Modulation of Host immunity
https://www.researchgate.net/publication/280639883_Modulation_of_host_immunity_by_tick_saliva
https://www.researchgate.net/publication/280639883_Modulation_of_host_immunity_by_tick_saliva
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Items: 1 to 20 of 37
1.
Adams PP, Flores Avile C, Popitsch N, Bilusic I, Schroeder R, Lybecker M, Jewett MW.
Nucleic Acids Res. 2017 Jan 25;45(2):775-792. doi: 10.1093/nar/gkw1180. Epub 2016 Dec 1.
- PMID:
- 27913725
2.
Smith AA, Navasa N, Yang X, Wilder CN, Buyuktanir O, Marques A, Anguita J, Pal U.
Cell Host Microbe. 2016 Jul 13;20(1):91-8. doi: 10.1016/j.chom.2016.06.001. Epub 2016 Jun 30.
- PMID:
- 27374407
3.
Bouquet J, Soloski MJ, Swei A, Cheadle C, Federman S, Billaud JN, Rebman AW, Kabre B, Halpert R, Boorgula M, Aucott JN, Chiu CY.
MBio. 2016 Feb 12;7(1):e00100-16. doi: 10.1128/mBio.00100-16.
Abstract
Lyme disease is a tick-borne illness caused by the bacterium Borrelia burgdorferi, and approximately 10 to 20% of patients report persistent symptoms lasting months to years despite appropriate treatment with antibiotics. To gain insights into the molecular basis of acute Lyme disease and the ensuing development of post-treatment symptoms, we conducted a longitudinal transcriptome study of 29 Lyme disease patients (and 13 matched controls) enrolled at the time of diagnosis and followed for up to 6 months. The differential gene expression signature of Lyme disease following the acute phase of infection persisted for at least 3 weeks and had fewer than 44% differentially expressed genes (DEGs) in common with other infectious or noninfectious syndromes. Early Lyme disease prior to antibiotic therapy was characterized by marked upregulation of Toll-like receptor signaling but lack of activation of the inflammatory T-cell apoptotic and B-cell developmental pathways seen in other acute infectious syndromes. Six months after completion of therapy, Lyme disease patients were found to have 31 to 60% of their pathways in common with three different immune-mediated chronic diseases. No differential gene expression signature was observed between Lyme disease patients with resolved illness to those with persistent symptoms at 6 months post-treatment. The identification of a sustained differential gene expression signature in Lyme disease suggests that a panel of selected human host-based biomarkers may address the need for sensitive clinical diagnostics during the "window period" of infection prior to the appearance of a detectable antibody response and may also inform the development of new therapeutic targets.IMPORTANCE:
Lyme disease is the most common tick-borne infection in the United States, and some patients report lingering symptoms lasting months to years despite antibiotic treatment. To better understand the role of the human host response in acute Lyme disease and the development of post-treatment symptoms, we conducted the first longitudinal gene expression (transcriptome) study of patients enrolled at the time of diagnosis and followed up for up to 6 months after treatment. Importantly, we found that the gene expression signature of early Lyme disease is distinct from that of other acute infectious diseases and persists for at least 3 weeks following infection. This study also uncovered multiple previously undescribed pathways and genes that may be useful in the future as human host biomarkers for diagnosis and that constitute potential targets for the development of new therapies.Free PMC Article
4.
Fazzino L, Tilly K, Dulebohn DP, Rosa PA.
Infect Immun. 2015 Dec;83(12):4800-10. doi: 10.1128/IAI.00925-15. Epub 2015 Oct 5.
- PMID:
- 26438790
5.
Drecktrah D, Lybecker M, Popitsch N, Rescheneder P, Hall LS, Samuels DS.
PLoS Pathog. 2015 Sep 15;11(9):e1005160. doi: 10.1371/journal.ppat.1005160. eCollection 2015 Sep. Erratum in: PLoS Pathog. 2015 Oct;11(10):e1005242.
- PMID:
- 26371761
6.
Martin CL, Sukarna TY, Akther S, Ramrattan G, Pagan P, Di L, Mongodin EF, Fraser CM, Schutzer SE, Luft BJ, Casjens SR, Qiu WG.
MBio. 2015 Apr 14;6(2). pii: e00011-15. doi: 10.1128/mBio.00011-15. Erratum in: MBio. 2015;6(4):e00999. Martin, Che I [Corrected to Martin, Che L].
- PMID:
- 25873371
7.
Iyer R, Caimano MJ, Luthra A, Axline D Jr, Corona A, Iacobas DA, Radolf JD, Schwartz I.
Mol Microbiol. 2015 Feb;95(3):509-38. doi: 10.1111/mmi.12882. Epub 2014 Dec 30.
- PMID:
- 25425211
8.
