Pneumonia: New Diagnostic and Therapeutic Options

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Medical Microbiology".

Deadline for manuscript submissions: 15 March 2025 | Viewed by 3205

Special Issue Editor


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Guest Editor
Department of Internal Medicine II, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria
Interests: immune activation; interferon-gamma mediated biochemical pathways; tryptophan catabolism; neopterin
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Special Issue Information

Dear Colleagues,

Pneumonia is a frequent disease, which can also impair the long-term health of infected patients. It can be caused by different pathogens, and its outcome is influenced by the virulence of the pathogen as well as the host’s immune response. In this Special Issue, studies investigating new diagnostic and therapeutic options in acute pneumonia will be presented. Additionally, this Special Issue will focus on the underlying pathomechanisms of pneumonia and metabolic changes induced by the different kinds of pathogens causing pneumonia. Also, as the host’s immune response strongly determines whether patients have a mild or severe course of disease, whether inflammatory processes are associated with genetic predisposition, gender, or other epigenetic/environmental factors will be examined. Furthermore, we also aim to characterize the relationship between symptoms of patients and metabolic alterations during acute infection and reconvalescence in more detail. All studies that intend to better understand the underlying pathomechanisms of pneumonia are welcome. Additionally, the long-term effects of pneumonia and their impact on patients’ quality of life will also be discussed. 

Dr. Katharina Kurz
Guest Editor

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Keywords

  • pneumonia
  • pathogens
  • immune activation
  • host
  • underlying pathomechanisms
  • diagnostics
  • therapy
  • long-term effects
  • symptoms

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Published Papers (3 papers)

