The role of mucins in host–parasite interactions: Part II – helminth parasites

Théodoropoulos, Georgios; Hicks, Sally J.; Corfield, Anthony P.; Miller, B. G.; Carrington, S.D.

doi:10.1016/s1471-4922(00)01775-x

Cited by 88 publications

(68 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…spiralis , T. muris and H . polygyrus 76, 77, 78, 79. It has yet to be determined whether these changes occur as a result of the inflammatory environment or to resolve the infection; clearly more research is required to define the precise role of mucin glycans.…”

Section: Gi Nematode Infection and Alterations In Mucin Glycomementioning

confidence: 99%

A sticky end for gastrointestinal helminths; the role of the mucus barrier

Sharpe

Thornton

Grencis

2018

Parasite Immunology

View full text Add to dashboard Cite

SummaryGastrointestinal (GI) nematodes are a group of successful multicellular parasites that have evolved to coexist within the intestinal niche of multiple species. It is estimated that over 10% of the world's population are chronically infected by GI nematodes, making this group of parasitic nematodes a major burden to global health. Despite the large number of affected individuals, there are few effective treatments to eradicate these infections. Research into GI nematode infections has primarily focused on defining the immunological and pathological consequences on host protection. One important but neglected aspect of host protection is mucus, and the concept that mucus is just a simple barrier is no longer tenable. In fact, mucus is a highly regulated and dynamic‐secreted matrix, underpinned by a physical hydrated network of highly glycosylated mucins, which is increasingly recognized to have a key protective role against GI nematode infections. Unravelling the complex interplay between mucins, the underlying epithelium and immune cells during infection are a major challenge and are required to fully define the protective role of the mucus barrier. This review summarizes the current state of knowledge on mucins and the mucus barrier during GI nematode infections, with particular focus on murine models of infection.

show abstract

Section: Gi Nematode Infection and Alterations In Mucin Glycomementioning

confidence: 99%

A sticky end for gastrointestinal helminths; the role of the mucus barrier

Sharpe

Thornton

Grencis

2018

Parasite Immunology

View full text Add to dashboard Cite

show abstract

“…The influx of both cell types is dependent on type 2 secreted cytokines, notably IL-4, IL-9 and IL-13 (McKenzie et al, 1998;Theodoropoulos et al, 2001;Artis et al, 2004;Pennock & Grencis, 2006). Eosinophils also aggregate in the mucosa at the sites of infection, their mobilization from the bone marrow appearing initially as a pronounced blood eosinophilia, which has come to be regarded as a hallmark of nematode infections (Klion & Nutman, 2003), but their numbers in the mucosa take longer to build up and often increase only after the worms have been expelled (Lammas et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

The mucosal cellular response to infection withAncylostoma ceylanicum

2008

View full text Add to dashboard Cite

Although hookworms are known to stimulate inflammatory responses in the intestinal mucosa of their hosts, there is little quantitative data on this aspect of infection. Here we report the results of experiments conducted in hamsters infected with Ancylostoma ceylanicum. Infection resulted in a marked increase in goblet cells in the intestinal mucosa, which was dependent on the number of adult worms present and was sustained as long as worms persisted (over 63 days) but returned to baseline levels within 7 days of the removal of worms by treatment with ivermectin. Increased mast cell responses were also recorded. Levels were again dependent on the intensity of worm burdens and lasted as long as 63 days after infection. When worms were eliminated, mast cell numbers took over 2 weeks to return to normal. Paneth cell numbers fell soon after infection, the degree of reduction being dependent on the worm burden. After clearance of worms, Paneth cell numbers returned to normal within a week, but then rebounded and numbers rose to higher levels than those in control naïve animals. The time course of the response was similar whether animals experienced a chronic low-intensity infection without loss of worms or a higher intensity infection during the course of which worm burdens were gradually reduced. Clearly, A. ceylanicum was able to induce a marked inflammatory response in its host's intestine which was sustained for over 9 weeks after infection, and which hamsters appeared able to tolerate well. Our data draw attention to the resilience of hookworms which, unlike many other nematodes, are able to survive for many weeks in a highly inflamed intestinal tract.

show abstract

“…Parasite, 2008, 15, 304-309 from protozoa and helminths (Hicks et al, 2000;Theodoropoulos et al, 2001), but also for other parasitic molecules displaying a VNTR region. Examples are the SOWgp cell surface proteins from the pathogenic fungi Coccidioides immitis (Hung et al, 2000) and different proteins from Plasmodium, the circomsporozoite proteins (CSP, (Nussenzweig & Nussenzweig, 1985)) or the merozoite surface proteins (Msp-1 and Msp-2, (Holder, 1988;Smythe et al, 1988)).…”

Section: Th Emop August 2008mentioning

confidence: 99%

“…Parasite-derived mucin or mucin-like molecules have been extensively described in different protozoan and helminth parasites, but their function has not yet been completely elucidated. They could have roles in host recognition, penetration, adhesion and invasion of host cells, immunoprotection, immunomodulation and in the avoidance of host immune processes (Hicks et al, 2000;Theodoropoulos et al, 2001). Among these molecules described in parasites, the mucin-like molecules of Trypanosoma cruzi have been extensively studied and share numerous characteristics with Sm PoMuc (see (Buscaglia et al, 2006) for review), such as their structure, a high level of glycosylation and polymorphism.…”

Section: Th Emop August 2008mentioning

confidence: 99%

The compatibility polymorphism in invertebrate host/trematodes interactions: research of molecular determinants

et al. 2008

View full text Add to dashboard Cite

Summary :The co-evolutionary dynamics that exist in many host-parasite interactions sometimes leads to compatibility polymorphism. This phenomenon is well documented in mollusc/trematodes interactions but its molecular base is unknown. In order to identify key molecules involved in this phenomenon, we developed several molecular approaches comparing compatible or incompatible strains of mollusc or parasite. These comparisons led to the identification of numerous candidate genes listed and discussed (some of them) in the present review.

show abstract

The role of mucins in host–parasite interactions: Part II – helminth parasites

Cited by 88 publications

References 40 publications

A sticky end for gastrointestinal helminths; the role of the mucus barrier

A sticky end for gastrointestinal helminths; the role of the mucus barrier

The mucosal cellular response to infection withAncylostoma ceylanicum

The compatibility polymorphism in invertebrate host/trematodes interactions: research of molecular determinants

Contact Info

Product

Resources

About