Lieskovská J, Páleníková J, Širmarová J, Elsterová J, Kotsyfakis M, Campos Chagas A, Calvo E, Růžek D, Kopecký J.
Parasite Immunol. 2015 Feb;37(2):70-8. doi: 10.1111/pim.12162.
- PMID:
- 25408129
9.
Narasimhan S, Rajeevan N, Liu L, Zhao YO, Heisig J, Pan J, Eppler-Epstein R, Deponte K, Fish D, Fikrig E.
Cell Host Microbe. 2014 Jan 15;15(1):58-71. doi: 10.1016/j.chom.2013.12.001.
- PMID:
- 24439898
10.
Wang P, Dadhwal P, Cheng Z, Zianni MR, Rikihisa Y, Liang FT, Li X.
Mol Microbiol. 2013 Sep;89(6):1140-53. doi: 10.1111/mmi.12337. Epub 2013 Aug 14.
- PMID:
- 23869590
11.
Schramm F, Kern A, Barthel C, Nadaud S, Meyer N, Jaulhac B, Boulanger N.
PLoS One. 2012;7(6):e40046. doi: 10.1371/journal.pone.0040046. Epub 2012 Jun 29.
- PMID:
- 22768217
12.
Lieskovska J, Kopecky J.
Parasite Immunol. 2012 Aug-Sep;34(8-9):421-9. doi: 10.1111/j.1365-3024.2012.01375.x.
- PMID:
- 22709526
13.
Lieskovská J, Kopecký J.
Parasite Immunol. 2012 Jan;34(1):32-9. doi: 10.1111/j.1365-3024.2011.01345.x.
Abstract
Dendritic cells
are a sentinel in defending against pathogens and tick saliva
facilitates transmission of tick-borne pathogens by modulating the host immune response. The maturation of dendritic cells
is inhibited by tick saliva. To elucidate the mechanism of this
inhibition, we tested the impact of Ixodes ricinus tick saliva on
signalling pathways activated by Toll-like receptor (TLR-2) ligand and Borrelia afzelii in spleen dendritic cells.
The activation of nuclear factor-κB (NF-κB) p65 and
phosphatidylinositol-3 kinase (PI3K)/Akt pathways was decreased by tick
saliva upon both TLR-2 and Borrelia
stimulation. Among the mitogen-activated protein kinases (MAPK), the
activation of extracellular matrix-regulated kinase (Erk1/2) was
suppressed by tick saliva, but not p38. In response to spirochaetes, the
amount of TNF-α decreased in the presence of tick saliva which was
mediated by selective suppression of Erk1/2, NF-κB and Akt as tick
saliva mimicked the effect of their specific inhibitors, UO126, IKK-IV
and LY294002, respectively. Saliva-induced enhancement of IL-10 was not
observed in the presence of specific inhibitor of Protein Kinase A
(PKA), H-89, suggesting the involvement of PKA pathway in IL-10
production. Our cumulative data show that tick saliva interferes with
several signalling pathways, thus modulating the immune functions of
dendritic cells.
© 2012 Blackwell Publishing Ltd.
- PMID:
- 22709526
- DOI:
- 10.1111/j.1365-3024.2012.01375.x
- [Indexed for MEDLINE]
14.
Sahay B, Singh A, Gnanamani A, Patsey RL, Blalock JE, Sellati TJ.
Am J Pathol. 2011 Feb;178(2):724-34. doi: 10.1016/j.ajpath.2010.10.025.
- PMID:
- 21281805
15.
Zhang X, Yang X, Kumar M, Pal U.
J Infect Dis. 2009 Oct 15;200(8):1318-30. doi: 10.1086/605846.
- PMID:
- 19754308
16.
Wang G, Petzke MM, Iyer R, Wu H, Schwartz I.
J Immunol. 2008 Jun 15;180(12):8306-15.
- PMID:
- 18523297
17.
Srivastava SY, de Silva AM.
J Bacteriol. 2008 May;190(10):3429-33. doi: 10.1128/JB.00085-08. Epub 2008 Mar 21.
- PMID:
- 18359818
18.
Cruz AR, Moore MW, La Vake CJ, Eggers CH, Salazar JC, Radolf JD.
Infect Immun. 2008 Jan;76(1):56-70. Epub 2007 Oct 15.
- PMID:
- 17938216
19.
Olson CM, Hedrick MN, Izadi H, Bates TC, Olivera ER, Anguita J.
Infect Immun. 2007 Jan;75(1):270-7. Epub 2006 Oct 30.
- PMID:
- 17074860
20.
Behera AK, Hildebrand E, Szafranski J, Hung HH, Grodzinsky AJ, Lafyatis R, Koch AE, Kalish R, Perides G, Steere AC, Hu LT.
Arthritis Rheum. 2006 Oct;54(10):3319-29.
- PMID:
- 17009305
