scholarly journals Enteric Expression of the Integrin αvβ6 Is Essential for Nematode-Induced Mucosal Mast Cell Hyperplasia and Expression of the Granule Chymase, Mouse Mast Cell Protease-1

2002 ◽  
Vol 161 (3) ◽  
pp. 771-779 ◽  
Author(s):  
Pamela A. Knight ◽  
Steven H. Wright ◽  
Jeremy K. Brown ◽  
Xiaozhu Huang ◽  
Dean Sheppard ◽  
...  
2003 ◽  
Vol 33 (1) ◽  
pp. 132-146 ◽  
Author(s):  
J. K. Brown ◽  
P. A. Knight ◽  
S. H. Wright ◽  
E. M. Thornton ◽  
H. R. P. Miller

2000 ◽  
Vol 68 (9) ◽  
pp. 4968-4971 ◽  
Author(s):  
Denis N. Onah ◽  
Fukumi Uchiyama ◽  
Yuuko Nagakui ◽  
Masao Ono ◽  
Toshiyuki Takai ◽  
...  

ABSTRACT A possible role for the γ subunit of immunoglobulin Fc receptors (FcR) in mucosal defenses against intestinal nematode parasites was studied using age-matched FcRγ-knockout (FcRγ−/−) and wild-type (FcRγ+/+) C57BL/6 mice. Mice were infected subcutaneously with 3,000 infective larvae of Strongyloides venezuelensis, and the degree of infection was monitored by daily fecal egg counts and adult worm recovery on days 8 and 13 postinfection. Mucosal mast cell (MMC) responses were assayed by in situ intestinal mast cell counts in stained histological sections of the jejunum and by measuring mouse mast cell protease 1 (MMCP-1) release in serum using sandwich enzyme-linked immunosorbent assay. FcRγ−/− mice had significantly higher egg counts (P < 0.01) and numbers of adult worms (P < 0.05) than FcRγ+/+mice, but mastocytosis and serum MMCP-1 release were comparable. It was concluded that MMCP-1 release may be spontaneous, does not depend on mast cell degranulation via the FcRγ signaling system, and appears to play no role in the expulsion of S. venezuelensis. The delay in worm expulsion in the FcRγ−/− mice might be related to inability of the MMC to degranulate and release effector molecules other than MMCP-1, since FcRγ deletion abrogates mast cell degranulative responses.


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

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.


2017 ◽  
Vol 139 (3) ◽  
pp. 987-996.e10 ◽  
Author(s):  
Asuka Honjo ◽  
Nobuhiro Nakano ◽  
Susumu Yamazaki ◽  
Mutsuko Hara ◽  
Koichiro Uchida ◽  
...  

Blood ◽  
1995 ◽  
Vol 86 (5) ◽  
pp. 1968-1976 ◽  
Author(s):  
GF Newlands ◽  
HR Miller ◽  
A MacKellar ◽  
SJ Galli

We assessed the effects of the c-kit ligand, stem cell factor (SCF), in the jejunal mucosal mast cell hyperplasia that occurs during infection with the intestinal nematodes, Nippostrongylus brasiliensis or Trichinella spiralis in rats. Compared with vehicle-treated rats, rats treated with SCF (25 micrograms/kg/d, intravenous [i.v.] for 14 days) during N brasiliensis infection exhibited significantly higher levels of the rat mucosal mast cell (MMC)-associated protease, rat mast cell protease II (RMCP II) in the jejunum and serum on day 8 of infection, but not on days 10 or 15 of infection. By contrast, in comparison to rats treated with normal sheep IgG, rats treated with a polyclonal sheep antirat SCF antibody exhibited markedly decreased numbers of jejunal MMCs, levels of jejunal RMCP II, and serum concentrations of RMCP II during infection with either nematode, particularly at the earlier intervals of infection (< or = day 10). Taken together, these findings indicate that SCF importantly contributes to MMC hyperplasia and/or survival during N brasiliensis or T spiralis infection in rats, but that levels of endogenous SCF are adequate to sustain near maximal MMC hyperplasia during infection with these nematodes. Notably, treatment of rats with SCF somewhat increased, and treatment with anti- SCF significantly decreased, parasite egg production during N brasiliensis infection. This finding raises the interesting possibility that certain activities of intestinal MMCs may contribute to parasite fecundity during infection with this nematode.


Parasitology ◽  
2008 ◽  
Vol 135 (6) ◽  
pp. 655-670 ◽  
Author(s):  
P. A. KNIGHT ◽  
J. K. BROWN ◽  
A. D. PEMBERTON

SUMMARYGastrointestinal infection with the nematodeTrichinella spiralisis accompanied by a rapid and reversible expansion of the mucosal mast cell and goblet cell populations in the intestinal epithelium, which is associated with the release of their mediators into the gut lumen. Both goblet cell and mast cell hyperplasia are highly dependent on mucosal T-cells and augmented by the cytokines IL-4 and IL-13. However, the contribution of both mast and goblet cells, and the mediators they produce, to the expulsion of the adults ofT. spiralisis only beginning to be elucidated through studies predominantly employingT. spiralis-mouse models. In the present article, we review the factors proposed to controlT. spiralis-induced mucosal mast cell (MMC) and goblet cell differentiation in the small intestine, and focus on some key MMC and goblet cell effector molecules which may contribute to the expulsion of adult worms and/or inhibition of larval development.


Sign in / Sign up

Export Citation Format

Share Document