Mycoplasma pneumoniae is the most common pathogen of respiratory tract infection in children and adults. Clinical observation shows that M. pneumoniae infection can cause massive mucus secretion in the respiratory tract, which makes the breathing of patients difficult. Studies have shown that M. pneumoniae infection can cause massive secretion of mucin 5AC (MUC5AC). Adhesin P1 plays an important role in the pathogenesis of M. pneumoniae infection by mediating the adhesion of pathogens to host cells, and the C-terminal residues of P1 (P1-C) are immunogenic. This study investigated the molecular mechanism of Wnt/β-catenin signaling pathway inhibitor Dickkopf-1 (DKK1) in the secretion of MUC5AC in mouse airway epithelial cells (MAECs) induced by P1-C. Scanning electron microscope and hematoxylin-eosin staining were used to observe the effect of P1-C on mucus secretion of MAECs. Protein chip was used to detect the secretion of cytokines and analyse the enrichment of related signaling pathways induced by P1-C in MAECs. Periodic acid schiff stain (PAS) staining, Tunel staining and Masson staining were used to detect the damage of the lungs of mouse exposed to P1-C. Immunohistochemistry was used to detect the secretion of MUC5AC expression, and Western blotting was used to reveal the molecular mechanism of DKK1-regulated secretion of MUC5AC induced by P1-C protein in MACES. The results showed that P1-C induced the massive secretion of mucus and inflammatory factors in MAECs. During P1-C infection, DKK1 down-regulated janus kinase 2 (JAK2), phosphorylation signaling and transcription activator 1 (p-STAT1) and phosphorylation signaling and activator of transcription 3 (p-STAT3) expression. Overexpression of DKK1 significantly up-regulated the expression of MUC5AC repressor transcription factor fork-head box protein A2 (FOXA2). At the same time, the expression of MUC5AC induced by P1-C was inhibited significantly. It is speculated that DKK1 can effectively reduce the secretion of MUC5AC in MAECs induced by P1-C by inhibiting the JAK/STAT1-STAT3 signaling pathway and up-regulating the expression of FOXA2.
Animals ; Mice ; Epithelial Cells ; Lung ; Mucin 5AC/metabolism* ; Mycoplasma pneumoniae/metabolism* ; Signal Transduction

We report a case of acute severe hepatitis with Mycoplasma pneumoniae (M. pneumoniae) infection and transient depression of multiple coagulation factors. A 5-year-old boy, previously healthy, was admitted with pneumonia. M. pneumoniae infection was confirmed by serology testing. Liver enzymes were elevated on admission without any past medical history. After treatment with azithromycin for 3 days, pneumonia improved, but the hepatitis was acutely aggravated. Partial thromboplastin time (PTT) was prolonged and depression of multiple coagulation factors developed. Liver biopsy revealed features consistent with acute hepatitis. A week later, liver enzymes were nearly normalized spontaneously. Normalization of prolonged PTT and coagulation factors were also observed several months later. This may be the first case of transient depression of multiple coagulation factors associated with M. pneumoniae infection.
Acute Disease ; Blood Coagulation Factors/metabolism ; Child, Preschool ; Hepatitis A/blood/diagnosis/*etiology ; Humans ; Male ; Mycoplasma pneumoniae/pathogenicity ; Partial Thromboplastin Time ; Pneumonia, Mycoplasma/blood/*complications

OBJECTIVETo explore the essential points for diagnosis of pulmonary embolism in children with mycoplasma pneumonia.

METHODRetrospective analysis of the clinical and laboratory data of a pediatric case who developed pulmonary embolism after mycoplasma pneumonia was performed for the key points for diagnosis.

