Статті в журналах: "Mybacterium tuberculosis - Inflammatory Response"

1

Friedland, Jon S. "Targeting the Inflammatory Response in Tuberculosis." New England Journal of Medicine 371, no. 14 (October 2, 2014): 1354–56. http://dx.doi.org/10.1056/nejmcibr1408663.

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2

Radović, Milan, Tatjana Pejčić, Ivana Stanković, Lidija Ristić, Milan Rančić, and Zorica Ćirić. "Acute–Phase Inflammatory Response in Patients with Pulmonary Tuberculosis." Acta Facultatis Medicae Naissensis 31, no. 3 (September 1, 2014): 183–91. http://dx.doi.org/10.2478/afmnai-2014-0023.

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Summary The main issue in patients with pulmonary tuberculosis (PTB) represents the impossibility of the host immune response to express bactericidal function and the sterilization of lesions depends exclusively on the specific antimicrobial chemotherapy. In order to investigate the value of acute-phase inflammatory response markers in patients with newly confirmed extensive PTB, there was designed a clinical study with 80 patients, of whom 40 had active disease (experimental group), while other 40 had inactive sequellar disease without comorbidity (control group). The examined groups were homogenous with respect to the patient’s general demographic characteristics. In the experimental group, 20.0% of the patients had an initial bacterial infection of the lower respiratory tract, while their average value of acute-phase systemic inflammatory markers was initially, before the antituberculosis treatment, significantly elevated compared to the control group. At the end of the treatment, values of erythrocyte sedimentation rate in the first hour (SE) and serum C-reactive protein (CRP) significantly decreased (SE-p <0.001, CRP-p<0.001), together with the value of the leukocyte count (Le) and serum fibrinogen (Le-p<0.001, fibrinogen-p<0.001). Multivariate linear regression analysis proved a significant correlation between baseline serum fibrinogen level with positive history of contact with active TB patient and initial radiological extent of PTB lung lesions. The values of the acute-phase inflammatory response markers in active PTB have its clinical significance in the assessment of unfavourable course of disease in extensive disseminated form of PTB as well as in the occurrence of complications associated with low respiratory tract bacterial superinfection.

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3

Bickett, Thomas E., and Sana D. Karam. "Tuberculosis–Cancer Parallels in Immune Response Regulation." International Journal of Molecular Sciences 21, no. 17 (August 26, 2020): 6136. http://dx.doi.org/10.3390/ijms21176136.

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Mycobacterium tuberculosis and cancer are two diseases with proclivity for the development of resistance to the host immune system. Mechanisms behind resistance can be host derived or disease mediated, but they usually depend on the balance of pro-inflammatory to anti-inflammatory immune signals. Immunotherapies have been the focus of efforts to shift that balance and drive the response required for diseases eradication. The immune response to tuberculosis has widely been thought to be T cell dependent, with the majority of research focused on T cell responses. However, the past decade has seen greater recognition of the importance of the innate immune response, highlighting factors such as trained innate immunity and macrophage polarization to mycobacterial clearance. At the same time, there has been a renaissance of immunotherapy treatments for cancer since the first checkpoint inhibitor passed clinical trials, in addition to work highlighting the importance of innate immune responses to cancer. However, there is still much to learn about host-derived responses and the development of resistance to new cancer therapies. This review examines the similarities between the immune responses to cancer and tuberculosis with the hope that their commonalities will facilitate research collaboration and discovery.

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4

Gold, Jeffrey A., Yoshihiko Hoshino, Naohiko Tanaka, William N. Rom, Bindu Raju, Rany Condos, and Michael D. Weiden. "Surfactant Protein A Modulates the Inflammatory Response in Macrophages during Tuberculosis." Infection and Immunity 72, no. 2 (February 2004): 645–50. http://dx.doi.org/10.1128/iai.72.2.645-650.2004.

