Sharni Hardcastle

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history
Jump to: navigation, search
Source: ResearchGate

Sharni Lee Hardcastle, BBioMedSc (Hons1) PhD, is a researcher and Immunology Lecturer at National Centre for Neuroimmunology and Emerging Diseases, Griffith University, School of Medical Science, Brisbane, Queensland, Australia.[1]

Awards[edit]

Notable studies[edit]

  • 2017, Impaired calcium mobilization in natural killer cells from chronic fatigue syndrome/myalgic encephalomyelitis patients is associated with transient receptor potential melastatin 3 ion channels FREE ACCESS/FULL TEXT[5]
  • 2015, Serum Immune Proteins in Moderate and Severe Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients[6]
  • 2015, Characterisation of cell functions and receptors in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME)
    "Conclusions: This study was the first to show significant differences in a number of receptors in NK, CD4+T and CD8+T cells in CFS/ME suggesting dysregulation in NK cell cytotoxic activity, receptor regulation and potentially cell adherence. Consistent with previous literature, our research suggests that CFS/ME patients have immunological dysregulation in the innate and adaptive immune cells. We have also highlighted significant differences in NK, CD4+T and CD8+T cells between moderate and severe CFS/ME patients, suggesting severity subgroups may have distinct immune perturbations and consequently aetiology. Further studies examining severity subgroups of CFS/ME patients may therefore contribute to the understanding of the pathomechanism associated with the illness."[7]
  • 2015, Longitudinal analysis of immune abnormalities in varying severities of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients
    "Conclusions: Severe CFS/ME patients differed from controls and moderate CFS/ME patients over time and expressed significant alterations in iNKT cell phenotypes, CD8+T cell markers, NK cell receptors and γδT cells at 6 months. This highlights the importance of further assessing these potential immune biomarkers longitudinally in both moderate and severe CFS/ME patients."[8]
  • 2014, The Role of Adaptive and Innate Immune Cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis FULL TEXT
    Abstract: "Perturbations in immune processes are a hallmark of a number of autoimmune and inflammatory disorders. Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is an inflammatory disorder with possible autoimmune correlates, characterized by reduced NK cell activity, elevations in regulatory T cells (Tregs) and dysregulation in cytokine levels. The purpose of this article is to examine innate and adaptive immune cell phenotypes and functional characteristics that have not been previously examined in CFS/ME patients. Thirty patients with CFS/ME and 25 non-fatigued controls were recruited for this study. Whole blood samples were collected from all participants for the assessment of cell phenotypes, functional properties, receptors, adhesion molecules, antigens and intracellular proteins using flow cytometric protocols. The cells investigated included NK cells, dendritic cells, neutrophils, B cells, T cells, γδT cells and Tregs. Significant changes were observed in B-cell subsets, Tregs, CD4+CD73+CD39+ T cells, cytotoxic activity, granzyme B, neutrophil antigens, TNF-α and IFN-γ in the CFS/ME patients in comparison with the non-fatigued controls. Alterations in B cells, Tregs, NK cells and neutrophils suggest significant impairments in immune regulation in CFS/ME and these may have similarities to a number of autoimmune disorders.[9]
  • 2014, Characterization of Natural Killer Cell Phenotypes in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis FULL TEXT
