Surgically treated reactive arthritis of the ankle after COVID-19 infection: A case report

A 37-year-old man developed right ankle pain and swelling six days after being diagnosed with coronavirus disease (COVID-19). Despite conservative treatment, his ankle symptoms persisted. Magnetic resonance imaging and computed tomography showed synovial hypertrophy and bone erosion in the ankle. Following arthroscopic synovectomy, performed 69 days after the COVID-19 diagnosis, the pain improved significantly. The clinical course was consistent with that of reactive arthritis following severe acute respiratory syndrome coronavirus 2 infection. The pathological findings resembled rheumatoid nodules. The bone erosion may have originated from the inflammatory pathway, which resembles the mechanism of rheumatoid arthritis.     

Overview of CF lung pathophysiology

Defects of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) protein affect the homeostasis of chloride, bicarbonate, sodium, and water in the airway surface liquid, influencing the mucus composition and viscosity, which induces a severe condition of infection and inflammation along the whole life of CF patients. The introduction of CFTR modulators, novel drugs directly intervening to rescue the function of CFTR protein, opens a new era of experimental research. The review summarizes the most recent advancements to understand the characteristics of the infective and inflammatory pathology of CF lungs.     

The key role of macrophage depolarization in the treatment of COPD with ergosterol both in vitro and in vivo

Macrophages are the most abundant immune cells in the lung, which play an important role in COPD. The anti-inflammatory and anti-oxidation of ergosterol are well documented. However, the effect of ergosterol on macrophage polarization has not been studied. The objective of this work was to investigate the effect of ergosterol on macrophage polarization in CSE-induced RAW264.7 cells and Sprague-Dawley (SD) rats COPD model. Our results demonstrate that CSE-induced macrophages tend to the M1 polarization via increasing ROS, IL-6 and TNF-α, as well as increasing MMP-9 to destroy the lung construction in both RAW264.7 cells and SD rats. However, treatment of RAW264.7 cells and SD rats with ergosterol inhibited CSE-induced inflammatory by decreasing ROS, IL-6 and TNF-α, and increasing IL-10 and TGF-β, shuffling the dynamic polarization of macrophages from M1 to M2 both in vitro and in vivo. Ergosterol also decreased the expression of M1 marker CD40, while increased that of M2 marker CD163. Moreover, ergosterol improved the lung characters in rats by decreasing MMP-9. Furthermore, ergosterol elevated HDAC3 activation and suppressed P300/CBP and PCAF activation as well as acetyl NF-κB/p65 and IKKβ, demonstrating that HDAC3 deacetylation was involved in the effect of ergosterol on macrophage polarization. These results also provide a proof in immunoregulation of ergosterol for therapeutic effects of cultured C. sinensis on COPD patients.     

Biochemical responses revealed in an amphibian species after exposure to a forgotten contaminant: An integrated biomarker assessment

Vanadium is a metal whose toxicity towards terrestrial and aquatic species has been under-reported to date.. The biochemical responses of vanadium in amphibian species have not been determined. To establish the effects of vanadium (V) on exposed adult Xenopus laevis, acute and chronic exposures were conducted, and biomarker analyses were performed on liver and muscle tissues from exposed frogs. Biomarkers of exposure, such as acetylcholinesterase (AChE) and metallothioneins (MT), were analysed. Biomarkers of effect were also analysed to determine possible increases in reactive oxygen species (ROS), and the effect of the exposure on the energy balance in the organisms. These included superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), protein carbonyls (PC), malondialdehyde (MDA), and cellular energy allocation (CEA) (energy available, energy consumption, lipids, proteins and glucose). In acute exposures, the energy balances in organisms were distinctly affected, possibly due to insulin mimetic properties of V. In chronic exposures, MT, AChE, SOD, CAT and GSH responses were more pronounced. Although AChE is generally inhibited by pollutant exposure, in this study, it was stimulated. There were significant inhibitions of SOD and CAT, previously observed in frog species. PC levels increased in the highest acute exposure concentration, indicating protein damage. The IBR.v2 revealed the biochemical responses of V more effectively than traditional statistical analysis.     

