Interactions ofGiardia sp.with the intestinal barrier: Epithelium, mucus, and microbiota

Abstract

Understanding how intestinal enteropathogens cause acute and chronic alterations has direct animal and human health perspectives. Significant advances have been made on this field by studies focusing on the dynamic crosstalk between the intestinal protozoan parasite model Giardia duodenalis and the host intestinal mucosa. The concept of intestinal barrier function is of the highest importance in the context of many gastrointestinal diseases such as infectious enteritis, inflammatory bowel disease, and post-infectious gastrointestinal disorders. This crucial function relies on 3 biotic and abiotic components, first the commensal microbiota organized as a biofilm, then an overlaying mucus layer, and finally the tightly structured intestinal epithelium. Herein we review multiple strategies used by Giardia parasite to circumvent these 3 components. We will summarize what is known and discuss preliminary observations suggesting how such enteropathogen directly and/ or indirectly impairs commensal microbiota biofilm architecture, disrupts mucus layer and damages host epithelium physiology and survival.

Pityriasis alba: Possible associations with intestinal helminths and pathogenic protozoa

“…It is possible that the shift towards a Th2 response and IgE elevation in PA patients could be stipulated by cross-reactivity of parasites and other exogenic allergens, for example, ascariasis increases human IgE responses to house dust mite-specific allergens. 33 More intense IgE responses in PA patients with parasites could be connected to an impairment of commensal microbiota biofilm architecture, disruption of mucus layer and damage to the intestinal barrier induced by G. lamblia 34 and helminths, influencing the epithelial permeability of the intestinal barrier through intrinsic (epithelial permeability) and extrinsic (mucin, bacterial peptides, commensal bacteria) elements. 35 The epithelial integrity of the intestinal Vitamin D deficiency/insufficiency has been detected in many cutaneous diseases, including autoimmune disorders, such as vitiligo, 37 psoriasis, 38 atopic dermatitis and other skin diseases.…”

“…We analysed the level of total serum IgE in PA patients and control individuals, taking into consideration the similarity of HP histology in PA patients and features of atopic dermatitis23 and elevation of IgE production in infections caused by helminths 12. More intense IgE responses in PA patients with parasites could be connected to an impairment of commensal microbiota biofilm architecture, disruption of mucus layer and damage to the intestinal barrier induced by G. lamblia34 and helminths, influencing the epithelial permeability of the intestinal barrier through intrinsic (epithelial permeability) and extrinsic (mucin, bacterial peptides, commensal bacteria) elements 35. In total, IgE concentrations ≤50-100 and 101-≥601 IU/ mL were found in 33.3% and 66.7% of PA patients and in 95% and 5% of the control individuals, respectively.…”

The compact genome of Giardia muris reveals important steps in the evolution of intestinal protozoan parasites

“…Giardiasis is also a problem in domestic animals, and the zoonotic potential of Giardia has been highlighted in recent years [5]. In vitro models of the interaction of G. intestinalis with human cells have helped to unravel clues to how Giardia causes disease [6–8], such as the importance of, the adhesive disc for attachment [9], flagella for motility [10, 11], secreted cysteine proteases for interference with host defenses [12–16], interactions with the intestinal microbiota [6, 17], differentiation into cysts for transmission [4, 18] and interference with nitric oxide (NO) production [19, 20]. Despite this progress it remains uncertain whether these in vitro models are representative of the natural infection, particularly because animal models of G. intestinalis infection have significant limitations.…”

Recent advances in the Giardia–host relationship reveal danger lurking behind the smile

“…Host responses play a pivotal role in pathogenesis in giardiasis as well, as hypermotility and sucrase deficiency are both reduced in immunodeficient animals, and studies of the intersection between parasite virulence factors and host immune response would also be of interest. Finally, the small intestine is home to a robust microbiota, and several studies suggest that interactions among Giardia , the host, and these additional microbes all contribute to the eventual outcome of Giardia infection [ 19 , 20 ].…”