β-Glucans are naturally occurring polysaccharides that are produced by bacteria, yeast, fungi, and many plants. Although their pharmacological activities, such as immunomodulatory, anti-infective and anti-cancer effects, have been well studied, it is still unclear how β-glucans exert their activities. However, recent studies on the β-glucan receptors shed some light on their mechanism of action. Since β-glucans have large molecular weights, they must bind surface receptors to activate immune cells. In this review, we summarize the immunopharmacological activities and the potential receptors of β-glucans in immune cells.

Population studies have suggested that lycopene, which is mostly found in tomato and tomato products, may reduce the risk of prostate cancer. We previously found that tomato sauce consumption prior to prostatectomy for prostate cancer decreased serum prostate specific antigen, decreased oxidative DNA damage, and increased lycopene concentrations in prostate tissue (Chen et al., 2001). Here, we extended those investigations to determine whether apoptotic cell death and associated Bcl-2 and Bax proteins were modulated by tomato sauce intervention. Thirty-two patients diagnosed by biopsy with prostate carcinoma were given tomato sauce pasta entrees (30 mg lycopene/day) for 3 wk before prostatectomy. Thirty-four patients with prostate cancer who did not consume tomato sauce and underwent prostatectomy served as controls. When tumor areas with the most apoptotic cells were compared in the biopsy (before) and resected prostate tissue (after), tomato sauce consumption increased apoptotic cells in benign prostate hyperplasia (BPH) from 0.66 +/- 0.10% to 1.38 +/- 0.31% (P = 0.013) and in carcinomas from 0.84 +/- 0.13% to 2.76 +/- 0.58% (P = 0.0003). When comparable morphological areas were counted, apoptotic cell death in carcinomas increased significantly with treatment, from 0.84 +/- 0.13% to 1.17 +/- 0.19% (P = 0.028), and apoptotic cell death in BPH showed a tendency toward an increase from 0.66 +/- 0.10% to 1.20 +/- 0.32% (P = 0.20). When the values of apoptotic cells in BPH and carcinomas of patients who consume tomato sauce were compared with corresponding control lesions of the patients who did not consume tomato sauce in resected prostate tissue, the differences of values were not significant [BPH 1.38 +/- 0.31% vs. 1.14 +/- 0.32% (P = 0.97); carcinomas 2.76 +/- 0.58% vs. 1.91 +/- 0.32% (P = 0.24)]. Tomato sauce consumption did not affect Bcl-2 expression but decreased Bax expression in carcinomas. These data provide the first in vivo evidence that tomato sauce consumption may suppress the progression of the disease in a subset of patients with prostate cancer by increasing apoptotic cell death. However, because of the relatively small number of control and tomato sauce-supplemented patients and the variability in the values of apoptotic cells in BPH and carcinomas, a much larger number of patients needs to be examined to support the data generated in this study.

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Summary What is known and objective Linezolid‐induced thrombocytopenia is one of the many confounding conditions in critically ill patients. It is rare but prognostic importance of linezolid‐induced thrombocytopenia in ICU population has not been well investigated. The study is to assess the incidence and risk factors of linezolid‐induced thrombocytopenia in ICU patients. Methods We conducted a retrospective study with ICU patients treated with linezolid between January 2005 and December 2015 at the adult medical, surgical, emergency, and neurological ICUs at 1500‐bed tertiary university medical center. Results and discussion There were 60 patients (mean age: 69.8 ± 11.9), 29 (48.3%) who developed linezolid‐induced thrombocytopenia determined by the Naranjo algorithm on a case‐by‐case basis during the study period. The patients with linezolid‐induced thrombocytopenia had a higher rate of any malignancy (41.4% vs 9.7%, P = 0.007), elevated baseline creatinine levels (median [interquartile range; IQR]: 1.7 mg/dL [0.9‐2.5] vs 0.9 mg/dL [0.6‐1.3]; P = 0.042), and lower baseline platelet counts (median [IQR] 160 × 109/L [128‐230] vs 194 × 109/L [118‐285]; P = 0.296) than patients without linezolid‐induced thrombocytopenia. The patients who developed thrombocytopenia received more platelet transfusions (34.5% vs 6.5%, P = 0.009) and had higher ICU mortality rates (62.1% vs 32.3%, P = 0.037). Logistic regression analysis revealed the following significant risk factors for linezolid‐induced thrombocytopenia: presence of any malignancy (odds ratio; OR [95% confidence interval; CI]: 8.667 [1.986‐37.831]) and an elevated baseline serum creatinine level (OR: 1.673, CI: 1.046‐2.675]). What is new and conclusion Critically ill patients with any malignancy or an elevated baseline creatinine level who were treated with linezolid in the ICU were more likely to develop thrombocytopenia. More importantly, mortality increased with patients who developed linezolid‐induced thrombocytopenia compared to those did not.

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Systemic lupus erythematosus (SLE) is a multi-organ autoimmune disease characterized by autoantibody production. Mesenchymal stem cells (MSCs) ameliorate SLE symptoms by targeting T cells, whereas the mechanisms of their efficacy remain incompletely understood. In this study, we show that transfer of human MSCs increased MRL.Faslpr mouse survival, decreased T cell infiltration in the kidneys, and reduced T cell cytokine expression. In vitro, allogeneic mouse MSCs inhibited MRL.Faslpr T cell proliferation and cytokine production. Time-lapse imaging revealed that MSCs recruited MRL.Faslpr T cells establishing long-lasting cellular contacts by enhancing T cell VCAM-1 expression in a CCL2-dependent manner. In contrast, CCL2 deficient MSCs did not induce T cell migration and VCAM-1 expression, resulting in insufficient cell-cell contact. Consequently, CCL2 deficient MSCs did not inhibit IFN-γ production by T cells and upon transfer no longer prolonged survival of MRL.Faslpr mice. Taken together, our imaging study demonstrates that CCL2 enables the prolonged MSC–T cell interactions needed for sufficient suppression of autoreactive T cells and helps to understand how MSCs ameliorate symptoms in lupus-prone MRL.Faslpr mice.

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