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ABSTRACT Tuberculosis leads to immune activation and increased human immunodeficiency virus type 1 (HIV-1) replication in the lung. However, in vitro models of mycobacterial infection of human macrophages do not fully reproduce these in vivo observations, suggesting that there are additional host factors. Surfactant protein A (SP-A) is an important mediator of innate immunity in the lung. SP-A levels were assayed in the human lung by using bronchoalveolar lavage (BAL). There was a threefold reduction in SP-A levels during tuberculosis only in the radiographically involved lung segments, and the levels returned to normal after 1 month of treatment. The SP-A levels were inversely correlated with the percentage of neutrophils in BAL fluid, suggesting that low SP-A levels were associated with increased inflammation in the lung. Differentiated THP-1 macrophages were used to test the effect of decreasing SP-A levels on immune function. In the absence of infection with Mycobacterium tuberculosis, SP-A at doses ranging from 5 to 0.01 μg/ml inhibited both interleukin-6 (IL-6) production and HIV-1 long terminal repeat (LTR) activity. In macrophages infected with M. tuberculosis, SP-A augmented both IL-6 production and HIV-1 LTR activity. To better understand the effect of SP-A, we measured expression of CAAT/enhancer binding protein beta (C/EBPβ), a transcription factor central to the regulation of IL-6 and the HIV-1 LTR. In macrophages infected with M. tuberculosis, SP-A reduced expression of a dominant negative isoform of C/EBPβ. These data suggest that SP-A has pleiotropic effects even at the low concentrations found in tuberculosis patients. This protein augments inflammation in the presence of infection and inhibits inflammation in uninfected macrophages, protecting uninvolved lung segments from the deleterious effects of inflammation.

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Valentin, Leonardo, Andrew DiNardo, Elizabeth Chiao, Laila Woc-Colburn, and Arun Nachiappan. "Case Report: Tuberculosis IRIS : a mediastinal problem." F1000Research 2 (February 18, 2013): 54. http://dx.doi.org/10.12688/f1000research.2-54.v1.

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We present a case of a 39-year-old male patient with Acquired Immune Deficiency Syndrome (AIDS) who developed Mycobacterium tuberculosis related Immune Reconstitution Inflammatory Syndrome (IRIS) after initiation of Highly Active Antiretroviral Therapy (HAART) treatment. The inflammatory response resulted in mediastinal necrotic lymphadenopathy and subsequent perforation of the esophageal wall.

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Valentin, Leonardo, Andrew DiNardo, Elizabeth Chiao, Laila Woc-Colburn, and Arun Nachiappan. "Case Report: Tuberculosis IRIS: a mediastinal problem." F1000Research 2 (August 7, 2013): 54. http://dx.doi.org/10.12688/f1000research.2-54.v2.

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We present a case of a 39-year-old male patient with Acquired Immune Deficiency Syndrome (AIDS) who developed Mycobacterium tuberculosis related Immune Reconstitution Inflammatory Syndrome (IRIS) after initiation of Highly Active Antiretroviral Therapy (HAART) treatment. The inflammatory response resulted in mediastinal necrotic lymphadenopathy and subsequent perforation of the esophageal wall.

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Muller, Beatriz Lima Alezio, Daniela Maria de Paula Ramalho, Paula Fernanda Gonçalves dos Santos, Eliene Denites Duarte Mesquita, Afranio Lineu Kritski, and Martha Maria Oliveira. "Inflammatory and immunogenetic markers in correlation with pulmonary tuberculosis." Jornal Brasileiro de Pneumologia 39, no. 6 (December 2013): 719–27. http://dx.doi.org/10.1590/s1806-37132013000600011.

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OBJECTIVE: To describe serum levels of the cytokines IL-10, TNF-α, and IFN-γ, as well as polymorphisms in the genes involved in their transcription, and their association with markers of the acute inflammatory response in patients with pulmonary tuberculosis.METHODS: This was a descriptive, longitudinal study involving 81 patients with pulmonary tuberculosis treated at two referral hospitals. We collected data on sociodemographic variables and evaluated bacteriological conversion at the eighth week of antituberculosis treatment, gene polymorphisms related to the cytokines studied, and serum levels of those cytokines, as well as those of C-reactive protein (CRP). We also determined the ESR and CD4+ counts.RESULTS: The median age of the patients was 43 years; 67 patients (82.7%) were male; and 8 patients (9.9%) were infected with HIV. The ESR was highest in the patients with high IFN-γ levels and low IL-10 levels. IFN-γ and TNF-α gene polymorphisms at positions +874 and −238, respectively, showed no correlations with the corresponding cytokine serum levels. Low IL-10 levels were associated with IL-10 gene polymorphisms at positions −592 and −819 (but not −1082). There was a negative association between bacteriological conversion at the eighth week of treatment and CRP levels.CONCLUSIONS: Our results suggest that genetic markers and markers of acute inflammatory response are useful in predicting the response to antituberculosis treatment.

