Abstract
Campylobacter jejuni is the leading cause of bacterial food-borne gastroenteritis worldwide and human infections are frequently associated with handling and consumption of contaminated poultry. The polysaccharide capsule of C. jejuni plays important roles in colonisation of the chicken gut, invasion of epithelial cells and serum resistance and is subject to modification with O-methyl phosphoramidate (MeOPN) in most strains. In this study, the cytokine responses of mouse bone marrow-derived macrophages (mBMMs), chicken bone marrow-derived macrophages (chBMMs) and human monocyte-derived macrophages (hMDMs) were measured following infection with C. jejuni 11168H wild-type (WT) or isogenic mutants lacking either the capsule (Δcj1439) or its MeOPN modification (Δcj1417). Consistent with previous observations using murine bone marrow-derived dendritic cells, mutants lacking the capsule or MeOPN elicited enhanced transcription of IL-6 and IL-10 in mBMMs compared to wild-type C. jejuni. However, the lack of capsule and MeOPN did not alter IL-6 and IL-10 expression in chBMMs and hMDMs compared to C. jejuni WT. Phagocytosis assays showed the acapsular mutant was not impaired in uptake or net intracellular survival after phagocytosis in both chicken and human macrophages; however, the phagocytosis of the MeOPN mutant was significantly decreased in both chicken and human macrophages. In conclusion, differences in the response of macrophages of varying host origin to Campylobacter were detected. The absence of MeOPN modification on the capsule of C. jejuni did not alter the levels of innate cytokine expression in both chicken and human macrophages compared to the 11168H WT, but affected phagocytosis by host macrophages.
Highlights
Campylobacter jejuni is the leading cause of bacterial food-borne gastroenteritis worldwide [1]
Important roles for the capsule and its O-methyl phosphoramidate (MeOPN) modification have been demonstrated in cell adherence, invasion, colonisation, serum resistance and host immune responses [26, 30, 31, 33]
We compared the cytokine responses of macrophages of different host origin known to differ in their symptoms upon infection with C. jejuni
Summary
Campylobacter jejuni is the leading cause of bacterial food-borne gastroenteritis worldwide [1]. The human immune response to C. jejuni, including the role of pattern recognition receptors and bacterial agonists of innate and adaptive immunity, remains poorly understood. As in other enteric infections, innate immune cells are likely to be involved in the initial response to C. jejuni infection [7, 8]. Upon C. jejuni infection, human monocytic cell line THP-1 and. Live C. jejuni induces a higher cytokine response in DCs than killed bacteria [11]. The pathogen recognition receptors, toll-like receptors (TLR) 2 and 4 have been shown to be involved in signalling and cytokine expression upon infection with C. jejuni in vitro using knock-out or knock-down technology [12, 13]. A luciferase-based TLR reporter assay, indicated that live C. jejuni did not directly activate human TLR2, TLR4, and TLR5 [14]. Human monocytes/ macrophages efficiently kill C. jejuni [15]
Sign-in/Register to view highlights & summary 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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
