◽  
Receptor Antagonists ◽  
Endothelin 1 ◽  
Eta Receptor ◽  
Etb Receptor

The effects of endothelin-1 (ET-1) on mucosal mast cells are of special interest, since they may be an important component of the tissue response that occurs during ischaemic preconditioning or ischaemia/re-oxygenation injuries. Increasing doses of ET-1 were administered intravenously to anaesthetized rats. In a second series of experiments, animals were pretreated with the ETA receptor antagonists BQ-610 or ETR-P1/fl peptide, or with the ETB receptor antagonist IRL-1038. Intestinal perfusion changes were recorded, and the proportion of degranulated mast cells and the degree of mucosal damage were determined in ileal biopsies. ET-1 induced dose-dependent alterations in the haemodynamic and morphological parameters, and caused significant mast cell degranulation. These changes were inhibited significantly by pretreatment with the ETA receptor antagonists, but not with the ETB receptor antagonist. We conclude that a cross-talk exists between endothelial cell-derived humoral mediators and the intestinal mast cell system.

Time course of human conjunctival mast cell degranulation in response to compound 48/80

2009 ◽  
Vol 67 (S192) ◽  
pp. 154-161 ◽  
Author(s):  
Ira J. Udell ◽  
Kenneth R. Kenyon ◽  
Laila A. Hanninen ◽  
Mark B. Abelson
Keyword(s):  
Mast Cell ◽  
Time Course ◽  
Mast Cell Degranulation
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