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8

Kolchin, Dmitriy, Yuliya Degtyareva, Viktor Ruzov, Baymurat Asanov, and Oleg Prokhorov. "PLATELET AGGREGATION IN PATIENTS WITH PULMONARY TUBERCULOSIS AND SYSTEMIC INFLAMMATORY RESPONSE SYNDROME." Ulyanovsk Medico-biological Journal, no. 1 (April 20, 2022): 29–38. http://dx.doi.org/10.34014/2227-1848-2022-1-29-38.

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Platelets play a special role in the systemic inflammatory response syndrome, as they acquire the ability to become activated and aggregate. Literature has no direct evidence of a link between platelet aggregation activity and the severity of the systemic inflammatory response syndrome in patients with pulmonary tuberculosis. The aim of the paper is to study platelet aggregation in patients with pulmonary tuberculosis with severe systemic inflammatory response syndrome. Materials and Methods. Spontaneous and induced by ADP (0.1, 1.0 and 5.0 ml) platelet aggregation was determined by Born turbodynamic method. The study enrolled 27 patients with severe and 33 patients with indolent systemic inflammatory response syndrome Spontaneous and induced by ADP (0.1 and 1.0 ml) platelet aggregation was evaluated in absorbance units (a.u.); platelet aggregation induced by 5.0 ml of ADP was measured in percentage terms. Statistica 10 was used to process the results. Discrepancy tests were used to determine the significance of differences of mean values; McNemar’s test and Fisher’s exact test were used to estimate event rate, p<0.05. Results. In Group 1 spontaneous and induced by ADP (0.1, 1.0 and 5 ml) platelet aggregation was 0.85–2.65 (1.210.1) a.u., 0.81–3.67 (3.030.38) a.u., 1.06–6.25 (6.50.51) a.u., 5–66 % (39.53.6); in Group 2 – 0.84–1.36 (1.10.04) a.u., 0.77–2.49 (2.10.26) a.u., 0.64–5.49 (2.200.08) a.u., 8–66 (35.74.14) %, respectively. Frequency of spontaneous and induced by ADP (0.1, 1.0 and 5 ml) platelet hypoaggregation in Groups 1 and 2 was 33.3 % and 27.3 %; 14.8 % and 24.2 %; 0 % and 39.4 %; 14.8 % and 24.2 %, respectively; frequency of hyperaggregation was 14.8 % and 0 %; 11.1 % and 9.1 %; 29.6 % and 0 %; 0 % and 0 %, respectively. Conclusion. Platelet aggregation activity in patients with pulmonary tuberculosis is determined by the severity of the systemic inflammatory response syndrome. A pronounced systemic inflammatory response syndrome is associated with increased spontaneous and induced by ADP (1.0 ml) platelet aggregation in 14.8 % and 29.6 % of cases, respectively.

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9

van Crevel, Reinout, Tom H. M. Ottenhoff, and Jos W. M. van der Meer. "Innate Immunity to Mycobacterium tuberculosis." Clinical Microbiology Reviews 15, no. 2 (April 2002): 294–309. http://dx.doi.org/10.1128/cmr.15.2.294-309.2002.

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SUMMARY The different manifestations of infection with Mycobacterium tuberculosis reflect the balance between the bacillus and host defense mechanisms. Traditionally, protective immunity to tuberculosis has been ascribed to T-cell-mediated immunity, with CD4+ T cells playing a crucial role. Recent immunological and genetic studies support the long-standing notion that innate immunity is also relevant in tuberculosis. In this review, emphasis is on these natural, innate host defense mechanisms, referring to experimental data (e.g., studies in gene knockout mice) and epidemiological, immunological, and genetic studies in human tuberculosis. The first step in the innate host defense is cellular uptake of M. tuberculosis, which involves different cellular receptors and humoral factors. Toll-like receptors seem to play a crucial role in immune recognition of M. tuberculosis, which is the next step. The subsequent inflammatory response is regulated by production of pro- and anti-inflammatory cytokines and chemokines. Different natural effector mechanisms for killing of M. tuberculosis have now been identified. Finally, the innate host response is necessary for induction of adaptive immunity to M. tuberculosis. These basic mechanisms augment our understanding of disease pathogenesis and clinical course and will be of help in designing adjunctive treatment strategies.

