Goblet cells: are they an unspecific barrier against Giardia intestinalis or a gate?

Abstract

Giardiosis is one of the major intestinal parasitic diseases of human beings as well as wild and domesticated animals. Several protective mechanisms against infection have been described. However, specific information about relationship between giardiosis and the increased proliferation of goblet cells (GC) in patients infected with Giardia intestinalis (Syn. G. duodenalis, G. lamblia) is scarce. In this work, we compare and quantify the number of GC, and have inferred their metabolic state in the small intestine of dogs parasitized with Giardia intestinalis compared to dogs without parasites. Small intestine segments were processed using routine methods for histology and electron microscopy; areas and cells were screened with an Axiovision Ver. 4.0 system. Data were analyzed by ANOVA and comparison of averages. Parasitized dogs showed higher GC numbers than nonparasitized ones. Averages were: 20+/-0.81 GC/25 microm(2) with independent mucin granules and 11+/-1.53 GC/25 microm(2) that were expelling mucus, compared to 11+/-0.94 GC/25 microm(2) and 1+/-0.27 GC/25 microm(2), respectively, in nonparasitized dogs (Tukey, p<0.001). The increases in GC number seem to be an unspecific defensive mechanism against Giardia trophozoites. However, we found some evidence supporting that GC hyperplasia could be a prejudicial to epithelial barrier that gives rise to gates allowing for Giardia-tissue invasion.

Morphologic Alterations of the Palpebral Conjunctival Epithelium in a Dry Eye Model

“…lung and airway epithelium 23, 24 and intestines 25, 26 . A few studies are available providing ultrastructural information on conjunctival goblet cells in different species e.g.…”

Goblet cells of the conjunctiva: A review of recent findings

“…Recent data from other mucosal epithelia in which goblet cells differentiate as well as from studies of conjunctival epithelium suggest that goblet cell differentiation can be manipulated extrinsically. Probably the best examples come from the tracheal bronchial epithelium in which goblet cell hyperplasia occurs in response to chronic pulmonary diseases including asthma, cystic fibrosis and chronic obstructive pulmonary disease (Park et al, 2007) and from the gut in response to parasitic infection(Ponce-Macotela et al, 2008). During chronic injury or exposure to allergens, epithelial cells lining the lung undergo metaplasia/hyperplasia associated with goblet cell hyperplasia and mucus hypersecretion, which are mediated by various cytokines and growth factors including IL-4, IL-13, and inducers of EGF signaling (for review see Park et al, 2007).…”

Expression of interferon gamma and proinflammatory cytokines in the cecal mucosa of rats experimentally infected with Blastocystis sp. strain RN94-9

“…The mucus layer is an important barrier between protozoans and host epithelial cells (Ponce-Macotela et al 2008;Tse and Chadee 1992); thus, to determine if any goblet cell alteration has occurred after Blastocystis infection, goblet cell numbers were counted in PASstained tissue sections of the cecum. As shown in Table 2, a slight but significant increase in the number of goblet cells was observed 2 weeks after infection.…”