Macrophages, whether M1 or M2 subtype, have been found to be implicated in the pathogenesis of osteoarthritis (OA). However, no study regarding the status of M1 and M2 macrophages has been reported in knee OA. To investigate the status of M1 and M2 macrophages in knee OA, synovial fluid as well as peripheral blood were collected from 80 patients with knee OA and 80 healthy controls. Reverse transcription-quantitative PCR was used to quantitatively detect the expression of CD11c as a marker for M1 macrophages and CD206 as a marker for M2 macrophages from synovial fluids. As confirmation, flow cytometry was employed to count the number of monocytes from whole blood using the CD86 (M1) and CD163 (M2) markers on monocytes. The ratio of M1 to M2 macrophages was shown to be markedly higher in knee OA than that of control and that the ratio was significantly positively correlated with level of Kellgren-Lawrence grade in knee OA, that is, the higher the ratio the more severe the knee OA seems to be. Thus, our study presented direct evidence for the involvement of macrophages in the pathogenesis of knee OA.

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BackgroundCystic fibrosis (CF) is a disease characterized by chronic airway infection with a high incidence and poor prognosis. Pseudomonas aeruginosa and Aspergillus fumigatus are pathogens commonly found in CF patients. Clinically, these two microorganisms often coexist in the airway of CF patients. Combined infection with P. aeruginosa and A. fumigatus results in worsening lung function and clinical condition.MethodsIn this review, we focus on the mutual inhibition and promotion mechanisms of P. aeruginosa and A. fumigatus in CF patients. We also summarized the mechanisms of the interaction between these pathogenic microorganisms.ResultsP. aeruginosa inhibits A. fumigatus growth through the effects of phenazines, the quorum sensing system, iron competition, bacteriophages, and small colony variants. P. aeruginosa induces A. fumigatus growth through volatile organic compounds and subbacteriostatic concentrations of phenazines. A. fumigatus interferes with P. aeruginosa, affecting its metabolic growth via phenazine metabolic transformation, gliotoxin production, and reduced antibiotic sensitivity.DiscussionCoexistence of P. aeruginosa and A. fumigatus can lead to both mutual inhibition and promotion. In different stages of CF disease, the interaction between these two pathogenic microorganisms may shift between promotion and inhibition. A discussion of the mechanisms of P. aeruginosa and A. fumigatus interaction can be beneficial for further treatment of CF patients and for improving the prognosis of the disease.

ObjectiveThis study aimed to evaluate the factors associated with death in patients with coronavirus disease 2019 by clarifying the clinical characteristics and immune responses.MethodsThe clinical characteristics and laboratory findings, including cytokine and lymphocyte subsets, were obtained from the electronic medical records of patients in Wuhan Tongji Hospital.ResultsThis study included 836 patients with confirmed COVID-19. In total, 699 (83.6%) were cured and discharged, and 137 (16.4%) died. Our analysis revealed that age ≥ 65 years, male sex, malignancy, chronic obstructive pulmonary disease, dyspnea, dizziness, respiratory rate > 20 bpm, heart rate > 100 bpm, systolic blood pressure < 90 mmHg, neutrophils > 6.3×109/L, lymphopenia, thrombocytopenia, D-dimer ≥ 0.5 mg/L, lactate dehydrogenase > 250 U/L, aspartate aminotransferase > 40 U/L, total bilirubin > 26 μmol/L, albumin < 35 g/L, blood urea nitrogen > 9.5 mmol/L, estimated glomerular filtration rate < 90 ml/min/1.73, elevated cardiac troponin I, N-terminal pro-brain natriuretic peptide ≥ 900 pg/ml, C-reactive protein ≥ 25 mg/L, procalcitonin ≥ 0.05 ng/ml and ferritin > 400 μg/L were associated with death in patients with COVID-19. The multivariate logistic regression analysis revealed that an estimated glomerular filtration rate < 90 ml/min/1.73, elevated cardiac troponin I, C-reactive protein ≥ 25 mg/L and procalcitonin ≥ 0.05 ng/ml were predictive of mortality. Regarding immune responses, IL-2R, IL-6, IL-8, IL-10, and TNFα were remarkably higher in the deceased group at admission, and the levels of IL-2R, IL-6, IL-8, IL-10, and TNFα in the deceased group showed a rapid increase; the dynamics of these cytokines were highly consistent with disease deterioration. Lymphocyte subset analysis revealed that the deceased patients showed significant decreases in lymphocyte counts, especially helper T cells, suppressor T cells and NK cells.ConclusionsThis study identified that an estimated glomerular filtration rate < 90 ml/min/1.73, elevated cardiac troponin I, C-reactive protein ≥ 25 mg/L and procalcitonin ≥ 0.05 ng/ml were predictors of mortality in COVID-19 patients. Elevated cytokine levels and a continued increasing trend, including in IL-2R, IL-6, IL-8, IL-10 and TNFα, and a decrease in lymphocyte subsets, especially helper T cells, suppressor T cells and NK cells, were associated with a poor prognosis.

The aim of this study was to evaluate the effects of quorum sensing (QS) systems in Pseudomonas aeruginosa (P. aeruginosa) on the expression of ampC gene induced by antibiotics. An in vitro dynamic model of P. aeruginosa biofilms was established in a silicon tube in once-flowthrough system at 37 °C. Biofilm generation was identified by argentation. Biofilm morphology of standard P. aeruginosa strain (PAO-1) and QS systems deficient strains (PDO100, rhlI deficient strain; PAO-JP1, lasI deficient strain; and PAO-MW1, rhlI and lasI deficient strain) were observed by optical microscope. The expression of ampC in PAO1, PAO1 with QS inhibitor (furanone C-30) and the QS deficient strains before and after induced by antibiotics were quantified by real-time quantitative PCR. The biofilms of PAO-1 and PDO100 were much thicker and denser than that of PAO-JP1 and PAO-MW1. Being induced by antibiotics, the expression of ampC in PAO1 and PDO100 was significantly higher than that in PAO-MW1 and PAO-JP1. With the effect of furanone C-30, the expression of ampC in PAO1 induced by antibiotics was reduced in a dose-dependent manner. QS system, especially the las system, plays an important role in both biofilm formation and antimicrobials induced ampC expression and furanone C-30 is a potent inhibitor for P. aeruginosa QS system.