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  • 1.
    Andersson, Lena
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Occupational and Environmental Medicine.
    Bryngelsson, Ing-Liss
    Department of Occupational and Environmental Medicine, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Hedbrant, Alexander
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Persson, Alexander
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Johansson, Anders
    Department of Occupational and Environmental Medicine, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Ericsson, Annette
    Department of Occupational and Environmental Medicine, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Lindell, Ina
    Department of Occupational and Environmental Medicine, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Stockfelt, Leo
    Unit of Occupational and Environmental Medicine, Sahlgrenska Academy, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
    Särndahl, Eva
    Örebro universitet, Institutionen för medicinska vetenskaper. Inflammatory Response and Infection Susceptibility Centre (iRiSC).
    Westberg, Håkan
    Örebro universitet, Institutionen för naturvetenskap och teknik. Department of Occupational and Environmental Medicine.
    Respiratory health and inflammatory markers: Exposure to respirable dust and quartz and chemical binders in Swedish iron foundries2019Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 14, nr 11, artikel-id e0224668Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    PURPOSE: To study the relationship between respirable dust, quartz and chemical binders in Swedish iron foundries and respiratory symptoms, lung function (as forced expiratory volume FEV1 and vital capacity FVC), fraction of exhaled nitric oxide (FENO) and levels of club cell secretory protein 16 (CC16) and CRP.

    METHODS: Personal sampling of respirable dust and quartz was performed for 85 subjects in three Swedish iron foundries. Full shift sampling and examination were performed on the second or third day of a working week after a work free weekend, with additional sampling on the fourth or fifth day. Logistic, linear and mixed model analyses were performed including, gender, age, smoking, infections, sampling day, body mass index (BMI) and chemical binders as covariates.

    RESULTS: The adjusted average respirable quartz and dust concentrations were 0.038 and 0.66 mg/m3, respectively. Statistically significant increases in levels of CC16 were associated with exposure to chemical binders (p = 0.05; p = 0.01) in the regression analysis of quartz and respirable dust, respectively. Non-significant exposure-responses were identified for cumulative quartz and the symptoms asthma and breathlessness. For cumulative chemical years, non-significant exposure-response were observed for all but two symptoms. FENO also exhibited a non significant exposure-response for both quartz and respirable dust. No exposure-response was determined for FEV1 or FVC, CRP and respirable dust and quartz.

    CONCLUSIONS: Our findings suggest that early markers of pulmonary effect, such as increased levels of CC16 and FENO, are more strongly associated with chemical binder exposure than respirable quartz and dust in foundry environments.

  • 2.
    Hedbrant, Alexander
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Andersson, Lena
    Region Örebro län. Örebro universitet, Institutionen för medicinska vetenskaper. Department of Occupational and Environmental Medicine.
    Bryngelsson, Ing-Liss
    Department of Occupational and Environmental Medicine, Örebro University Hospital, Örebro, Sweden.
    Eklund, Daniel
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Westberg, Håkan
    Department of Medical Sciences, School of Medicine and Health, Örebro University, Örebro, Sweden; Inflammatory Response and Infection Susceptibility Centre (iRiSC), Örebro University, Örebro, Sweden; Department of Occupational and Environmental Medicine, Örebro University Hospital, Örebro, Sweden.
    Särndahl, Eva
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Persson, Alexander
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Quartz Dust Exposure Affects NLRP3 Inflammasome Activation and Plasma Levels of IL-18 and IL-1Ra in Iron Foundry Workers2020Ingår i: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, artikel-id 8490908Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Purpose: To study the association between inhalation of particulate matter or quartz in Swedish iron foundries and the effects on NLRP3 inflammasome activation. 

    Methods: Particle exposure measurements were performed during an eight-hour work day for 85 foundry workers at three Swedish iron foundries. Personal sampling was used for measurement of respirable quartz and dust and stationary measurements to obtain exposure measurements for inhalable dust and PM10. The NLRP3 inflammasome markers, interleukin- (IL-) 1β and IL-18, and inhibitors IL-1 receptor antagonist (IL-1Ra) and IL-18 binding protein (IL-18BP) were measured in plasma. Inflammasome activation was measured by caspase-1 enzymatic activity in monocytes in whole blood by flow cytometry, and expression of inflammasome-related genes was quantified using real-time PCR. Multiple linear regression analysis was used to investigate associations between PM exposures and inflammatory markers. Sex, age, smoking, current infection, BMI, and single nucleotide polymorphism in the inflammasome regulating genes CARD8 (C10X) and NLRP3 (Q705K) were included as covariates. 

    Results: The average exposure levels of respirable dust and quartz were 0.85 and 0.052 mg/m3, respectively. A significant exposure-response was found for respirable dust and IL-18 and for inhalable dust and IL-1Ra. Whole blood, drawn from study participants, was stimulated ex vivo with inflammasome priming stimuli LPS or Pam3CSK4, resulting in a 47% and 49% increase in caspase-1 enzymatic activity in monocytes. This increase in caspase-1 activity was significantly attenuated in the higher exposure groups for most PM exposure measures. 