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Research

13 pages, 1418 KiB  
Article
QuantiFERON® Monitor Test as a Potential Tool for Stratifying Patients by Infection Risk and Tailoring Follow-Up Care in Lung Transplant Recipients: A Single-Center Retrospective Experience
by Paolo Solidoro, Antonio Curtoni, Filippo Patrucco, Eleonora Russo, Francesca Sidoti, Giorgia Piccinini, Alessandro Bondi, Paolo Valesella, Mattia Genco, Massimo Boffini, Rocco Francesco Rinaldo and Cristina Costa
Microorganisms 2025, 13(2), 316; https://doi.org/10.3390/microorganisms13020316 - 1 Feb 2025
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Abstract
Background: Lung transplantation is a life-saving option for patients with end-stage respiratory diseases, but risk of infections remains critical for ensuring long-term organ function. This study aimed to assess immune recovery in lung transplant recipients by measuring IFN-γ levels using the QuantiFERON Monitor [...] Read more.
Background: Lung transplantation is a life-saving option for patients with end-stage respiratory diseases, but risk of infections remains critical for ensuring long-term organ function. This study aimed to assess immune recovery in lung transplant recipients by measuring IFN-γ levels using the QuantiFERON Monitor Test (QFM). Results were correlated with episodes of infection and organ rejection to explore the assay’s predictive potential. Methods: A retrospective study was conducted on 15 lung transplant recipients at the Lung Transplant Centre of Turin (Città della Salute e della Scienza di Torino, Italy) between December 2019 and January 2023. Patients were divided into a High Infection (HI) group (with >3 infections) and Low Infection (LI) group (with ≤3 infections). QFM assays were performed after 18 months post-transplant. Results: HI patients had lower QFM levels compared to LI (68.84 ± 21.98 vs. 380.54 ± 104.64 UI/mL, p = 0.033). A QFM value <89.5 UI/mL was associated with increased infection risk (p < 0.05). Patients with lower QFM levels also exhibited higher rates of MRSA bacteremia during hospitalization (50% HI vs. 0% LI, p = 0.04). No differences were observed in acute or chronic rejection rates, but LI patients showed more frequent alveolar neutrophilia at the fourth month post-transplant (0% HI vs. 55.5% LI, p = 0.04). Conclusion: lower QFM values were associated with higher infection risk, highlighting the assay’s potential for immune monitoring. In this study, a QFM value of 89.5 UI/mL showed good predictive accuracy for infections beyond 18 months. Further studies are needed to refine QFM’s role in post-transplant care. Full article
(This article belongs to the Special Issue Pneumonia: New Diagnostic and Therapeutic Options)
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13 pages, 3561 KiB  
Article
Establishment of a Mouse Model of Mycoplasma pneumoniae-Induced Plastic Bronchitis
by Peng Jin, Lin-Sheng Zhao, Tong-Qiang Zhang, Han Di and Wei Guo
Microorganisms 2024, 12(6), 1132; https://doi.org/10.3390/microorganisms12061132 - 1 Jun 2024
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Abstract
Plastic bronchitis (PB) constitutes a life-threatening pulmonary disorder, predominantly attributed to Mycoplasma pneumoniae (MP) infection. The pathogenic mechanisms involved remain largely unexplored, leading to the absence of reliable approaches for early diagnosis and clear treatment. Thus, the present investigation aimed to develop an [...] Read more.
Plastic bronchitis (PB) constitutes a life-threatening pulmonary disorder, predominantly attributed to Mycoplasma pneumoniae (MP) infection. The pathogenic mechanisms involved remain largely unexplored, leading to the absence of reliable approaches for early diagnosis and clear treatment. Thus, the present investigation aimed to develop an MP-induced mouse model of PB, thereby enhancing our understanding of this complex condition. In the first stage, healthy BALB/c mice were utilized to investigate the optimal methods for establishing PB. This involved the application of nebulization (15–20 min) and intratracheal administration (6–50 μL) with 2-chloroethyl ethyl sulfide (CEES) concentrations ranging from 4.5% to 7.5%. Subsequently, the MP model was induced by administering an MP solution (2 mL/kg/day, 108 CFU/50 μL) via the intranasal route for a duration of five consecutive days. Ultimately, suitable techniques were employed to induce plastic bronchitis in the MP model. Pathological changes in lung tissue were analyzed, and immunohistochemistry was employed to ascertain the expression levels of vascular endothelial growth factor receptor 3 (VEGFR-3) and the PI3K/AKT/mTOR signaling pathway. The administration of 4.5% CEES via a 6 µL trachea was the optimal approach to establishing a PB model. This method primarily induced neutrophilic inflammation and fibrinous exudate. The MP-infected group manifested symptoms indicative of respiratory infection, including erect hair, oral and nasal secretions, and a decrease in body weight. Furthermore, the pathological score of the MP+CEES group surpassed that of the groups treated with MP or CEES independently. Notably, the MP+CEES group demonstrated significant activation of the VEGFR-3 and PI3K/AKT/mTOR signaling pathways, implying a substantial involvement of lymphatic vessel impairment in this pathology. This study successfully established a mouse model of PB induced by MP using a two-step method. Lymphatic vessel impairment is a pivotal element in the pathogenetic mechanisms underlying this disease entity. This accomplishment will aid in further research into treatment methods for patients with PB caused by MP. Full article
(This article belongs to the Special Issue Pneumonia: New Diagnostic and Therapeutic Options)
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15 pages, 1505 KiB  
Article
CRP/Neopterin Ratio and Neuropsychiatric Symptoms in Patients with Different Forms of Pneumonia: Results of a Pilot Study
by Katharina Konstanze Lilly Wagner, Daniele Corda, Andreas Steinmayr, Francesco Burkert, Dietmar Fuchs, Johanna Gostner, Stefanie Hofer, Lucia Parrakova, Irina Gasslitter, Günter Weiss, Christian Irsara, Sarah Maier, Andrea Griesmacher, Rosa Bellmann-Weiler and Katharina Kurz
Microorganisms 2024, 12(6), 1099; https://doi.org/10.3390/microorganisms12061099 - 29 May 2024
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Abstract
Background: Pneumonia is one of the most common infectious diseases, mostly caused by viruses or bacteria. In response to bacteria or viruses which are different but which also are partly overlapping, innate and adaptive immune responses are induced, which can be quantified using [...] Read more.
Background: Pneumonia is one of the most common infectious diseases, mostly caused by viruses or bacteria. In response to bacteria or viruses which are different but which also are partly overlapping, innate and adaptive immune responses are induced, which can be quantified using the determination of specific biomarkers. Among these, C-reactive protein (CRP) has been established as a marker of innate immune function, whereas Neopterin, which is mainly produced upon stimulation with interferon-gamma, reflects cellular immune activation. Aim: We investigated inflammation markers in patients with microbiologically confirmed viral or bacterial pneumonia, and studied the potential of CRP, Neopterin, and the CRP/Neopterin ratio to distinguish between viral and bacterial pathogenesis. Furthermore, we examined, how often neuropsychiatric symptoms occur in patients suffering from different kinds of pneumonia. Patients and method: A total of 194 patients diagnosed with either coronavirus disease 2019 (COVID-19) (n = 63), bacterial pneumonia (n = 58), Influenza infection (n = 10), Influenza and a bacterial superinfection (n = 9), and COVID-19 patients with a bacterial superinfection (n = 54) were included in our pilot study. Clinical as well as laboratory parameters were determined shortly after admission. Results: We found significantly higher CRP/Neopterin ratios in patients with bacterial pneumonia (median: 0.34) and lower CRP/Neopterin ratios in patients hospitalized with COVID-19 infection (median: 0.03; p < 0.001). Both in men and in women, the CRP/Neopterin ratio was able to distinguish between viral and bacterial pathogens, but also was able to detect bacterial super-infection (BSI) in subjects with initial viral pneumonia (p < 0.001). Patients with BSI presented with significantly lower CRP/Neopterin ratios (median 0.08) than patients with bacterial infection only (median 0.34; p < 0.001). Interestingly, COVID-19 patients had a decreased physical functioning (as reflected in the ECOG score) and a higher frequency of fatigue (84.1%) and neurological symptoms (54.8%) than patients with pneumonia, due to other underlying pathogens. Patients that reported fatigue during viral and bacterial pneumonia presented with lower CRP concentrations than patients without it. Conclusions: The CRP/Neopterin ratio is useful to differentiate between viral and bacterial pathogenesis. The occurrence of neuropsychiatric symptoms in pneumonia appears to depend on the kind of pathogen causing the infection. Lower CRP concentrations at admission appear to be related to fatigue during acute viral and bacterial infection. Full article
(This article belongs to the Special Issue Pneumonia: New Diagnostic and Therapeutic Options)
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