Neutrophil infiltration is the characteristic pathological feature of M. pneumoniae pneumonia (MPP). This study aimed to explore the associations among neutrophil activity, clinical presentation, and role of the M. pneumoniae/interleukin-8 (IL-8)/neutrophil axis in the pathogenesis of MPP. A total of 42 patients with MPP were prospectively enrolled in the study. Neutrophil activity, including matrix metalloproteinase-9 (MMP-9), myeloperoxidase (MPO), and neutrophil elastase (NE), were measured. Clinical information was collected for all patients and control group. In vitro, IL-8 production was measured at different time points after M. pneumoniae infection of bronchial epithelial cells, and neutrophil activity was analyzed after IL-8 stimulation. The percentage of neutrophil in the bronchoalveolar lavage fluid was higher in the group of patients with high levels of M. pneumoniae DNA than in those with low levels of M. pneumoniae DNA (P < 0.05). IL-8, MMP-9, and NE in patients with MPP significantly increased compared with controls and decreased after treatment (P < 0.05). MPO and MMP-9 were associated with duration of fever (r = 0.332, P < 0.05) and length of stay (r = 0.342, P < 0.05), respectively. In vitro, M. pneumoniae induced IL-8 production by bronchial epithelial cells in a time dependent manner. MPO, MMP-9 and NE production by neutrophils significantly increased compared with medium controls after IL-8 stimulation. In summary, the M. pneumoniae/IL-8/neutrophil axis likely plays a vital role in the pathogenesis of MPP.

It is urgent to identify and validate biomarkers for early diagnosis and efficient treatment of nasopharyngeal carcinoma (NPC). Recent studies have proposed p38 gamma (p38γ) as a cyclin-dependent kinase (CDK)-like kinase that phosphorylates retinoblastoma (Rb) to promote cyclins expression and tumorigenesis. Here the Gene Expression Profiling Interactive Analysis (GEPIA) database and results from the local NPC tissues demonstrate that p38γ is significantly upregulated in NPC tissues, correlating with poor overall survival. Furthermore, p38γ mRNA and protein expression is elevated in established NPC cell lines (CNE-1 HONE-1 and CNE-2) and primary human NPC cells, but low expression detected in human nasal epithelial cells. In established and primary NPC cells, p38γ depletion, using the shRNA strategy or the CRISPR/Cas9 gene-editing method, largely inhibited cell growth, proliferation and migration, and induced significant apoptosis activation. Contrarily, ectopic p38γ overexpression exerted opposite activity and promoted NPC cell proliferation and migration. Retinoblastoma (Rb) phosphorylation and cyclin E1/A expression were decreased in NPC cells with p38γ silencing or knockout, but increased after p38γ overexpression. Moreover, mitochondrial subcellular p38γ localization was detected in NPC cells. Significantly, p38γ depletion disrupted mitochondrial functions, causing mitochondrial depolarization, reactive oxygen species production, oxidative injury and ATP depletion in NPC cells. In vivo, intratumoral injection of adeno-associated virus-packed p38γ shRNA potently inhibited primary human NPC xenograft growth in nude mice. In p38γ shRNA virus-injected NPC xenograft tissues, p38γ expression, Rb phosphorylation, cyclin E1/A expression and ATP levels were dramatically decreased. Taken together, we conclude that p38γ overexpression is required for NPC cell growth, acting as a promising therapeutic target of NPC.

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We aim to analyze the clinical characteristics of obstructive sleep apnea hypopnea syndrome (OSAHS) in children. Polysomnography (PSG) and nasopharynx lateral film were performed, and clinical data were collected in 469 children who came to the outpatient department due to "snoring during sleep with mouth opening breathing, hard breathing or suffocation". Among the enrolled children, 123 (22.6%) were diagnosed with OSAHS, with 70 were mild and 53 were moderate-severe. Percentage of adenoid hypertrophy was higher in OSAHS patients (p <0.01), instead of tonsil enlargement. The OSAHS children were agged 5 (4, 7). Compared with PS, the percentage of snoring, apnea, dyspnea, increased nocturia, and daytime sleepness were significsntly higher in moderate-severe patients (p <0.01). In OSAHS groups, AHI, ODI, Longest time of apnea were increased, while minimum SpO2 and mean SpO2 during sleep were decreased significantly (p <0.01) than PS. Time ratio of NREM1 was elevated in moderate-severe OSAHS patients (p <0.01). Time ratio of REM was elevated in mild patients(p <0.01). Compared with the preschoolers, the percentage of leg movement and sleepness were significsntly higher in school-agers (p <0.05). The youngers had higher time ratio of NREM3 and better sleep efficieny (p<0.01). However, AHI(p<0.05) and ODI(p<0.01) were higher in elder OSAHS significantly. Snoring (OR =5.745, p < 0.01), adenoid hypertrophy (OR =4.381, p < 0.01), apnea (OR =2.670, p < 0.001), dyspnea (OR =1.975, p < 0.01), and CRP (OR =1.172, p < 0.001) were independent risk factors for OSAHS. Conclusion AHI, ODI, Longest time of apnea, minimum SpO2 and mean SpO2 should be considered and analyzed simultaneously in diagnosis. The school-age OSAHS patients seems to more serious than the preschoolers. Snoring, apnea, dyspnea, adenoid hypertrophy, and CRP are risk factors for OSAHS.