    Conclusions: The results indicate that exposure levels of PM in the iron foundry environment can affect the NLRP3 inflammasome and systemic inflammation.

  • 3.
    Hedbrant, Alexander
    et al.
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Erlandsson, Ann
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för läkarutbildning.
    Wijkander, Jonny
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Conditioned media from human macrophages of M1 phenotype attenuate the cytotoxic effect of 5-fluorouracil on the HT-29 colon cancer cell line2015Ingår i: International Journal of Oncology, ISSN 1019-6439, Vol. 46, nr 1, s. 37-46Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Resistance of tumor cells to chemotherapy, such as 5-fluorouracil (5-FU), is an obstacle for successful treatment of cancer. As a follow-up of a previous study we have investigated the effect of conditioned media (CM) from macrophages of M1 or M2 phenotypes on 5-FU cytotoxicity on the colon cancer cell lines HT-29 and CACO-2. HT-29 cells, but not CACO-2 cells, having been treated with a combination of M1 CM and 5-FU recovered their cell growth to a much larger extent compared to cells having been treated with 5-FU alone when further cultured for 7 days in fresh media. M1 CM treatment of HT-29, but not CACO-2 cells, induced cell cycle arrest in the G(0)/G(1) and G(2)/M phases. 5-FU treatment induced accumulation of cells in S-phase in both HT-29 and CACO-2 cells. This accumulation of cells in S-phase was attenuated by combined M1 CM and 5-FU treatment in HT-29 cells, but not in CACO-2 cells. The mRNA expression of cell cycle regulatory proteins and 5-FU metabolic enzymes were analyzed in an attempt to find possible mechanisms for the M1 CM induced attenuation of 5-FU cytotoxicity in HT-29. Thymidylate synthetase (TS) and thymidine phosphorylase (TP) were found to be substantially downregulated and upregulated, respectively, in HT-29 cells treated with M1 CM, making them unlikely as mediators of reduced 5-FU cytotoxicity. Among cell cycle regulating proteins, p21 was induced in HT-29 cells, but not in CACO-2 cells, in response to M1 CM treatment. However, small interfering RNA (siRNA) knockdown of p21 had no effect on the M1 CM induced cell cycle arrest seen in HT-29 and neither did it change the growth recovery after combined treatment of HT-29 cells with M1 CM and 5-FU. In conclusion, treatment of HT-29 cells with M1 CM reduces the cytotoxic effect of 5-FU and this is mediated by a M1 CM induced cell cycle arrest in the G(0)/G(1) and G(2)/M phases. So far, we lack an explanation why this action is absent in the CACO-2 cells. The current findings may be important for optimization of chemotherapy in colon cancer.

  • 4.
    Hedbrant, Alexander
    et al.
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Wijkander, Jonny
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Seidal, Tomas
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för läkarutbildning.
    Erlandsson, Ann
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Macrophages of M1 phenotype have properties that influence lung cancer cell progression2015Ingår i: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 36, nr 11, s. 8715-8725Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Stromal macrophages of different phenotypes can contribute to the expression of proteins that affects metastasis such as urokinase-type plasminogen activator (uPA), its receptor uPAR, and plasminogen activator inhibitor-1 (PAI-1), but knowledge of how essential their contribution is in comparison to the cancer cells in small cell lung cancer (SCLC) and lung squamous cell carcinoma (SCC) is lacking. The expression of uPA, uPAR, and PAI-1 and of the matrix metalloproteinases (MMP)-2 and MMP-9 were studied in human macrophages of M1 and M2 phenotype and compared to a lung SCC (NCI-H520) and a SCLC (NCI-H69) cell line. Effects of treatment with conditioned media (CM) from M1 and M2 macrophages on the expression of these genes in H520 and H69 cells as well as effects on the cell growth were investigated. In addition, data on the stromal macrophages immunoreactivity of uPAR, MMP-2, and MMP-9 in a few SCC and SCLC biopsies was included. uPAR, MMP-2, and MMP-9 were confirmed in stromal cells including macrophages in the SCC and SCLC biopsies. In vitro, both macrophage phenotypes expressed considerably higher mRNA levels of uPA, uPAR, PAI-1, and MMP-9 compared to the cancer cell lines, and regarding uPAR, the highest level was found in the M1 macrophage phenotype. Furthermore, M1 CM treatment not only induced an upregulation of PAI-1 in both H520 and H69 cells but also inhibited cell growth in both cell lines, giving M1 macrophages both tumor-promoting and tumor-killing potential.