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10

Lin, Yuanguang, Ming Zhang, and Peter F. Barnes. "Chemokine Production by a Human Alveolar Epithelial Cell Line in Response to Mycobacterium tuberculosis." Infection and Immunity 66, no. 3 (March 1, 1998): 1121–26. http://dx.doi.org/10.1128/iai.66.3.1121-1126.1998.

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ABSTRACT To investigate the role of chemokines during the initial local response to Mycobacterium tuberculosis in the human lung, we studied chemokine production by the human alveolar epithelial cell line A549 after infection with M. tuberculosis. M. tuberculosis-infected A549 cells produced mRNAs and protein for monocyte chemotactic protein-1 (MCP-1) and interleukin-8 (IL-8) but not mRNAs for macrophage inflammatory protein 1α (MIP-1α), MIP-1β, and RANTES. Chemokine production in response to M. tuberculosis was not dependent on production of tumor necrosis factor alpha, IL-1β, or IL-6. Two virulent clinical M. tuberculosis isolates, the virulent laboratory strain H37Rv, and the avirulent strain H37Ra elicited production of comparable concentrations of MCP-1 and IL-8, whereas killed M. tuberculosis and three Mycobacterium avium strains did not. The three virulent M. tuberculosis strains grew more rapidly than the avirulent M. tuberculosisstrain in the alveolar epithelial cell line, and the threeM. avium strains did not grow intracellularly. These findings suggest that intracellular growth is necessary for mycobacteria to elicit production of MCP-1 and IL-8 by alveolar epithelial cells but that virulence and the rate of intracellular growth do not correlate with chemokine production. Alveolar epithelial cells may contribute to the local inflammatory response in human tuberculosis by producing chemokines which attract monocytes, lymphocytes, and polymorphonuclear cells.

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Alcantara, Cheldon Ann, Ira Glassman, Kevin H. Nguyen, Arpitha Parthasarathy, and Vishwanath Venketaraman. "Neutrophils in Mycobacterium tuberculosis." Vaccines 11, no. 3 (March 12, 2023): 631. http://dx.doi.org/10.3390/vaccines11030631.

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Mycobacterium tuberculosis (M. tb) continues to be a leading cause of mortality within developing countries. The BCG vaccine to promote immunity against M. tb is widely used in developing countries and only in specific circumstances within the United States. However, current the literature reports equivocal data on the efficacy of the BCG vaccine. Critical within their role in the innate immune response, neutrophils serve as one of the first responders to infectious pathogens such as M. tb. Neutrophils promote effective clearance of M. tb through processes such as phagocytosis and the secretion of destructive granules. During the adaptative immune response, neutrophils modulate communication with lymphocytes to promote a strong pro-inflammatory response and to mediate the containment M. tb through the production of granulomas. In this review, we aim to highlight and summarize the role of neutrophils during an M. tb infection. Furthermore, the authors emphasize the need for more studies to be conducted on effective vaccination against M. tb.

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12

Belyaeva, E. N., M. E. Dyakova, D. S. Esmedlyaeva, N. V. Sapozhnikova, and A. A. Starshinova. "MARKERS OF INFLAMMATORY RESPONSE IN PATIENTS WITH DRUG RESISTANCE OF MYCOBACTERIUM TUBERCULOSIS." Journal Infectology 9, no. 4 (January 1, 2017): 31–36. http://dx.doi.org/10.22625/2072-6732-2017-9-4-31-36.

