Objective To observe the change of immunologic function in children with mycoplasma pneumoniae pneumonia (MMP).Methods Totally 114 children diagnosed with MPP were selected as experimental group,and MPIgM were positively detected in the course of 7 to 10 days,and the blood samples were collected.At the same time,50 healthy children in health clinic were selected as control group,and peripheral blood samples were collected.The levels of T cell subsets (CD3,CD4,CD8,CD4/CD8,NK) and humoral immunity (IgG,IgA,IgM,C3,C4) in peripheral blood samples were detected respectively.Results The serum CD3,CD4,CD4/CD8 ratio and NK value in the experimental group were significantly lower than those in the control group (P ＜ 0.05),and IgA,C3 and C4 were significantly lower than those in the control group (P ＜ 0.05),but there was no significant difference in IgG and IgM values (P ＞ 0.05).Conclusion Mycoplasma pneu moniae (MP) infection can cause immune dysfunction,inhibit cellular immunity and humoral immunity.

Objective To observe the change of immunologic function in children with mycoplasma pneumoniae pneumonia (MMP).Methods Totally 114 children diagnosed with MPP were selected as experimental group,and MPIgM were positively detected in the course of 7 to 10 days,and the blood samples were collected.At the same time,50 healthy children in health clinic were selected as control group,and peripheral blood samples were collected.The levels of T cell subsets (CD3,CD4,CD8,CD4/CD8,NK) and humoral immunity (IgG,IgA,IgM,C3,C4) in peripheral blood samples were detected respectively.Results The serum CD3,CD4,CD4/CD8 ratio and NK value in the experimental group were significantly lower than those in the control group (P ＜ 0.05),and IgA,C3 and C4 were significantly lower than those in the control group (P ＜ 0.05),but there was no significant difference in IgG and IgM values (P ＞ 0.05).Conclusion Mycoplasma pneu moniae (MP) infection can cause immune dysfunction,inhibit cellular immunity and humoral immunity.

Emerging evidence indicates that the gut microbiome contributes to the host immune response to infectious diseases. Here, to explore the role of the gut microbiome in the host immune responses in COVID-19, we conducted shotgun metagenomic sequencing and immune profiling of 14 severe/critical and 24 mild/moderate COVID-19 cases as well as 31 healthy control samples. We found that the diversity of the gut microbiome was reduced in severe/critical COVID-19 cases compared to mild/moderate ones. We identified the abundance of some gut microbes altered post-SARS-CoV-2 infection and related to disease severity, such as Enterococcus faecium, Coprococcus comes, Roseburia intestinalis, Akkermansia muciniphila, Bacteroides cellulosilyticus and Blautia obeum. We further analyzed the correlation between the abundance of gut microbes and host responses, and obtained a correlation map between clinical features of COVID-19 and 16 severity-related gut microbe, including Coprococcus comes that was positively correlated with CD3⁺/CD4⁺/CD8⁺ lymphocyte counts. In addition, an integrative analysis of gut microbiome and the transcriptome of peripheral blood mononuclear cells (PBMCs) showed that genes related to viral transcription and apoptosis were up-regulated in Coprococcus comes low samples. Moreover, a number of metabolic pathways in gut microbes were also found to be differentially enriched in severe/critical or mild/moderate COVID-19 cases, including the superpathways of polyamine biosynthesis II and sulfur oxidation that were suppressed in severe/critical COVID-19. Together, our study highlighted a potential regulatory role of severity related gut microbes in the immune response of host.
COVID-19 ; Clostridiales ; Gastrointestinal Microbiome ; Humans ; Immunity ; Leukocytes, Mononuclear ; SARS-CoV-2