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1.  CD161 Expression Defines a Th1/Th17 Polyfunctional Subset of Resident Memory T Lymphocytes in Bronchoalveolar Cells 
PLoS ONE  2015;10(4):e0123591.
Alveolar resident memory T cells (TRM) comprise a currently uncharacterized mixture of cell subpopulations. The CD3+CD161+ T cell subpopulation resides in the liver, intestine and skin, but it has the capacity for tissue migration; however, the presence of resident CD3+CD161+ T cells in the bronchoalveolar space under normal conditions has not been reported. Bronchoalveolar cells (BACs) from healthy volunteers were evaluated and found that 8.6% (range 2.5%-21%) of these cells were CD3+ T lymphocytes. Within the CD3+ population, 4.6% of the cells (2.1–11.3) expressed CD161 on the cell surface, and 74.2% of the CD161+CD3+ T cells expressed CD45RO. The number of CD3+CD161+ T cells was significantly lower in the bronchoalveolar space than in the blood (4.6% of BACs vs 8.4% of peripheral blood mononuclear cells (PBMCs); P<0.05). We also found that 2.17% of CD4+ T lymphocytes and 1.52% of CD8+ T lymphocytes expressed CD161. Twenty-two percent of the alveolar CD3+CD161+ T lymphocytes produced cytokines upon stimulation by PMA plus ionomycin, and significantly more interferon gamma (IFN-γ) was produced compared with other cytokines (P = 0.05). Most alveolar CD3+CD161+ T cells produced interleukin-17 (IL-17) and IFN-γ simultaneously, and the percentage of these cells was significantly higher than the percentage of CD3+CD161− T cells. Moreover, the percentage of alveolar CD3+CD161+ T lymphocytes that produced IFN-γ/IL-17 was significantly higher than those in the peripheral blood (p<0.05). In conclusion, Th1/Th17-CD3+CD161+ TRM could contribute to compartment-specific immune responses in the lung.
doi:10.1371/journal.pone.0123591
PMCID: PMC4408072  PMID: 25906076
2.  Humoral and cellular responses to a non-adjuvanted monovalent H1N1 pandemic influenza vaccine in hospital employees 
BMC Infectious Diseases  2013;13:544.
Background
The efficacy of the H1N1 influenza vaccine relies on the induction of both humoral and cellular responses. This study evaluated the humoral and cellular responses to a monovalent non-adjuvanted pandemic influenza A/H1N1 vaccine in occupationally exposed subjects who were previously vaccinated with a seasonal vaccine.
Methods
Sixty healthy workers from a respiratory disease hospital were recruited. Sera and peripheral blood mononuclear cells (PBMCs) were obtained prior to and 1 month after vaccination with a non-adjuvanted monovalent 2009 H1N1 vaccine (Influenza A (H1N1) 2009 Monovalent Vaccine Panenza, Sanofi Pasteur). Antibody titers against the pandemic A/H1N1 influenza virus were measured via hemagglutination inhibition (HI) and microneutralization assays. Antibodies against the seasonal HA1 were assessed by ELISA. The frequency of IFN-γ-producing cells as well as CD4+ and CD8+ T cell proliferation specific to the pandemic virus A/H1N peptides, seasonal H1N1 peptides and seasonal H3N2 peptides were assessed using ELISPOT and flow cytometry.
Results
At baseline, 6.7% of the subjects had seroprotective antibody titers. The seroconversion rate was 48.3%, and the seroprotection rate was 66.7%. The geometric mean titers (GMTs) were significantly increased (from 6.8 to 64.9, p < 0.05). Forty-nine percent of the subjects had basal levels of specific IFN-γ-producing T cells to the pandemic A/H1N1 peptides that were unchanged post-vaccination. CD4+ T cell proliferation in response to specific pandemic A/H1N1 virus peptides was also unchanged; in contrast, the antigen-specific proliferation of CD8+ T cells significantly increased post-vaccination.
