PurposeTo evaluate the association of serum levels of adipokines and cytokines with psoriasis.Materials and MethodsA comprehensive literature search was performed in PubMed, ScienceDirect and Web of Science for the available relevant studies published before December 1, 2016. Differences in serum marker levels between patients and controls were pooled as standardized mean differences (SMDs) with 95% confidence interval to combine the effect estimations. We also conducted stratified analysis, meta-regression analysis and sensitivity analysis.ResultsSixty-three studies containing 2876 psoriasis patients and 2237 healthy controls were included in this meta-analysis. The pooled serum levels of TNF-α, IFN-γ, IL-2, IL-6, IL-8, IL-18, IL-22, chemerin, lipocalin-2, resistin, sE-selectin, fibrinogen and C3 were higher in psoriasis patients compared with healthy controls (all P < 0.05). In contrast, adiponectin levels were lower. Serum levels of IL-1β, IL-4, IL-10, IL-12, IL-17, IL-21, IL-23, visfatin and omentin were not significantly different between psoriasis patients and controls (all P > 0.05). However, increased serum levels of IL-17 correlated with psoriasis in men. For other biomarkers, age, gender and psoriasis area and severity index did not explain the differences in effect size between the studies.ConclusionsSerum levels of TNF-α, IFN-γ, IL-2, IL-6, IL-8, IL-18, IL-22, chemerin, lipocalin-2, resistin, sE-selectin, fibrinogen, complement 3, and adiponectin correlate with psoriasis and can be used as potential biomarkers for psoriasis and response to the treatment. Future studies are needed to identify additional players involved in the pathogenesis of psoriasis and to fully decipher the underlying mechanism.

B1 cells are evolutionarily conserved innate-like cells that share many features with macrophages. It has also been established that B1 cells have a close developmental relationship with macrophages. However, whether B1 cells are able to act as professional phagocytic cells is not clear. In this study, we report that mouse peritoneal cavity (PerC) B cells demonstrate in vivo and in vitro phagocytic activities for Staphylococcus aureus, Escherichia coli, and polystyrene fluorescent microspheres. Approximately 5% of PerC B cells, mainly B1b cells, showed phagocytic activity. Ingested microbes were killed efficiently in the phagolysosome. The antigen-specific B-cell antigen receptor promoted B-cell phagocytosis, resulting in antigen presentation to T cells after uptake of bacteria. Our results reveal for the first time that mouse B1 cells have active phagocytic capabilities and thereby act as a bridge linking innate and adaptive immunity.

A growing corpus of evidence implicates the involvement of the commensal microbiota and immune cytokines in the initiation and progression of systemic lupus erythematosus (SLE). Glucocorticoids have been widely used in the treatment of SLE patients, however, glucocorticoid treatment carries a higher risk of other diseases. Using the 16S rRNA technique, we investigated the differences between the gut microbiota associated with the immune cytokines of SLE and relevant glucocorticoid treatment in a female cohort of 20 healthy control subjects (HC), 17 subjects with SLE (SLE-G), and 20 SLE patients having undergone glucocorticoid treatment (SLE+G). We observed that the diversity and structure of the microbial community in SLE+G patients were significantly changed compared to that of SLE-G patients, whereas the gut microbial community of the SLE+G group showed a similarity with the HC group, which implicate that the shift in the gut microbiome could represent a return to homeostasis. Furthermore, the up-regulations of immune cytokines in SLE-G were identified as closely related to gut dysbiosis, which indicates that the overrepresented genera in SLE patients may play roles in regulating expression level of these immune cytokines. This associated analysis of gut microbiota, glucocorticoid therapy, and immune factors might provide novel and insightful clues revealing the pathogenesis of SLE patients.

The purpose of this study was to review the clinical features of maxillofacial space infection (MSI), and to identify the potential risk factors predisposing to life-threatening complications. A retrospective review of the medical charts of patients with MSI treated at Peking University School and Hospital of Stomatology from August 2008 to September 2013 was conducted. A total of 127 patients [75 men (59.1%) and 52 women (40.9%); mean age, 45.39 ± 21.18 years, with a range of 1–85 years] formed the study cohort. The most common cause of MSI was odontogenic infection (57.5%). The most common space involved was the submandibular space. All patients were treated by antibiotics as well as surgical incision and drainage. Sixteen patients developed life-threatening complications, and the dominant complication was respiratory obstruction. Multivariate logistic regression analysis revealed the percentage of neutrophils (NEUT%) upon hospital admission ≥85.0% to be associated with life-threatening complications (P < 0.05). Even though adequate antibiotic therapy and incision and drainage of abscess were given, MSI patients with NEUT% upon hospital admission ≥85.0% carry a higher risk of life-threatening complications. In these patients, an aggressive treatment strategy is mandatory.

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Scabies moderately affected the QoL of the patients. Sulphur could be considered as an effective treatment for patients with scabies.

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