To investigate the effect of ILC2s on Th2-type adaptive immunity during the acute exacerbation of chronic obstructive pulmonary disease (AECOPD), the study enrolled healthy people, stable COPD patients, and AECOPD patients. Flow cytometry was used to detect Th1, Th2, and ILC2 in the peripheral blood and CD80 and MHC II levels on ILC2. The mRNA levels of GATA3, RORα, and CRTH2 of ILC2s were detected by RT-PCR. In addition, ILC2s from the peripheral blood of AECOPD patients were cocultured with CD4+ T cells from the peripheral blood of healthy controls. Cytokine levels in serum of the three groups and the in vitro coculture supernatants were measured by ELISA. Compared with the stable COPD group or the healthy control group, Th2 in the peripheral blood of AECOPD group increased dramatically, inducing an increase of Th2/Th1 ratio in AECOPD patients. Meanwhile, the level of IL-4 in the serum of this group was also increased. However, we also detected ILC2s in the peripheral blood of the AECOPD group and found that it was also increased, alone with the increased GATA3, RORα, and CRTH2 mRNA levels. We also found that the CD80 and MHC II on ILC2 were significantly upregulated and the proportion of MHC II+ ILC2 cells was significantly positively correlated with the proportion of Th2 cells in AECOPD patients. To further demonstrate the effect of ILC2 on Th2 cells, we cocultured ILC2 with CD4+ T cells in vitro, which also showed a significant increase of Th2 ratio as well as Th2-associated cytokines IL-4, IL-5, and IL-13. However, we found that this effect of ILC2s on Th2 cells could be inhibited by the addition of anti-MHC II. The Th2/Th1 balance shifts to Th2 in AECOPD. ILC2s may function as APC by the upregulation of MHC II and regulate adaptive immunity shift to Th2-type response in AECOPD.

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Antiwei was effective and well tolerated in treatment of natural influenza infection in adults. Antiwei represents a clinically valuable intervention in the management of influenza.

The aim of the present study was to investigate the roles of type 2 innate lymphoid cells (ILC2s) and interleukin-33 (IL-33) in chronic obstructive pulmonary disease (COPD). Serum and peripheral blood mononuclear cells (PBMCs) were isolated from healthy controls and COPD patients. ILC2 cells from the peripheral blood of COPD patients were stimulated with IL-33 or neutralizing ST2 antibody+IL-33 in vitro. The cell viability was assessed using a Cell Counting Kit-8 assay. ELISA was used to detect serum IL-33 and the levels of IL-4, IL-5, IL-6, IL-13 and soluble ST2 (sST2) in the culture supernatant. The percentage of ILC2 cells was measured by flow cytometry. The mRNA expression levels of GATA binding protein 3 (GATA3), RAR-related orphan receptor (ROR)α, ST2 and prostaglandin D2 receptor 2 (CRTH2) were detected by reverse transcription-quantitative PCR. It was revealed that IL-33, IL-5, IL-6 and IL-13 were significantly elevated in peripheral blood of patients with COPD. The proportion of ILC2s in peripheral blood of COPD patients was significantly increased, and the expression of RORA and CRTH2 was increased. The proportion of ST2 + ILC2 cells was significantly increased. After 48 h of IL-33 stimulation in vitro, the ratio of linage-CD45 + CD127 + CRTH2 + cells reached a maximum. In addition, the viability of ILC2 cells, the expression levels of RORA, GATA3, ST2 and CRTH2 mRNA and the cytokines IL-4, IL-6, IL-5, IL-13 and sST2 were significantly increased. These effects were abrogated by treatment with anti-ST2. In conclusion, IL-33 is upregulated in the serum of patients with COPD and the proportion of ILC2s among the PBMCs is increased. IL-33 may promote the proliferation of ILC2 cells and secrete type 2 T-helper cell cytokines to participate in the immune response in COPD.

Background:A Chinese herb formula Yufeining (YFN) has showed promise in the treatment of stable chronic obstructive pulmonary disease (COPD), less is known that the impact of YFN in combination with standard Western treatments on lung inflammation. This study evaluated the safety and efficacy of YFN as a treatment for stable COPD and as an anti-inflammatory agent.Methods:Sixty patients with stable COPD were randomly assigned to two treatment groups (YFN treatment, N = 30; placebo treatment, N = 30). Both groups received inhaled steroids and bronchodilators during an 8-week intervention, and patient status was assessed at 8 weeks later and 4 months after treatment. The primary outcome included clinical efficacy. The secondary outcomes involved CAT score, mMRC grade, six-minute walking distance (6MWD). IL-8, TNF-α, IL-17A, LTB4, TGF-β1 and CRP were also detection in peripheral serum, as well as adverse reaction conditions.Results:The YFN group demonstrated a significant improvement in clinical efficacy (compare 89.3% to 63.3% in the placebo group; P < 0.05). CAT scores and mMRC grades significantly decreased (P < 0.05, P < 0.01), and 6MWD significantly increased (P<0.05), after YFN treatment. The levels of IL-8, TNF-α, LTB4 and CRP decreased significantly after 8 weeks of treatment compared to baseline levels in both groups. Only in the YFN treatment group, the levels of IL-17A decreased significantly after treatment compared to baseline levels (P < 0.05). No changes were observed inTGF-β1 from pre-to post-treatment in either group (P > 0.05). Serum levels of IL-8, TNF-α, IL-17A, LTB4 and CRP decreased significantly after YFN treatment compared to the placebo group (P < 0.05).Conclusion:A combinatorial treatment approach with YFN, inhaled steroids and bronchodilators produced a clinically effective treatment for stable COPD, leading to a significant decrease in circulating inflammatory mediators. The study appeared YFN was safety.Clinical trial registration number:No. ChiCTR-IOR-17013577.