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13

Choi, Rihwa, Kyunga Kim, Min-Ji Kim, Su-Young Kim, O. Jung Kwon, Kyeongman Jeon, Hye Yun Park, et al. "Serum inflammatory profiles in pulmonary tuberculosis and their association with treatment response." Journal of Proteomics 149 (October 2016): 23–30. http://dx.doi.org/10.1016/j.jprot.2016.06.016.

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Harishankar, M., K. Afsal, V. V. Banurekha, N. Meenakshi, and P. Selvaraj. "1,25-Dihydroxy vitamin D3 downregulates pro-inflammatory cytokine response in pulmonary tuberculosis." International Immunopharmacology 23, no. 1 (November 2014): 148–52. http://dx.doi.org/10.1016/j.intimp.2014.08.021.

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Weijer, Sebastiaan, Catharina W. Wieland, Sandrine Florquin, and Tom van der Poll. "A thrombomodulin mutation that impairs activated protein C generation results in uncontrolled lung inflammation during murine tuberculosis." Blood 106, no. 8 (October 15, 2005): 2761–68. http://dx.doi.org/10.1182/blood-2004-12-4623.

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AbstractThrombomodulin (TM) plays an essential role in the generation of activated protein C (APC), a mediator with both anticoagulant and anti-inflammatory properties, and is preferentially expressed in lungs. To investigate the role of TM in the coagulant and inflammatory response in the lung during tuberculosis, mice with a mutation in the TM gene (Thbd), which results in a minimal capacity for APC generation (TMpro/pro mice), were intranasally infected with live virulent Mycobacterium tuberculosis. Whereas pulmonary tuberculosis was not associated with activation of coagulation in either wild-type or TMpro/pro mice, 5 weeks after infection TMpro/pro mice displayed an uncontrolled inflammatory response in their lungs, as reflected by higher lung weights, a diminished ability to form well-shaped granulomas, elevated levels of proinflammatory cytokines, and concurrently reduced concentrations of anti-inflammatory cytokines. During a 36-week follow-up after infection with a lower dose of M tuberculosis, 35% of TMpro/pro mice died from week 28 onward versus none of the wild-type mice, and the surviving TMpro/pro mice displayed increased lung inflammation accompanied by higher mycobacterial loads in liver and spleen. These data suggest that a TM mutation that impairs APC generation results in uncontrolled lung inflammation during tuberculosis.

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Ravesloot-Chávez, Mariëtta M., Erik Van Dis, and Sarah A. Stanley. "The Innate Immune Response to Mycobacterium tuberculosis Infection." Annual Review of Immunology 39, no. 1 (April 26, 2021): 611–37. http://dx.doi.org/10.1146/annurev-immunol-093019-010426.

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Infection with Mycobacterium tuberculosis causes >1.5 million deaths worldwide annually. Innate immune cells are the first to encounter M. tuberculosis, and their response dictates the course of infection. Dendritic cells (DCs) activate the adaptive response and determine its characteristics. Macrophages are responsible both for exerting cell-intrinsic antimicrobial control and for initiating and maintaining inflammation. The inflammatory response to M. tuberculosis infection is a double-edged sword. While cytokines such as TNF-α and IL-1 are important for protection, either excessive or insufficient cytokine production results in progressive disease. Furthermore, neutrophils—cells normally associated with control of bacterial infection—are emerging as key drivers of a hyperinflammatory response that results in host mortality. The roles of other innate cells, including natural killer cells and innate-like T cells, remain enigmatic. Understanding the nuances of both cell-intrinsic control of infection and regulation of inflammation will be crucial for the successful development of host-targeted therapeutics and vaccines.

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Poladian, Nicole, Davit Orujyan, William Narinyan, Armani K. Oganyan, Inesa Navasardyan, Prathosh Velpuri, Abraham Chorbajian та Vishwanath Venketaraman. "Role of NF-κB during Mycobacterium tuberculosis Infection". International Journal of Molecular Sciences 24, № 2 (16 січня 2023): 1772. http://dx.doi.org/10.3390/ijms24021772.

