Premium
Giardia lamblia attenuation of proinflammatory signaling in intestinal epithelial cells is partially dependent on parasitic modulations to the NF‐κB pathway
Author(s) -
Cotton James A,
Sayer Heather L,
Buret Andre G
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.117.4
Subject(s) - proinflammatory cytokine , giardia lamblia , biology , stimulation , microbiology and biotechnology , chemistry , endocrinology , immunology , inflammation
Giardia lamblia is a non‐invasive, protozoan parasite that causes diarrheal disease in humans. Intestinal epithelial cells (IECs) do not release proinflammatory mediators, such as interleukin (IL)‐8, following exposure to G. lamblia trophozoites. The nuclear factor κB (NF‐κB) pathway regulates the expression of proinflammatory factors, such as IL‐8, and its inhibition reduces the expression of these mediators. Aims To determine if human adenocarcinoma (Caco‐2) monolayers, incubated with G. lamblia trophozoites, reduce secreted levels of IL‐8, following stimulation with proinflammatory IL‐1β, and if this reduction occurs through modulations to the NF‐κB pathway. Results Caco‐2 monolayers secreted significantly lower levels of IL‐8 when incubated with G. lamblia for 24 hours prior to stimulation with IL‐1β; this result did not require physical contact between trophozoites and monolayers. G. lamblia reduced total levels of the NF‐κB p65 subunit in a strain dependent manner. All strains induced cleavage of p65 into a fragment approximately 37 kDa in size that translocated to the nucleus following IL‐1β stimulation. NF‐κB p65 cleavage requires physical contact between trophozoites and monolayers. Conclusion Attenuation of proinflammatory signaling in IECs incubated with G. lamblia is at least partially dependent on parasitic modulations to the NF‐κB pathway. Funding was provided by NSERC.