Conclusion
Our results indicate that a cellular immune response that is cross-reactive to pandemic influenza antigens may be present in populations exposed to the circulating seasonal influenza virus prior to pandemic or seasonal vaccination. Additionally, we found that the pandemic vaccine induced a significant increase in CD8+ T cell proliferation.
doi:10.1186/1471-2334-13-544
PMCID: PMC3835617  PMID: 24238117
Pandemic influenza; H1N1; Vaccine; Cellular response; Proliferation; Humoral response
3.  Nordihydroguaiaretic Acid Attenuates the Oxidative Stress-Induced Decrease of CD33 Expression in Human Monocytes 
Nordihydroguaiaretic acid (NDGA) is a natural lignan with recognized antioxidant and beneficial properties that is isolated from Larrea tridentata. In this study, we evaluated the effect of NDGA on the downregulation of oxidant stress-induced CD33 in human monocytes (MNs). Oxidative stress was induced by iodoacetate (IAA) or hydrogen peroxide (H2O2) and was evaluated using reactive oxygen species (ROS) production, and cell viability. NDGA attenuates toxicity, ROS production and the oxidative stress-induced decrease of CD33 expression secondary to IAA or H2O2 in human MNs. It was also shown that NDGA (20 μM) attenuates cell death in the THP-1 cell line that is caused by treatment with either IAA or H2O2. These results suggest that NDGA has a protective effect on CD33 expression, which is associated with its antioxidant activity in human MNs.
doi:10.1155/2013/375893
PMCID: PMC3596923  PMID: 23533689
4.  High glucose concentrations induce TNF-α production through the down-regulation of CD33 in primary human monocytes 
BMC Immunology  2012;13:19.
Background
CD33 is a membrane receptor containing a lectin domain and a cytoplasmic immunoreceptor tyrosine-based inhibitory motif (ITIM) that is able to inhibit cytokine production. CD33 is expressed by monocytes, and reduced expression of CD33 correlates with augmented production of inflammatory cytokines, such as IL-1β, TNF-α, and IL-8. However, the role of CD33 in the inflammation associated with hyperglycemia and diabetes is unknown. Therefore, we studied CD33 expression and inflammatory cytokine secretion in freshly isolated monocytes from patients with type 2 diabetes. To evaluate the effects of hyperglycemia, monocytes from healthy donors were cultured with different glucose concentrations (15-50 mmol/l D-glucose), and CD33 expression and inflammatory cytokine production were assessed. The expression of suppressor of cytokine signaling protein-3 (SOCS-3) and the generation of reactive oxygen species (ROS) were also evaluated to address the cellular mechanisms involved in the down-regulation of CD33.
Results
CD33 expression was significantly decreased in monocytes from patients with type 2 diabetes, and higher levels of TNF-α, IL-8 and IL-12p70 were detected in the plasma of patients compared to healthy donors. Under high glucose conditions, CD33 protein and mRNA expression was significantly decreased, whereas spontaneous TNF-α secretion and SOCS-3 mRNA expression were increased in monocytes from healthy donors. Furthermore, the down-regulation of CD33 and increase in TNF-α production were prevented when monocytes were treated with the antioxidant α-tocopherol and cultured under high glucose conditions.
Conclusion
Our results suggest that hyperglycemia down-regulates CD33 expression and triggers the spontaneous secretion of TNF-α by peripheral monocytes. This phenomenon involves the generation of ROS and the up-regulation of SOCS-3. These observations support the importance of blood glucose control for maintaining innate immune function and suggest the participation of CD33 in the inflammatory profile associated with type 2 diabetes.
doi:10.1186/1471-2172-13-19
PMCID: PMC3353220  PMID: 22500980
Antioxidant; Cytokines; Monocytes; ROS; Siaglec-3; Type 2 diabetes
5.  A polytrauma patient with an unusual posterior fracture-dislocation of the femoral head: a case report 
We report a case of a 27-year-old man who was involved in a high-speed car accident. He sustained multiple organ damage including multiple brain petechiae suggesting diffuse axonal damage, aortic dissection, retroperitoneal haematoma and a fracture-dislocation of the right hip with a femoral head fracture and an ipsilateral intertrochanteric fracture. Due to the general condition of the patient, physiological stabilisation was prioritized, and at 2 weeks the fracture-dislocation of the hip was treated with a proximal femoral nail for the intertrochanteric fracture and Herbert screws for the femoral head fracture. Postoperatively, two episodes of recurrent hip dislocation occurred, and this was stabilized eventually with a Steinman pin inserted across the hip joint and taken out 1 month later. Weight-bearing was allowed according to clinical and radiographical assessments. Heterotopic ossification developed around the hip joint, but without evidence of AVN or osteoarthritis. At 18-months follow-up, the fractures had healed and the patient had a Harris Hip score of 79.1. Anatomical reduction and stable fixation of fracture-dislocations of the hip are important for achieving an acceptable result.