RESULTA-six-year old boy was admitted with chief complaint of fever and cough for half a month, combined with chest pain and mild labored breath. Vital signs were stable. Breathing movement of the left side weakened and there was left lower lobe percussion dullness. Breath sound was found weakened in the left lung, and a few fine crackles were audible. The results of laboratory tests were as follows: mycoplasma antibody (IgM) 1:128, cold agglutinin test 1:1024, blood D dimer 14.81 mg/L; anticardiolipin antibody was positive; plasma protein C activity was 60% (normal range 70% - 130%). Pulmonary artery computed tomographic angiography revealed a mass opaque shadow in left lower lobe, the branch of left lower bronchial artery was partially obstructed. Echocardiography showed tricuspid valve mild regurgitation, estimated pulmonary pressure was 5.1 kPa. Single-photon emission computed tomography indicated that radioactivity distribution was apparently sparse in the dorsal segment, anterior basal segment, outer basal segment and inferior lingular segment of the left lung. The preliminary diagnosis on admission was mycoplasma pneumonia with pleural effusion, pulmonary embolism. Intravenous erythromycin combined with meropenem were administered. Anticoagulation therapy was initiated with low molecular weight heparin and then oral warfarin tablets. Pleural effusion disappeared soon, D dimer descended to 0.38 mg/L, and pulmonary artery pressure declined. After 3-month follow-up, anti-cardiolipin antibody was negative, plasma protein C activity recovered, and lung lesions were absorbed.

CONCLUSIONWhen mycoplasma pneumonia is accompanied by chest pain or dyspnea and there are bloody pleural effusion, pulmonary hypertension, positive antiphospholipid antibody and elevated D dimer, pulmonary embolism should be considered. Diagnosis could be clarified by the result of pulmonary artery computed tomographic angiography.

Antibodies, Antiphospholipid ; blood ; Child ; Fibrin Fibrinogen Degradation Products ; metabolism ; Humans ; Male ; Mycoplasma pneumoniae ; Pneumonia, Mycoplasma ; complications ; diagnosis ; Pulmonary Embolism ; complications ; diagnosis ; Retrospective Studies

OBJECTIVETo investigate the effects of Huchang Qingfei concentrated pellets on the expression of E-cadherin (E-cd) in the lung tissue from mice infected with Mycoplasma pneumoniae (MP).

METHODA mice model of Mycoplasmal pneumonia (MPP) was developed by repeatedly intranasal infectious route. Transmission electronic microscope (TEM) and immunohistochemistry stain were performed to observe the pathological changes and expression of E-cd in lung tissues.

RESULTUnder TEM it was found that the cellular membrane was ruptured, mitochondria was denatured, crista was broken in the pulmonary cells of the model group; the all above parameters in Huchang medicated group were improved obviously. The immunohistochemistry test showed that strong positive brown stain of E-cd expression was found in the pulmonary epithelial cell membrane and bronchial periphery in the model group, however, in the medicated group, the E-cd expression level in the cellular membrane was decreased and the expression ratio was dropped significantly as compared with the model controls.

CONCLUSIONHuchang Qingfei concentrated pellets can inhibit the overexpression of E-cd in the lung tissue of mice with MP-infection, which may be helpful for prevention and treatment of pulmonary injury caused by MPP.

Animals ; Cadherins ; metabolism ; Cell Membrane ; metabolism ; Drug Combinations ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Epithelial Cells ; metabolism ; Female ; Lung ; metabolism ; pathology ; Male ; Mice ; Mycoplasma pneumoniae ; isolation & purification ; Plants, Medicinal ; chemistry ; Pneumonia, Mycoplasma ; metabolism ; microbiology ; pathology ; Random Allocation

Amino Acid Sequence ; Animals ; Bacterial Proteins ; genetics ; metabolism ; Bacterial Toxins ; genetics ; metabolism ; Base Sequence ; Community-Acquired Infections ; microbiology ; Gene Expression Regulation, Bacterial ; Humans ; Lung ; microbiology ; pathology ; Mycoplasma pneumoniae ; Pneumonia, Mycoplasma ; microbiology ; Respiratory Distress Syndrome, Adult ; microbiology

BACKGROUNDMycoplasma pneumoniae is a common pathogen that caused community-acquired pneumonia (CAP). P1 protein served as major adhesion and immunodominant protein in Mycoplasma pneumoniae, but little about P1 gene was learned and the relationship between P1 genotype and macrolide resistance has yet to be explored.