A neuroglia-based interpretation of glaucomatous neuroretinal rim thinning in the optic nerve head

Neuroretinal rim thinning (NRR) is a characteristic glaucomatous optic disc change. However, the precise mechanism of the rim thinning has not been completely elucidated. This review focuses on the structural role of the glioarchitecture in the formation of the glaucomatous NRR thinning. The NRR is a glia-framed structure, with honeycomb geometry and mechanically reinforced astrocyte processes along the transverse plane. When neural damage selectively involves the neuron and spares the glia, the gross structure of the tissue is preserved. The disorganization and loss of the glioarchitecture are the two hallmarks of optic nerve head (ONH) remodeling in glaucoma that leads to the thinning of NRR tissue upon axonal loss. This is in contrast to most non-glaucomatous optic neuropathies with optic disc pallor where hypertrophy of the glioarchitecture is associated with the seemingly absent optic disc cupping. Arteritic anterior ischemic optic neuropathy is an exception where pan-necrosis of ONH tissue leads to NRR thinning. Milder ischemia indicates selective neuronal loss that spares glia in non-arteritic anterior ischemic optic neuropathy. The biological reason is the heterogeneous glial response determined by the site, type, and severity of the injury. The neuroglial interpretation explains how the cellular changes underlie the clinical findings. Updated understandings on glial responses illustrate the mechanical, microenvironmental, and microglial modulation of activated astrocytes in glaucoma. Findings relevant to the possible mechanism of the astrocyte death in advanced glaucoma are also emerging. Ultimately, a better understanding of glaucomatous glial response may lead to glia-targeting neuroprotection in the future.     

Role of Toll-like receptor 2 against Streptococcus uberis infection in primary mouse mammary epithelial cells

Mammary epithelial cells (MECs) play an important role against Streptococcus uberis infection which is one of the main causes of bovine mastitis and a potential threat to human health. Toll-like receptors (TLRs) and their mediated signaling pathways are critical in both innate and infection responses, yet their roles in anti-S. uberis infection in MECs remains poorly defined. In this work we investigated the regulatory mechanisms of TLR2 in inflammatory responses, where WT and TLR2^−/− mice were euthanized at 15–18 days gestation, and mammary gland tissues were collected aseptically. The mouse MECs (MMECs) were isolated by combined digestion with type I collagenase, hyaluronidase and trypsin. We challenged MMECs with S. uberis and quantified antioxidant capacity as well as reactive oxygen species (ROS), proinflammatory cytokines and cell damage at different times. The loss of TLR2 function in MMECs results in more serious cell damage, increased cell adhesion, and significantly decreased ROS and mitochondrial ROS (mROS) with bactericidal function in response to S. uberis infection. Moreover, it was observed that the antioxidant capacity declined, and the production of TLR2-mediated cytokines (except CXC ligand 15) also were reduced. We demonstrated that TLR2 can mediate cellular anti-infective processes in MMECs by regulating the production of ROS and mROS and the secretion of cytokines. The results suggest an unpredicted role of TLR2 in MMECs in response to S. uberis infection.     

外源性胆绿素对中波紫外线诱导的角质形成细胞光损伤的保护作用和机制

【摘要】 目的 探讨外源性胆绿素对中波紫外线（UVB）照射的HaCaT细胞光损伤的保护作用。方法 将HaCaT细胞分为加入0、0.1、1、10 μmol/L胆绿素并照射UVB的UVB组、0.1 μmol/L UVB组、1 μmol/L UVB组、10 μmol/L UVB组及不做处理的对照组。UVB照射剂量为30 mJ/cm2，照射后继续培养24 h，分别检测细胞活性氧（ROS）水平、超氧化物歧化酶（SOD）活力、丙二醛（MDA）含量，ELISA法检测各组细胞的炎症因子白细胞介素6（IL-6）、IL-8水平。多组间均数比较采用单因素方差分析，组间两两比较采用LSD-t检验。结果 UVB组、0.1 μmol/L UVB 组、1 μmol/L UVB组、10 μmol/L UVB组、对照组细胞ROS水平（3 613.33 ± 206.61、2 958.67 ± 193.87、2 678.33 ± 178.24、2 274.67 ± 118.81、1 905.67 ± 250.25）、SOD活力（24.41 ± 1.78、28.96 ± 2.21、29.75 ± 1.75、30.19 ± 2.29、37.52 ± 2.31）、MDA含量（5.61 ± 0.32、5.46 ± 0.55、4.65 ± 0.22、2.55 ± 0.93、1.31 ± 0.05）、IL-6水平、IL-8水平差异均有统计学意义（F值分别为 34.02、57.36、214.09、29.73、11.40，均P < 0.05），UVB组ROS水平、MDA含量及IL-6、IL-8水平均高于另4组（均P < 0.05），SOD活力均低于另4组（均P < 0.05）。结论 外源性胆绿素减轻UVB引起的HaCaT细胞的氧化损伤、减轻炎症反应和抑制脂质过氧化作用，对细胞光损伤有一定的保护作用。