scholarly journals The Role of QuantiFERON-TB Gold Plus in Mycobacterium Tuberculosis Detection in a Severe HIV Immunocompromised Patient—Case Report

Pathogens ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1523
Author(s):  
Florentina Dumitrescu ◽  
Cătălina-Gabriela Pisoschi ◽  
Vlad Pădureanu ◽  
Andreea Cristina Stoian ◽  
Livia Dragonu ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Immunocompromised Patient ◽  
Symptomatic Treatment ◽  
Pneumocystis Pneumonia ◽  
Hiv Positive ◽  
Patient Case ◽  
Mycobacterium Tuberculosis Infection ◽  
Antituberculosis Therapy ◽  
Antituberculosis Treatment

Tuberculosis (TB) is an important opportunistic infection in HIV-positive people. We are reporting a case of a 31-year-old HIV-infected patient who was hospitalized in July 2021 for dyspnea, cough with mucopurulent sputum and asthenia. He was confirmed to have Serratia liquefaciens pneumonia and acute respiratory failure. The evolution was unfavorable despite the antibiotic, pathogenic and symptomatic treatment. Because the patient had severe immunosuppression (CD4 count = 37 cell/mm3), we used QuantiFERON-TB Gold Plus for the detection of the Mycobacterium tuberculosis infection. The antituberculosis therapy was initiated, which resulted in a significant improvement of the general condition and the patient was discharged with the recommendation to continue antiretroviral therapy, antituberculosis treatment and Trimethoprim/Sulfamethoxazole—single tablet daily for the prophylaxis of Pneumocystis pneumonia.

scholarly journals Obesity-Induced Dysbiosis Exacerbates IFN-γ Production and Pulmonary Inflammation in the Mycobacterium tuberculosis Infection

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1732
Author(s):  
Sandra Patricia Palma Albornoz ◽  
Thais Fernanda de Campos Fraga-Silva ◽  
Ana Flávia Gembre ◽  
Rômulo Silva de Oliveira ◽  
Fernanda Mesquita de Souza ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Gut Microbiota ◽  
Inflammatory Diseases ◽  
Pulmonary Inflammation ◽  
Host Susceptibility ◽  
Chronic Infections ◽  
Mycobacterium Tuberculosis Infection ◽  
Pulmonary Damage ◽  
Ifn Γ

The microbiota of the gut–lung axis affects local and far-reaching immune responses and might also trigger chronic and inflammatory diseases. We hypothesized that gut dysbiosis induced by obesity, which coexists in countries with a high tuberculosis burden, aggravates the host susceptibility and the pulmonary damage tolerance. To assess our hypothesis, we used a model of high-fat diet (HFD)-induced obesity, followed by infection of C57BL/6 mice with Mycobacterium tuberculosis. We showed that obesity increased the susceptibility, the pulmonary inflammation and IFN-γ levels in M. tuberculosis-infected mice. During the comorbidity obesity and tuberculosis, there is an increase of Bacteroidetes and Firmicutes in the lungs, and an increase of Firmicutes and butyrate in the feces. Depletion of gut microbiota by antibiotic treatment in the obese infected mice reduced the frequencies of CD4+IFN-γ+IL-17− cells and IFN-γ levels in the lungs, associated with an increase of Lactobacillus. Our findings reinforce the role of the gut–lung axis in chronic infections and suggest that the gut microbiota modulation may be a potential host-directed therapy as an adjuvant to treat TB in the context of IFN-γ-mediated immunopathology.

scholarly journals Alveolar Epithelial Cells in Mycobacterium tuberculosis Infection: Active Players or Innocent Bystanders?

2015 ◽  
Vol 8 (1) ◽  
pp. 3-14 ◽  
Author(s):  
Julia M. Scordo ◽  
Daren L. Knoell ◽  
Jordi B. Torrelles
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial Cells ◽  
Mycobacterium Tuberculosis Infection ◽  
Alveolar Epithelial ◽  
Immune Balance ◽  
Global Threat ◽  
Cell Crosstalk

Tuberculosis (TB) is a disease that kills one person every 18 s. TB remains a global threat due to the emergence of drug-resistant Mycobacterium tuberculosis (M.tb) strains and the lack of an efficient vaccine. The ability of M.tb to persist in latency, evade recognition following seroconversion, and establish resistance in vulnerable populations warrants closer examination. Past and current research has primarily focused on examination of the role of alveolar macrophages and dendritic cells during M.tb infection, which are critical in the establishment of the host response during infection. However, emerging evidence indicates that the alveolar epithelium is a harbor for M.tb and critical during progression to active disease. Here we evaluate the relatively unexplored role of the alveolar epithelium as a reservoir and also its capacity to secrete soluble mediators upon M.tb exposure, which influence the extent of infection. We further discuss how the M.tb-alveolar epithelium interaction instigates cell-to-cell crosstalk that regulates the immune balance between a proinflammatory and an immunoregulatory state, thereby prohibiting or allowing the establishment of infection. We propose that consideration of alveolar epithelia provides a more comprehensive understanding of the lung environment in vivo in the context of host defense against M.tb.