METHODSThe DNA sequence of the entire P1 gene from 35 strains isolated from clinical specimens collected in Beijing, China, in 2010 was determined. The resulting sequences were checked for known macrolide resistance mutations, such as A2063G, A2064G, C2617G in domain V of 23S rRNA. Antibiotic susceptibility test was done to further identify macrolide resistant strains.

RESULTSThirty-four clinical strains were type 1, and were identical to type 1 reference strain MP129. Only one clinical strain, MpYYM22, was type 2, and proved to be variant 2c. One synonymous point mutation in the P1 type 1 gene from two isolates was identified relative to the MP129 P1 sequence at nucleotide position (nt) 552 (C>A), while another two isolates had missense mutations at nt 2504 (G>A). This point mutation caused an amino acid change from glycine to glutamic acid. An AGT tri-nucleotide variable-number tandem repeat (VNTR), coding for serine and repeating 6-11 times, up to 15-16 times, was found in the region between the RepMP4 and RepMP2/3 elements in the 35 isolates examined. All 35 clinical strains, including MpYYM22, demonstrated macrolide resistance with the range of minimum inhibitory concentration (MIC) of erythromycin from 64 to 256 µg/ml, having an A2063G transition in domain V of the 23S rRNA gene.

CONCLUSIONSP1 type 1 was the dominant type of Mycoplasma pneumoniae in Beijing in 2010, although variant 2c strains were present. More samples are needed to determine whether there is a relationship between the P1 genotype and macrolide resistance, as the 35 strains examined did not allow a conclusive result. However, the AGT tri-nucleotide VNTR may be a more informative locus for multi-locus VNTR analysis.

Anti-Bacterial Agents ; pharmacology ; DNA, Bacterial ; Drug Resistance, Bacterial ; Genotype ; Humans ; Macrolides ; pharmacology ; Microbial Sensitivity Tests ; Mycoplasma pneumoniae ; drug effects ; genetics ; metabolism

Diagnosis of Mycoplasma pneumoniae infection is important due to its variable clinical manifestations and absence of response to beta-lactams. Introduction of enzyme immunoassays (EIAs) for serologic diagnosis of M. pneumoniae has made it possible to separate the analyses of specific IgG and IgM antibodies. We compared four different commercial EIAs, ImmunoWELL IgG, IgM (GenBio), Medac IgG, IgA, IgM (Medac), Platelia IgG, IgM (Sanofi Pasteur), and Ridascreen IgG, IgA, IgM (r-Biopharm) with indirect particle agglutination assay (PA), Serodia-MycoII (Fujirebio). We tested 91 specimens from 73 pediatric patients (2-17 yr) hospitalized at a tertiary-care hospital between December 2005 and January 2006. The measurements of IgM EIAs were correlated with PA titers (Spearman's correlation coefficient, from 0.89 to 0.92) with high concordance rates, ranging from 82.4% to 92.3%. However, some negative IgM-EIA results in PA-positive specimens indicated that serial samplings with convalescent sera would be necessary to confirm M. pneumoniae infection.
Adolescent ; Antibodies, Bacterial/chemistry ; Child ; Child, Preschool ; Female ; Humans ; Immunoenzyme Techniques/*methods ; Immunoglobulin G/*chemistry ; Immunoglobulin M/*chemistry ; Infant ; Male ; Microbiology ; Mycoplasma pneumoniae/chemistry/*immunology/metabolism ; Pneumonia, Mycoplasma/*diagnosis/*immunology ; Polymerase Chain Reaction ; Serologic Tests