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Mycobacterium tuberculosis (M. tb) causes tuberculosis infection in humans worldwide, especially among immunocompromised populations and areas of the world with insufficient funding for tuberculosis treatment. Specifically, M. tb is predominantly exhibited as a latent infection, which poses a greater risk of reactivation for infected individuals. It has been previously shown that M. tb infection requires pro-inflammatory and anti-inflammatory mediators to manage its associated granuloma formation via tumor necrosis factor-α (TNF-α), interleukin-12 (IL-12), interferon-γ (IFN-γ), and caseum formation via IL-10, respectively. Nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) has been found to play a unique mediator role in providing a pro-inflammatory response to chronic inflammatory disease processes by promoting the activation of macrophages and the release of various cytokines such as IL-1, IL-6, IL-12, and TNF-α. NF-κB’s role is especially interesting in its mechanism of assisting the immune system’s defense against M. tb, wherein NF-κB induces IL-2 receptors (IL-2R) to decrease the immune response, but has also been shown to crucially assist in keeping a granuloma and bacterial load contained. In order to understand NF-κB’s role in reducing M. tb infection, within this literature review we will discuss the dynamic interaction between M. tb and NF-κB, with a focus on the intracellular signaling pathways and the possible side effects of NF-κB inactivation on M. tb infection. Through a thorough review of these interactions, this review aims to highlight the role of NF-κB in M. tb infection for the purpose of better understanding the complex immune response to M. tb infection and to uncover further potential therapeutic methods.

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Lin, YuanGuang, JianHua Gong, Ming Zhang, Wanfen Xue, and Peter F. Barnes. "Production of Monocyte Chemoattractant Protein 1 in Tuberculosis Patients." Infection and Immunity 66, no. 5 (May 1, 1998): 2319–22. http://dx.doi.org/10.1128/iai.66.5.2319-2322.1998.

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ABSTRACT To investigate the role of monocyte chemoattractant protein 1 (MCP-1) in the immune response to Mycobacterium tuberculosis, we studied MCP-1 production in tuberculosis patients. CD14+ blood monocytes from tuberculosis patients spontaneously expressed higher levels of MCP-1 mRNA and protein than CD14+ monocytes from healthy tuberculin reactors. MCP-1 production in lymph nodes from tuberculosis patients was also markedly increased. These findings suggest that MCP-1 can contribute to the antimycobacterial inflammatory response by attracting monocytes and T lymphocytes.

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Torres-Juarez, Flor, Albertina Cardenas-Vargas, Alejandra Montoya-Rosales, Irma González-Curiel, Mariana H. Garcia-Hernandez, Jose A. Enciso-Moreno, Robert E. W. Hancock, and Bruno Rivas-Santiago. "LL-37 Immunomodulatory Activity during Mycobacterium tuberculosis Infection in Macrophages." Infection and Immunity 83, no. 12 (September 8, 2015): 4495–503. http://dx.doi.org/10.1128/iai.00936-15.

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Tuberculosis is one of the most important infectious diseases worldwide. The susceptibility to this disease depends to a great extent on the innate immune response against mycobacteria. Host defense peptides (HDP) are one of the first barriers to counteract infection. Cathelicidin (LL-37) is an HDP that has many immunomodulatory effects besides its weak antimicrobial activity. Despite advances in the study of the innate immune response in tuberculosis, the immunological role of LL-37 duringM. tuberculosisinfection has not been clarified. Monocyte-derived macrophages were infected withM. tuberculosisstrain H37Rv and then treated with 1, 5, or 15 μg/ml of exogenous LL-37 for 4, 8, and 24 h. Exogenous LL-37 decreased tumor necrosis factor alpha (TNF-α) and interleukin-17 (IL-17) while inducing anti-inflammatory IL-10 and transforming growth factor β (TGF-β) production. Interestingly, the decreased production of anti-inflammatory cytokines did not reduce antimycobacterial activity. These results are consistent with the concept that LL-37 can modulate the expression of cytokines during mycobacterial infection and this activity was independent of the P2X7 receptor. Thus, LL-37 modulates the response of macrophages during infection, controlling the expression of proinflammatory and anti-inflammatory cytokines.

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Xu, Guangxian, Hao Jia, Yong Li, Xiaoming Liu, Min Li, and Yujiong Wang. "Hemolytic phospholipaseRv0183of Mycobacterium tuberculosis induces inflammatory response and apoptosis in alveolar macrophage RAW264.7 cells." Canadian Journal of Microbiology 56, no. 11 (November 2010): 916–24. http://dx.doi.org/10.1139/w10-079.