doi:10.1007/s11751-009-0078-8
PMCID: PMC2839317  PMID: 20360877
Hip dislocation; Femoral head fracture; Heterotopic ossification; Prognosis
6.  A polytrauma patient with an unusual posterior fracture-dislocation of the femoral head: a case report 
We report a case of a 27-year-old man who was involved in a high-speed car accident. He sustained multiple organ damage including multiple brain petechiae suggesting diffuse axonal damage, aortic dissection, retroperitoneal haematoma and a fracture-dislocation of the right hip with a femoral head fracture and an ipsilateral intertrochanteric fracture. Due to the general condition of the patient, physiological stabilisation was prioritized, and at 2 weeks the fracture-dislocation of the hip was treated with a proximal femoral nail for the intertrochanteric fracture and Herbert screws for the femoral head fracture. Postoperatively, two episodes of recurrent hip dislocation occurred, and this was stabilized eventually with a Steinman pin inserted across the hip joint and taken out 1 month later. Weight-bearing was allowed according to clinical and radiographical assessments. Heterotopic ossification developed around the hip joint, but without evidence of AVN or osteoarthritis. At 18-months follow-up, the fractures had healed and the patient had a Harris Hip score of 79.1. Anatomical reduction and stable fixation of fracture-dislocations of the hip are important for achieving an acceptable result.
doi:10.1007/s11751-009-0078-8
PMCID: PMC2839317  PMID: 20360877
Hip dislocation; Femoral head fracture; Heterotopic ossification; Prognosis
7.  Chloroquine-Resistant Plasmodium falciparum: Effect of Substrate on Chloroquine and Amodiaquin Accumulation 
Glucose stimulates the high-affinity processes of chloroquine and amodiaquin accumulation in owl monkey erythrocytes infected with a chloroquine-susceptible strain of Plasmodium falciparum. Although these erythrocytes have greater ability to accumulate amodiaquin than chloroquine, glucose has relatively less effect on amodiaquin accumulation than on chloroquine accumulation. In contrast to these findings with chloroquine-susceptible P. falciparum, glucose stimulates amodiaquin but not chloroquine accumulation in erythrocytes infected with chloroquine-resistant P. falciparum. This lack of function of a substrate-dependent component of chloroquine accumulation distinguishes chloroquine-resistant from chloroquine-susceptible P. falciparum.
PMCID: PMC444732  PMID: 4217585
8.  High-Affinity Accumulation of Chloroquine by Mouse Erythrocytes Infected with Plasmodium berghei 
Washed erythrocytes infected with chloroquine-susceptible (CS) or with chloroquine-resistant (CR) P. berghei were used in model systems in vitro to study the accumulation of chloroquine with high affinity. The CS model could achieve distribution ratios (chloroquine in cells: chloroquine in medium) of 100 in the absence of substrate. 200—300 in the presence of 10 mM pyruvate or lactate, and over 600 in the presence of 1 mM glucose or glycerol. In comparable studies of the CR model, the distribution ratios were 100 in the absence of substrate and 300 or less in the presence of glucose or glycerol. The presence of lactate stimulated chloroquine accumulation in the CR model, whereas the presence of pyruvate did not. Lactate production from glucose and glycerol was undiminished in the CR model, and ATP concentrations were higher than in the CS model. Cold, iodoacetate, 2,4-dinitrophenol, or decreasing pH inhibited chloroquine accumulation in both models. These findings demonstrate substrate involvement in the accumulation of chloroquine with high affinity.
In studies of the CS model, certain compounds competitively inhibited chloroquine accumulation, while others did not. This finding is attributable to a specific receptor that imposes structural constraints on the process of accumulation. For chloroquine analogues, the position and length of the side chain, the terminal nitrogen atom of the side chain, and the nitrogen atom in the quinoline ring are important determinants of binding to this receptor.
PMCID: PMC301521  PMID: 4600044

Results 1-8 (8)