  • 5.
    Lindsten, Therése
    et al.
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden.
    Hedbrant, Alexander
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Ramberg, Anna
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden; School of Medical Sciences, Örebro University, Örebro, Sweden.
    Wijkander, Jonny
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Solterbeck, Anja
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden.
    Eriksson, Margareta
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden; Faculty of Medicine and Health, Örebro University, Örebro, Sweden; Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Erlandsson, Ann
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Environmental and Life Sciences/Biology, Karlstad University, Karlstad, Sweden; Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Effect of macrophages on breast cancer cell proliferation, and on expression of hormone receptors, uPAR and HER-22017Ingår i: International Journal of Oncology, ISSN 1019-6439, Vol. 51, nr 1, s. 104-114Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Malignant tumors, including breast cancers, are frequently infiltrated with innate immune cells and tumor-associated macrophages (TAMs) represent the major inflammatory component in stroma of many tumors. In this study, we examined the immunoreactivity of the macrophage markers CD68 and CD163 as well as the hormone receptors estrogen receptor alpha (ER alpha), progesterone receptor (PR), estrogen receptor beta 1 (ER beta 1), human epidermal growth factor receptor 2 (HER-2), matrix metalloproteinase 9 (MMP-9), urokinase-type plasminogen activator receptor (uPAR) and the proliferations marker Ki67 in 17 breast cancer biopsies. The quantitative score for CD68(+) and CD163(+) strongly indicate M2 phenotype dominance in the currently investigated biopsies. We found that an increasing level of macrophages was negatively associated with ER alpha or PR, whereas a positive association was observed for Ki-67 or uPAR. No significant association could be seen between the level of macrophage and HER-2, ER beta 1 or MMP-9 expression. Effect of conditioned media (CM) generated from cultured human M1 and M2 macrophage phenotypes were investigated on the proliferation and expression of selected markers in the T47D breast cancer cell line. We found that in contrast to the in vivo situation, in particularly the CM from M1 macrophages decreased the growth and Ki67 expression in T47D, and significantly increased ER beta 1 mRNA levels. Moreover, in accordance to the in vivo situation the CM from the macrophages decreased the expression of ER alpha protein as well as ER alpha or PR mRNA. In conclusion our results show that macrophages alone have the capability to decrease the tumor cell expression of ER alpha and PR in vitro. In the tumor environment in vivo macrophages also contribute to an increase in tumor cell expression of uPAR and Ki67, suggesting that macrophages are involved in impairing the prognosis for breast cancer patients.

  • 6.
    Westberg, Håkan
    et al.
    Örebro universitet, Institutionen för naturvetenskap och teknik. Department of Occupational and Environmental Medicine Örebro University Hospital, Örebro, Sweden.
    Hedbrant, Alexander
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Persson, Alexander
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Bryngelsson, Ing-Liss
    Department of Occupational and Environmental Medicine, Faculty of Medicine and Health, Örebro University, Sweden.
    Johansson, Anders
    Department of Occupational and Environmental Medicine, Faculty of Medicine and Health, Örebro University, Sweden.
    Ericsson, Annette
    Örebro universitet, Institutionen för hälsovetenskaper. Department of Occupational and Environmental Medicine.
    Sjögren, Bengt
    Work Environment Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Stockfelt, Leo
    Department of Occupational and Environmental Medicine, University of Gothenburg, Sweden.
    Särndahl, Eva
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Andersson, Lena
    Region Örebro län. Örebro universitet, Institutionen för medicinska vetenskaper. Department of Occupational and Environmental Medicine.
    Inflammatory and coagulatory markers and exposure to different size fractions of particle mass, number and surface area air concentrations in Swedish iron foundries, in particular respirable quartz2019Ingår i: International Archives of Occupational and Environmental Health, ISSN 0340-0131, E-ISSN 1432-1246, Vol. 92, nr 8, s. 1087-1098Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    PURPOSE: To study the relationship between inhalation of airborne particles and quartz in Swedish iron foundries and markers of inflammation and coagulation in blood.

    METHODS: Personal sampling of respirable dust and quartz was performed for 85 subjects in three Swedish iron foundries. Stationary measurements were used to study the concentrations of respirable dust and quartz, inhalable and total dust, PM10 and PM2.5, as well as the particle surface area and the particle number concentrations. Markers of inflammation, namely interleukins (IL-1β, IL-6, IL-8, IL-10 and IL-12), C-reactive protein, and serum amyloid A (SAA) were measured in plasma or serum, together with markers of coagulation including fibrinogen, factor VIII (FVIII), von Willebrand factor and D-dimer. Complete sampling was performed on the second or third day of a working week after a work-free weekend, and follow-up samples were collected 2 days later. A mixed model analysis was performed including sex, age, smoking, infections, blood group, sampling day and BMI as covariates.

    RESULTS: The average 8-h time-weighted average air concentrations of respirable dust and quartz were 0.85 mg/m3 and 0.052 mg/m3, respectively. Participants in high-exposure groups with respect to some of the measured particle types exhibited significantly elevated levels of SAA, fibrinogen and FVIII.

    CONCLUSIONS: These observed relationships between particle exposure and inflammatory markers may indicate an increased risk of cardiovascular disease among foundry workers with high particulate exposure.

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