Journal of Microbiology Immunology and Infection最新文献

A case of H5N6 avian influenza was reported in Anhui Province, China. The viral titers in the patient's lungs and pharynx decreased rapidly after oseltamivir treatment, yet it still fatal. The whole genome sequencing suggested that it derived from four distinct sources and classified within the 2.3.4.4b clade.

Background: Eosinophilic AECOPD is a specific phenotype; however, the clinical outcomes and the short-term changes in sputum microbiome remain unclear.

Methods: We retrospectively included AECOPD patients admitted to National Cheng Kung Universal Hospital from January 2013 to December 2022. The primary outcome was respiratory failure rate. In addition, self-expectorated sputum was prospectively collected on days 1 and 5 of hospitalization between June 2020 and May 2021, and 16S rRNA gene segments (V3-V4) were amplified for sputum microbiome identification. Eosinophilic AECOPD were defined as blood eosinophils (bEOS) exceeding 2 % at admission.

Results: From the analysis of 202 AECOPD hospitalizations, patients with bEOS ≥2 % had shorter hospital stays and respiratory failure days (β-coefficient: 2.98 and -3.86, P < 0.001 and = 0.049, respectively), a lower risk of respiratory failure and intensive care unit admission (odds ratio: 0.29 and 0.35, P = 0.007 and = 0.029, respectively). In a sub-cohort of 30 AECOPD patients undergoing sputum microbiome analysis, 12 had bEOS ≥2 %, a significant decrease in Shannon diversity at the phylum level after 5 days of treatment was observed only in the bEOS <2 % group. Moreover, the relative abundance of Proteobacteria increased after treatment in the patients with bEOS ≥ 2 % while a trend of decrease was observed in those with bEOS<2 %.

Conclusions: Patients with eosinophilic AECOPD demonstrate better short-term clinical outcomes. The sputum microbiota in the eosinophilic and non-eosinophilic patients also respond differently to the treatment for AECOPD.

Background: Cavitary lung disease caused by Mycobacterium tuberculosis (TB) and nontuberculous mycobacteria (NTM) presents overlapping radiologic features but potentially distinct immunopathologic mechanisms. Macrophage polarization and prothymosin-α (PTMA) expression may contribute to disease progression, but their roles in surgically treated patients remain unclear.

Methods: We retrospectively analyzed 33 patients who underwent pulmonary resection for TB (n = 17) or NTM (n = 16) infection. Clinical characteristics, CT-based cavity wall thickening scores, and immunohistochemical staining for PTMA, CD68, iNOS, and Arginase-1 were compared. A monocyte migration assay was also performed to evaluate PTMA function.

Results: NTM patients exhibited lower body mass index and fewer comorbidities than TB patients but had a higher relapse rate. Cavity wall thickness correlated with increased PTMA and CD68 expression, particularly in NTM lesions. No significant difference in iNOS or Arginase-1 expression or M1/M2 ratio was observed. M. kansasii was more often linked to severe cavitary disease. PTMA enhanced monocyte migration in a dose-dependent manner in vitro.

Conclusion: Radiologic cavity wall thickness may reflect underlying immune dynamics, particularly in NTM. PTMA and CD68 are associated with immune activation and cavity progression in chronic mycobacterial infections. PTMA may serve a dual role as both a histologic marker and a functional regulator of monocyte recruitment. Immunohistochemical analysis revealed no clear M1/M2 polarization shift, suggesting a non-classical or depolarized macrophage phenotype. These findings underscore the potential of PTMA as both a tissue marker and a bioactive mediator in chronic pulmonary infection.

Background/purpose(s): Psoriasis is a skin-specific autoimmune disease that causes scaling, erythema and thickening. The disease involves immune cell infiltration and keratinocyte proliferation in skin lesions. Previous studies have demonstrated that Th17 cells and IL-22 play prominent roles in the pathogenesis of psoriasis via IL-17, IL-22 and IL-23 signaling. However, the role of innate cells in this process remains unclear.

Methods: In this study, using the TLR7/8 agonist imiquimod (IMQ) in a well-established murine model, we demonstrated that natural killer (NK) cells play an important role in the pathogenesis of psoriasis. Non-obese diabetic (NOD) mice are prone to Th1 and Th17 responses, and the lack of NK cell activity and macrophages in these animals contribute to their value as a model for type I diabetes.

Results: The NOD mice treated with IMQ (NOD-IMQ) exhibit markedly attenuated skin lesions compared to BALB/c mice treated with IMQ (BALB/c-IMQ). An analysis of immune cell types revealed that the number of macrophages, plasmacytoid dendritic cells (pDCs), neutrophils and Th1, Th2, Th17, Treg, and NK cells increased in the BALB/c-IMQ mice compared to the NOD-IMQ mice. Testing NK cell activity and macrophage function, NK cell cytotoxicity and macrophage phagocytosis, but not macrophage migration, were decreased in the NOD mice compared with the BALB/c mice. After NK cell depletion, normal BALB/c-IMQ mice exhibited milder skin lesions than the NOD-IMQ mice.

Conclusion: These results suggest that NK cells play a critical role in IMQ-induced skin inflammation. Controlling NK cell activity may be a potential therapeutic approach for psoriasis.