ORCID Profile
0000-0001-6303-6076
Current Organisation
Karolinska Institutet
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Publisher: Cold Spring Harbor Laboratory
Date: 19-04-2021
DOI: 10.1101/2021.04.18.440186
Abstract: Intestinal helminth parasites can alter immune responses to vaccines, other infections, allergens and autoantigens, indicating effects on host immune responses in distal barrier tissues. We herein show that C57BL/6 mice infected with the strictly intestinal nematode Heligmosomoides polygyrus have impaired capacity to initiate skin immune responses and develop skin-resident memory cells to mycobacterial antigens, both during infection and months after deworming therapy. Surprisingly, and in contrast to a previously noted loss of T cells in peripheral lymph nodes, the skin of worm-infected mice harboured higher numbers of CD4+ T cells compared to skin of uninfected controls. H. polygyrus- specific T H 2 cells accumulated during infection and remained after worm expulsion. Accumulation of T H 2 cells in the skin was associated with increased expression of the skin-homing chemokine receptors CCR4 and CCR10 on CD4+ T cells in blood and mesenteric lymph nodes draining intestinal tissues, indicating gut-to-skin trafficking of cells. In conclusion, we show that infection by a strictly intestinal helminth has long-term effects on immune cell composition and local immune responses to unrelated antigens in the skin, revealing a novel mechanism for T cell colonization and worm-mediated immunosuppression in this organ.
Publisher: American Association for the Advancement of Science (AAAS)
Date: 09-06-2017
Abstract: Infection, especially by helminths or bacteria, can cause tissue damage (see the Perspective by Bouchery and Harris). Minutti et al. studied mouse models of helminth infection and fibrosis. They expressed surfactant protein A (a member of the complement component C1q family) in the lung, which enhanced interleukin-4 (IL-4)-mediated proliferation and activation of alveolar macrophages. This activation accelerated helminth clearance and reduced lung injury. In the peritoneum, C1q boosted macrophage activation for liver repair after bacterial infection. By a different approach, Bosurgi et al. discovered that after wounding caused by migrating helminths in the lung or during inflammation in the gut of mice, IL-4 and IL-13 act only in the presence of apoptotic cells to promote tissue repair by local macrophages. Science , this issue p. 1076 , p. 1072 see also p. 1014
Publisher: Elsevier BV
Date: 03-2011
DOI: 10.1016/J.IJPARA.2010.09.011
Abstract: Giardia intestinalis is one of the major causes of parasite-induced diarrhea. The disease, giardiasis, is caused by trophozoites attaching to the intestinal epithelium, resulting in apoptosis of intestinal epithelial cells, disrupted epithelial barrier function and malabsorption. Microarray studies have detected extensive gene expression changes in intestinal epithelial cells (IECs) during interaction with Giardia trophozoites in vitro. In the present study, we examined this host-parasite interaction further by transcriptional profiling of interacting trophozoites using Giardia microarrays. A total of 200 Giardia transcripts were significantly changed due to the interaction, lasting up to 18 h in complete growth medium. Quantitative reverse transcriptase PCR confirmed the changes in all 12 genes tested using mRNA isolated in separate experiments. Genes encoding proteins previously suggested to be important during host-parasite interactions such as arginine deiminase, enolase and cysteine proteinases were up-regulated early but down-regulated later during the interaction. Cell ision and attachment genes were down-regulated in the late time-points of interaction. The most highly up-regulated genes encode oxygen defense proteins and several members of the high cysteine membrane protein (HCMp) and Gly-rich repeat (GRREAT) families. Putative small RNAs were up-regulated, whereas the 5S rRNA was slightly down-regulated during the interaction with IECs. Thus, there are extensive gene expression changes in Giardia trophozoites and IECs during host-parasite interactions which can be important for establishment of infection and the induction of giardiasis.
No related grants have been discovered for Emma Ringqvist.