| 11. |
|
|
| 12. |
|
|
| 13. |
|
|
| 14. |
- Eliasson, Mette, et al.
(author)
-
Characterization of Released Polypeptides During an Interferon-γ-Dependent Antibacterial Response in Airway Epithelial Cells.
- 2012
-
In: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1557-7465 .- 1079-9907. ; 32:11, s. 524-533
-
Journal article (peer-reviewed)abstract
- When pathogenic bacteria breach the epithelial lining at mucosal surfaces, rapidly available innate immune mechanisms are critical to halt the infection. In the present study, we characterized the production of antibacterial polypeptides released by epithelial cells. IFN-γ, but neither TNF nor IL-1β alone, induced release of antibacterial activity to a cell culture medium, causing a lytic appearance of killed bacteria as revealed by electron microscopy. Addition of the protein streptococcal inhibitor of complement, derived from Streptococcus pyogenes, known for its ability to neutralize antimicrobial polypeptides (AMPs), reduced the antibacterial activity of the medium. Characterization of the antibacterial incubation medium using mass spectrometric approaches and ELISAs, displayed presence of several classical AMPs, antibacterial chemokines, as well as complement factors and proteases that may interfere with bacterial killing. Many were constitutively produced, that is, being released by cells incubated in a medium alone. While a combination of IFN-γ and TNF did not increase bacterial killing, the presence of TNF boosted the amounts and detectable number of AMPs, including antibacterial chemokines. However, the methods applied in the study failed to single out certain AMPs as critical mediators, but rather demonstrate the broad range of molecules involved. Since many AMPs are higly amphiphatic in nature (i.e., cationic and hydrophobic), it is possible that difficulties in optimizing recovery present limitations in the context investigated. The findings demonstrate that epithelial cells have a constitutive production of AMPs and that IFN-γ is an important inducer of an antibacterial response in which is likely to be a critical part of the innate host defense against pathogenic bacteria at mucosal surfaces.
|
|
| 15. |
- Fellström, Bengt, 1947-, et al.
(author)
-
Associations Between Apolipoprotein A1, High-Density Lipoprotein Cholesterol, and Urinary Cytokine Levels in Elderly Males and Females
- 2019
-
In: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1079-9907 .- 1557-7465. ; 40:2, s. 71-74
-
Journal article (peer-reviewed)abstract
- There exists a close relationship between cardiovascular diseases and chronic kidney disease. Apolipoprotein A1 and high-density lipoprotein (HDL) cholesterol are widely used as cardiovascular risk markers but they also have anti-inflammatory properties. The aim of this study was to investigate any associations between HDL levels and cytokine levels in urine. We randomly selected 90 urine samples from the Prospective Investigation of the Vasculature in Uppsala Seniors Study (41 males and 49 females). The samples were analyzed with 2 multiplex assays, Multiplex Inflammation I and Cardiovascular II kits (Olink Bioscience, Uppsala, Sweden). We analyzed the correlations between 158 cytokines in urine with apolipoprotein A1, HDL cholesterol, apolipoprotein B, and low-density lipoprotein cholesterol. There were strong correlations for apolipoprotein A1 and HDL cholesterol with individual cytokines. After adjustment for multiplicity testing, there were 33 significant correlations between apolipoprotein A1 and cytokine levels and 14 of these were also significantly correlated with HDL cholesterol. The strongest associations were observed for IL-1α, SPON2, RAGE, PAR-1, TRAIL-R2, IL-4RA, TNFRSF11A, and SCF. A total of 28 out of 33 correlations were negative, indicating a negative relationship between apolipoprotein A1 and urinary cytokines. The study shows a negative correlation between apolipoprotein A1 and HDL cholesterol and urinary cytokine levels. The finding is in agreement with the anti-inflammatory properties of HDL.
|
|
| 16. |
- Fellström, Bengt, 1947-, et al.
(author)
-
Strong Associations Between Early Tubular Damage and Urinary Cytokine, Chemokine, and Growth Factor Levels in Elderly Males and Females
- 2021
-
In: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1079-9907 .- 1557-7465. ; 41:8, s. 283-290
-
Journal article (peer-reviewed)abstract
- Acute tubular necrosis is associated with high mortality rates and it is important to develop new biomarkers for tubular damage. The aim of this study was to investigate the effect of early tubular damage on a large number of urinary cytokines, chemokines, and growth factors. We selected 90 urine samples from the Prospective Investigation of the Vasculature in Uppsala Seniors Study (41 males and 49 females). The tubular damage markers cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1) were analyzed in the urine samples and urinary cytokine levels were analyzed with 2 multiplex assays (proximity extension assay). After adjustment for sex, body mass index, estimated glomerular filtration rate, smoking, and multiplicity testing using the false discovery rate approach, there remained 26 cytokines that correlated significantly with urine cystatin C, 27 cytokines that correlated with NGAL, and 66 cytokines that correlated with KIM-1. Tubular damage shows a strong association with urinary cytokines, chemokines, and growth factors. Our findings indicate that multiplex proteomics could be a promising new approach to explore the complex effects of tubular damage.
|
|
| 17. |
|
|
| 18. |
|
|
| 19. |
- Hedman Hjorth, Maria, 1978-, et al.
(author)
-
Nicotinamide reduces high secretion of IFN-γ in high-risk relatives even though it does not prevent type 1 diabetes
- 2006
-
In: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1079-9907 .- 1557-7465. ; 26:4, s. 207-213
-
Journal article (peer-reviewed)abstract
- Type 1 diabetes (T1D) is an autoimmune disease suggested to be of a T helper (Th)1-like origin. This study aimed to investigate the Th1-like and Th2-like profile in high-risk individuals during the prediabetic phase and the immunologic effect of treatment with nicotinamide. High-risk first-degree relatives of T1D patients participating in the European Nicotinamide Diabetes Intervention Trial (ENDIT) were treated with either nicotinamide or placebo. Peripheral blood mononuclear cells (PBMC) were obtained during the prediabetic phase and close to the onset of manifest T1D and from nondiabetic high-risk individuals. Using the sensitive enzyme-linked immunospot (ELISPOT) technique to distinguish Th1-like from Th2-like lymphocytes, secretion of interferon-γ (IFN-γ) and interleukin-4 (IL-4) was analyzed from PBMCs spontaneously and after in vitro stimulation with the diabetes-associated autoantigens, glutamic acid decarboxylase 65 (GAD65, protein and peptide, aa 247-279), recombinant tyrosine phosphatase (IA-2), and heat shock protein (HSP, aa 437-460). High-risk individuals showed high spontaneous as well as autoantigen-induced IFN-γ secretion. Secretion of IFN-γ and the IFN-γ/IL-4 ratio, induced by autoantigens, decreased in individuals developing T1D (p < 0.05), whereas nondiabetic individuals showed an increased IL-4 response (p < 0.05). Thus, a Th1-dominated cytokine profile observed in high-risk individuals inclined toward a diagnosis of diabetes. Nicotinamide caused decreased spontaneous (p = 0.05) and in vitro autoantigen-induced IFN-γ secretion (p < 0.05) and may play a role in immune regulation, even though it has not been shown to prevent T1D. © Mary Ann Liebert, Inc.
|
|
| 20. |
|
|