scholarly journals MAIT cell-directed therapy of Mycobacterium tuberculosis infection

2020 ◽  
Vol 14 (1) ◽  
pp. 199-208 ◽  
Author(s):  
Shunsuke Sakai ◽  
Keith D. Kauffman ◽  
Sangmi Oh ◽  
Christine E. Nelson ◽  
Clifton E. Barry ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
Cd4 T Cell ◽  
Mycobacterium Tuberculosis Infection ◽  
Mait Cells ◽  
T Cell Priming ◽  
Draining Lymph Nodes ◽  
Mait Cell

AbstractMucosal-associated invariant T (MAIT) cells are potential targets of vaccination and host-directed therapeutics for tuberculosis, but the role of MAIT cells during Mycobacterium tuberculosis (Mtb) infection in vivo is not well understood. Here we find that following Mtb infection MAIT cells mount minimal responses, and MAIT cell-deficient MR1−/− mice display normal survival. Preinfection expansion of MAIT cells through 5-OP-RU vaccination fails to protect against subsequent Mtb challenge. In fact, 5-OP-RU vaccination delays Mtb-specific CD4 T cell priming in lung-draining lymph nodes, and conversely MR1 deficiency or blockade accelerates T cell priming. The MAIT cell-mediated delay in T cell priming is partly dependent on TGF-β. Surprisingly, 5-OP-RU treatment during chronic infection drives MAIT cell expansion and an IL-17A-dependent reduction in bacterial loads. Thus, during early infection MAIT cells directly contribute to the notoriously slow priming of CD4 T cells, but later during infection MAIT cell stimulation may be an effective host-directed therapy for tuberculosis.

scholarly journals Acute inflammation, mediated by lung neutrophils, confers enhanced protection against Mycobacterium tuberculosis infection in mice

2021 ◽  
Author(s):  
Tucker J. Piergallini ◽  
Julia M. Scordo ◽  
Paula A. Pino ◽  
Jordi B. Torrelles ◽  
Joanne Turner
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Acute Inflammation ◽  
Mycobacterium Tuberculosis Infection ◽  
Positive Role ◽  
Innate Capacity ◽  
Time Of Infection ◽  
Lps Treatment ◽  
Partial Depletion

AbstractInflammation plays a crucial role in the control of Mycobacterium tuberculosis (M.tb) infection. In this study, we demonstrate that an inflammatory pulmonary environment at the time of infection mediated by liposaccharide (LPS) treatment in mice confers enhanced protection against M.tb for up to 6 months post infection. This transient protective inflammatory environment was associated with a neutrophil and monocyte/macrophage influx as well as increased inflammatory cytokines. In vitro infection of neutrophils from LPS treated mice demonstrated that LPS neutrophils exhibited increased recognition of M.tb, and had a greater innate capacity for killing M.tb. Finally, partial depletion of neutrophils in LPS treated mice showed an increase in M.tb burden, suggesting neutrophils conferred the enhanced protection observed in LPS treated mice. These results indicate a positive role of an inflammatory environment during initial M.tb infection, and suggests that acute inflammation at the time of M.tb infection can positively alter disease outcome.

GPR183 regulates interferons and bacterial growth during Mycobacterium tuberculosis infection: interaction with type 2 diabetes and TB disease severity

2020 ◽  
Author(s):  
Stacey Bartlett ◽  
Adrian Tandhyka Gemiarto ◽  
Minh Dao Ngo ◽  
Haressh Sajiir ◽  
Semira Hailu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Mycobacterium Tuberculosis ◽  
Disease Severity ◽  
Mycobacterial Infection ◽  
Mycobacterium Tuberculosis Infection ◽  
Important Regulator ◽  
Chest X Ray ◽  
Mycobacterial Growth

AbstractOxidized cholesterols have emerged as important signaling molecules of immune function, but little is known about the role of these oxysterols during mycobacterial infections. We found that expression of the oxysterol-receptor GPR183 was reduced in blood from patients with tuberculosis (TB) and type 2 diabetes (T2D) compared to TB patients without T2D and was associated with TB disease severity on chest x-ray. GPR183 activation by 7α,25-hydroxycholesterol (7α,25-OHC) reduced growth of Mycobacterium tuberculosis (Mtb) and Mycobacterium bovis BCG in primary human monocytes, an effect abrogated by the GPR183 antagonist GSK682753. Growth inhibition was associated with reduced IFN-β and IL-10 expression and enhanced autophagy. Mice lacking GPR183 had significantly increased lung Mtb burden and dysregulated IFNs during early infection. Together, our data demonstrate that GPR183 is an important regulator of intracellular mycobacterial growth and interferons during mycobacterial infection.Graphical Abstract

Sign in / Sign up

Export Citation Format

Share Document