    Abstract - "Objective: Natural Killer (NK) cells are classified into different phenotypes according to the expression of the surface markers CD56 and CD16. Each NK cell phenotype has a role in the immune response through cytotoxic activity or cytokine production. Reduced NK cell cytotoxic activity is a consistent finding in patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) and investigations into the potential causes of reduced NK cell cytotoxic activity have predominantly focused on total NK cells. The purpose of this study was to investigate and characterize four NK cell phenotypes in CFS/ME. Methods: Twenty nine CFS/ME patients (mean age ± SEM=48.28 ± 2.63) meeting the 1994 Fukuda definition and 27 healthy controls (mean age ± SEM=49.15 ± 2.51) were included in this study. Flow cytometric protocols identified CD56bright CD16-/dim, CD56dimCD16-, CD56dimCD16+ or CD56-CD16+ NK cells for the measurement of surface markers including adhesion molecules CD2, CD18, CD11a, CD11b and CD11c, natural cytotoxicity receptors, Killer Immunoglobulin Like Receptors, signalling lymphocytic activation molecules and cell maturation (CD57). Following stimulation, NK cell phenotype expression of CD107a and CD107b was measured as a marker for degranulation. Intracellular staining measured lytic proteins including perforin, Granzyme A and Granzyme B in the four NK cell phenotypes. Results: In the CFS/ME group, CD56brightCD16-/dim NK cell co-expression of adhesion molecules CD2 and CD18 was significantly reduced. Granzyme B was significantly decreased in CD56dimCD16+ and CD56-CD16+ NK cells from CFS/ME patients. CD57 expression on CD56dimCD16+ NK cells from CFS/ME patients was significantly increased. Conclusion: This is the first study to characterize four NK cell phenotypes in CFS/ME by investigating surface and intracellular molecules necessary for NK cell effector function. The data suggests that a combination of impairments in CD56dimCD16+ NK cells from CFS/ME patients may contribute to reduced cytotoxic activity of this phenotype."[10]
  • 2014, Analysis of the Relationship between Immune Dysfunction and Symptom Severity in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) FULL TEXT
    Abstract - "Objective: Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is a disabling illness, characterised by persistent, debilitating fatigue and a multitude of symptoms. Immunological alterations are prominent in CFS/ME cases, however little is known about the relationship between CFS/ME severity and the extent of immunological dysfunction. The purpose of this study was to assess innate and adaptive immune cell phenotypes and function of two groups of CFS/ME patients, bedridden (severe) and mobile (moderate). Methods: CFS/ME participants were defined using the Centres for Disease Prevention and Control (1994 CDC) Criteria for CFS/ME. Participants were grouped into healthy controls (n=22, age=40.14 ± 2.38), moderate/ mobile (n=23; age=42.52 ± 2.63) and severe/bedridden (n=18; age=39.56 ± 1.51) CFS/ME patients. Flow cytometric protocols were used to examine neutrophil, monocyte, dendritic cells (DCs), iNKT, Treg, B, γδ and CD8+ T cell phenotypes, NK cytotoxic activity and receptors. Results: The present data found that CFS/ME patients demonstrated significant decreases in NK cytotoxic activity, transitional and regulatory B cells, γδ1T cells, KIR2DL1/DS1, CD94+ and KIR2DL2/L3. Significant increases in CD56-CD16+NKs, CD56dimCD16- and CD56brightCD16-/dim NKs, DCs, iNKT phenotypes, memory and naive B cells were also shown in CFS/ME participants. Severe CFS/ME patients demonstrated increased CD14-CD16+ DCs, memory and naïve B cells, total iNKT, iNKT cell and NK phenotypes compared to moderate CFS/ME patients. Conclusion: This study is the first to determine alterations in NK, iNKT, B, DC and γδ T cell phenotypes in both moderate and severe CFS/ME patients. Immunological alterations are present in innate and adaptive immune cells and sometimes, immune deregulation appears worse in CFS/ME patients with more severe symptoms. It may be appropriate for CFS/ME patient severity subgroups to be distinguished in both clinical and research settings to extricate further immunological pathologies that may not have been previously reported.[11]
  • 2012, Longitudinal investigation of natural killer cells and cytokines in chronic fatigue syndrome/myalgic encephalomyelitis[12]

Talks & interviews[edit]

Online presence[edit]

Learn more[edit]

See also[edit]

References[edit]