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The metabolic pathway of phospholipids is one of the most important physiologic pathways in Mycobacterium tuberculosis , a typical intracellular bacterium. The hemolytic phospholipase lip gene (Rv0183) is one of 24 phospholipase genes that have been demonstrated to play critical roles in the metabolism of phospholipids in M. tuberculosis. Quantitative RT–PCR and flow cytometry were used to elucidate the immunological and pathogenic implications of the Rv0183 gene on the inflammatory response following persistent expression of Rv0183 in mouse alveolar macrophage RAW264.7 cells. Our results demonstrate that a time-course-dependent ectopic expression of Rv0183 significantly elevated the expression of IL-6, NF-κB, TLR-2, TLR-6, TNFα, and MyD88 in these alveolar macrophage cells. Furthermore, the persistent expression of Rv0183 induced RAW264.7 cell apoptosis in vitro. These findings demonstrate that the expression of Rv0183 induces an inflammatory response and cell apoptosis in the host cells, suggesting that Rv0183 may play an important role in the virulence and pathogenesis of M. tuberculosis infection.

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Zhang, Qingwen, Xinru Jiang, Weigang He, Kailin Wei, Jinxia Sun, Xiangyang Qin, Yuejuan Zheng та Xin Jiang. "MCL Plays an Anti-Inflammatory Role inMycobacterium tuberculosis-Induced Immune Response by Inhibiting NF-κB and NLRP3 Inflammasome Activation". Mediators of Inflammation 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/2432904.

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Mycobacterium tuberculosis(Mtb) remains a significant menace to global health as it induces granulomatous lung lesions and systemic inflammatory responses during active tuberculosis (TB). Micheliolide (MCL), a sesquiterpene lactone, was recently reported to have a function of relieving LPS-induced inflammatory response, but the regulative role of MCL on the immunopathology of TB still remains unknown. In this experiment, we examined the inhibitory effect of MCL on Mtb-induced inflammatory response in mouse macrophage-like cell line Raw264.7 by downregulating the activation of nuclear factor kappa B (NF-κB) and NLRP3 inflammasome. Evidences showed that MCL decreased the secretion of Mtb-induced inflammatory cytokines (IL-1βand TNF-α) in a dose-dependent manner. Meanwhile, MCL dramatically suppressed Mtb-induced activation of iNOS and COX2 as well as subsequent production of NO. Furthermore, MCL inhibited Mtb-induced phosphorylation of Akt (Ser 473) in Raw264.7. According to our results, MCL plays an important role in modulating Mtb-induced inflammatory response through PI3K/Akt/NF-κB pathway and subsequently downregulating the activation of NLRP3 inflammasome. Therefore, MCL may represent as a potential drug candidate in the adjuvant treatment of TB by regulating host immune response.

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Di Liberto, Diana, Massimo Locati, Nadia Caccamo, Annunciata Vecchi, Serena Meraviglia, Alfredo Salerno, Guido Sireci, et al. "Role of the chemokine decoy receptor D6 in balancing inflammation, immune activation, and antimicrobial resistance in Mycobacterium tuberculosis infection." Journal of Experimental Medicine 205, no. 9 (August 11, 2008): 2075–84. http://dx.doi.org/10.1084/jem.20070608.

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D6 is a decoy and scavenger receptor for inflammatory CC chemokines. D6-deficient mice were rapidly killed by intranasal administration of low doses of Mycobacterium tuberculosis. The death of D6−/− mice was associated with a dramatic local and systemic inflammatory response with levels of M. tuberculosis colony-forming units similar to control D6-proficient mice. D6-deficient mice showed an increased numbers of mononuclear cells (macrophages, dendritic cells, and CD4 and CD8 T lymphocytes) infiltrating inflamed tissues and lymph nodes, as well as abnormal increased concentrations of CC chemokines (CCL2, CCL3, CCL4, and CCL5) and proinflammatory cytokines (tumor necrosis factor α, interleukin 1β, and interferon γ) in bronchoalveolar lavage and serum. High levels of inflammatory cytokines in D6−/− infected mice were associated with liver and kidney damage, resulting in both liver and renal failure. Blocking inflammatory CC chemokines with a cocktail of antibodies reversed the inflammatory phenotype of D6−/− mice but led to less controlled growth of M. tuberculosis. Thus, the D6 decoy receptor plays a key role in setting the balance between antimicrobial resistance, immune activation, and inflammation in M. tuberculosis infection.

