Mucin gene deficiency in mice impairs host resistance to an enteric parasitic infection

Hasnain, Sumaira Z., Wang, Huaqing, Ghia, Jean-Eric, Haq, Nihal, Deng, Yikang, Velcich, Anna, Grencis, Richard K., Thornton, David J. and Khan, Waliul I. (2010) Mucin gene deficiency in mice impairs host resistance to an enteric parasitic infection. Gastroenterology, 138 5: 1763-1771.e5. doi:10.1053/j.gastro.2010.01.045


Author Hasnain, Sumaira Z.
Wang, Huaqing
Ghia, Jean-Eric
Haq, Nihal
Deng, Yikang
Velcich, Anna
Grencis, Richard K.
Thornton, David J.
Khan, Waliul I.
Title Mucin gene deficiency in mice impairs host resistance to an enteric parasitic infection
Journal name Gastroenterology   Check publisher's open access policy
ISSN 0016-5085
1528-0012
Publication date 2010-05
Sub-type Article (original research)
DOI 10.1053/j.gastro.2010.01.045
Open Access Status DOI
Volume 138
Issue 5
Start page 1763
End page 1771.e5
Total pages 14
Place of publication Maryland Heights, MO, United States
Publisher W.B. Saunders
Language eng
Formatted abstract
Background & Aims: Hyperplasia of mucin-secreting intestinal goblet cells accompanies a number of enteric infections, including infections by nematode parasites. Nevertheless, the precise role of mucins in host defense in nematode infection is not known. We investigated the role of the mucin (Muc2) in worm expulsion and host immunity in a model of nematode infection.

Methods: Resistant (BALB/c, C57BL/6), susceptible (AKR), and Muc2-deficient mouse strains were infected with the nematode, Trichuris muris, and worm expulsion, energy status of the whipworms, changes in mucus/mucins, and inflammatory and immune responses were investigated after infection.

Results: The increase in Muc2 production, observed exclusively in resistant mice, correlated with worm expulsion. Moreover, expulsion of the worms from the intestine was significantly delayed in the Muc2-deficient mice. Although a marked impairment in the development of periodic acid Schiff (PAS)-stained intestinal goblet cells was observed in Muc2-deficient mice, as infection progressed a significant increase in the number of PAS-positive goblet cells was observed in these mice. Surprisingly, an increase in Muc5ac, a mucin normally expressed in the airways and stomach, was observed after infection of only the resistant animals. Overall, the mucus barrier in the resistant mice was less permeable than that of susceptible mice. Furthermore, the worms isolated from the resistant mice had a lower energy status.

Conclusions: Mucins are an important component of innate defense in enteric infection; this is the first demonstration of the important functional contribution of mucins to host protection from nematode infection.
Keyword Enteric infection
Goblet cell
Host resistance
Innate immunity
Muc2
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: Mater Research Institute-UQ (MRI-UQ)
 
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