  1. https://www.griffith.edu.au/health/national-centre-neuroimmunology-emerging-diseases/our-team
  2. http://iacfsme.org/Organization/Former-IACFS-ME-Awardees.aspx
  3. http://goldcoastwomeninbusinessawards.com.au/past-winners/
  4. https://www.researchgate.net/profile/Sharni_Hardcastle/info
  5. Nguyen, T.; Hardcastle, S.; Clarke, L.; Smith, P.; Staines, D.; Marshall-Gradisnik, S. (2017), "Impaired calcium mobilization in natural killer cells from chronic fatigue syndrome/myalgic encephalomyelitis patients is associated with transient receptor potential melastatin 3 ion channels", Clinical and Experimental Immunology, 187 (2): 284–293, doi:10.1111/cei.12882 
  6. Hardcastle, SL; Brenu, EW; Johnston, S; Nguyen, T; Huth, T; Wong, N; Ramos, S; Staines, DR; Marshall-Gradisnik, SM (2015), "Serum Immune Proteins in Moderate and Severe Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients", International Journal of Medical Sciences, 12 (10): 764-772, doi:10.7150/ijms.12399 
  7. Hardcastle, SL; Brenu, EW; Johnston, S; Nguyen, T; Huth, T; Wong, N; Ramos, S; Staines, DR; Marshall-Gradisnik, SM (2015), "Characterisation of cell functions and receptors in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME)", BMC Immunology, 16 (35), doi:10.1186/s12865-015-0101-4 
  8. Hardcastle, Sharni Lee; Brenu, Ekua Weba; Johnston, Samantha; Nguyen, Thao; Huth, Teilah; Ramos, Sandra; Staines, Donald; Marshall-Gradisnik, Sonya (2015), "Longitudinal analysis of immune abnormalities in varying severities of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients", Journal of Translational Medicine, 13 (299), doi:10.1186/s12967-015-0653-3 
  9. Brenu, EW; Huth, TK; Hardcastle, SL; Fuller, K; Kaur, M; Johnston, S; Ramos, Sandra; Staines, Donald; Marshall-Gradisnik, Sonya (2014), "The Role of adaptive and innate immune cells in chronic fatigue syndrome/myalgic encephalomyelitis", International Immunology, 26 (4): 233-42, PMID 24343819, doi:10.1093/intimm/dxt068 
  10. Huth, Teilah K.; Brenu, Ekua; Nguyen, Thao; Hardcastle, Sharni L.; Johnston, Samantha; Ramos, Sandra; Staines, Donald R.; Marshall-Gradisnik, Sonya M. (2014), "Characterization of Natural Killer Cell Phenotypes in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis", Journal of Clinical & Cellular Immunology, 5 (3), doi:10.4172/2155-9899.1000223 
  11. Hardcastle, Sharni Lee; Brenu, Ekua Weba; Johnston, Samantha; Nguyen, Thao; Huth, Teilah; Kaur, Manprit; Ramos, Sandra; Salajegheh, Ali; Staines, Donald R; Marshall-Gradisnik, Sonya (2014), "Analysis of the Relationship between Immune Dysfunction and Symptom Severity in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME)", Journal of Clinical & Cellular Immunology, 5 (190), doi:10.4172/2155-9899.1000190 
  12. Brenu, Ekua W; van Driel, Mieke L; Staines, Donald R; Ashton, Kevin J; Hardcastle, Sharni L; Keane, James; Tajouri, Lotti; Peterson, Daniel; Ramos, Sandra B; Marshall-Gradisnik, Sonya M (2012), "Longitudinal investigation of natural killer cells and cytokines in chronic fatigue syndrome/myalgic encephalomyelitis", Journal of Translational Medicine, 10: 88, doi:10.1186/1479-5876-10-88 
  13. http://internationalstudentresearch.com/previous-forums/
  14. https://www.griffith.edu.au/health/national-centre-neuroimmunology-emerging-diseases/news-and-events
  15. https://www.griffith.edu.au/__data/assets/pdf_file/0009/566118/CFS-Symposium-2013-Program.pdf


The information provided at this site is not intended to diagnose or treat any illness.

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history