Abstract
Human giardiasis, caused by the protozoan parasite Giardia duodenalis (syn. Giardia lamblia, Giardia intestinalis, Lamblia intestinalis), is one of the most commonly-identified parasitic diseases worldwide. Chronic G. duodenalis infections cause a malabsorption syndrome that may lead to failure to thrive and/or stunted growth, especially in children in developing countries. Understanding the parasite/epithelial cell crosstalk at the mucosal surfaces of the small intestine during human giardiasis may provide novel insights into the mechanisms underlying the parasite-induced immunopathology and epithelial tissue damage, leading to malnutrition. Efforts to identify new targets for intervening in the development of intestinal immunopathology and the progression to malnutrition are critical. Translating these findings into a clinical setting will require analysis of these pathways in cells and tissues from humans and clinical trials could be devised to determine whether interfering with unwanted mucosal immune responses developed during human giardiasis provide better therapeutic benefits and clinical outcomes for G. duodenalis infections in humans.
Highlights
Human giardiasis, caused by the protozoan parasite Giardia duodenalis
Consistent with the observations that G. duodenalis strains differ in their ability to induce pathological changes at the upper intestinal epithelial surface [50, 66, 68, 76], calves infected with assemblage E neither showed increased rates of apoptotic cells nor did they exhibit any signs of villus shortening as compared with uninfected controls [77]
As a major mucosal surface interfacing between the “self” and the “non-self”, the intestinal epithelium participates in host defense against a wide range of lumen-dwelling intestinal pathogens by secreting multiple immune mediators with direct anti-microbial properties
Summary
Human giardiasis, caused by the protozoan parasite Giardia duodenalis (syn. Giardia lamblia, Giardia intestinalis, Lamblia intestinalis), is one of the most prevalent enteric parasitic protozoan infections globally, with prevalence rates ranging from 2-5% in the developed world and 20-30% in the developing countries [1,2,3]. The dysfunctional intestinal epithelial barrier during Giardia infection is characterized by altered expression of TJ proteins (i.e., ZO-1, claudins, occludin), increased intestinal permeability, and reduced transepithelial electrical resistance (TEER) in both murine models of giardiasis as well as in humans [51, 53].
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call