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Peng, Xuan, Tao Luo, Xiaoqian Zhai, Chunxi Zhang, Jing Suo, Pengjiao Ma, Chuhan Wang, and Lang Bao. "PPE11 of Mycobacterium tuberculosis can alter host inflammatory response and trigger cell death." Microbial Pathogenesis 126 (January 2019): 45–55. http://dx.doi.org/10.1016/j.micpath.2018.10.031.

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Andersson, Henrik, Blanka Andersson, Daniel Eklund, Eyler Ngoh, Alexander Persson, Kristoffer Svensson, Maria Lerm, Robert Blomgran, and Olle Stendahl. "Apoptotic Neutrophils Augment the Inflammatory Response to Mycobacterium tuberculosis Infection in Human Macrophages." PLoS ONE 9, no. 7 (July 7, 2014): e101514. http://dx.doi.org/10.1371/journal.pone.0101514.

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Alvarez-Sekely, Magaly, Ana Lopez-Bago, Renata Báez-Saldaña, Rodolfo E. Pezoa-Jares, Patricia Gorocica, Edgar Zenteno, Ricardo Lascurain, and Alfredo Saldívar-González. "Major Depressive Disorder and Pulmonary Tuberculosis Comorbidity Exacerbates Proinflammatory Immune Response—A Preliminary Study." Pathogens 12, no. 3 (February 21, 2023): 361. http://dx.doi.org/10.3390/pathogens12030361.

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Background: Major depressive disorders (MDDs) occurs frequently in patients with tuberculosis (TB). Elevated serum pro-inflammatory cytokine levels in MDD patients is a well-established fact. Therefore, an integrated clinical practice should be considered. However, the inflammatory status of MDD-TB patients is unknown. In this study, we analyze cytokines in activated-cells and sera from MDD-TB, TB, MDD patients, and healthy controls. Methods: Flow cytometry was used to evaluate the intracellular production of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-12, and IL-10 by peripheral blood mononuclear cells after a polyclonal stimulation. A Bio-Plex Luminex system was used to measure serum cytokine and chemokine levels in the study groups. Results: We observed a 40.6% prevalence of MDD in TB patients. The proportion of IFN-gamma-producing cells was higher in MDD-TB patients than other pathological groups. Nevertheless, the percentage of TNF-alpha- and IL-12-producing cells was similar between MDD-TB and TB patients. Likewise, MDD-TB and TB patients showed similar serum pro-inflammatory cytokine and chemokine levels, which were significantly lower than those in MDD patients. By multiple correspondence analyses, we observed that low levels of serum IL-4, IL-10, and IL-13 were powerfully associated with TB comorbidities with MDD. Conclusions: A high frequency of IFN-γ-producing cells is associated with low levels of serum anti-inflammatory cytokines in MDD-TB patients.

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Zanozin, A. S., Y. S. Berezovsky, E. A. Kogan, and S. E. Kochetkova. "Primary tuberculosis with miliary hematogenous generalization in old age." Clinical Medicine (Russian Journal) 101, no. 1 (March 27, 2023): 63–67. http://dx.doi.org/10.30629/0023-2149-2023-101-1-63-67.

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Currently, the problems of the mechanisms of immune and inflammatory response aging, which determine the mechanisms of the development of the inflammatory process in the elderly, are being actively studied. A sectional observation of senile tuberculosis in a patient K., 78 years old, who had been treated for 4 months in the University Clinical Hospital No. 4 of the First Sechenov Moscow State Medical University in 2018 is presented. After autopsy, histological, histochemical and PCR examination, the following pathoanatomical diagnosis was made: primary (senile) tuberculosis with hematogenous and lympho-vascular generalization, with a focus of caseous pneumonia in the III segment of the right lung; caseous lymphadenitis of bifurcation, thoracic and abdominal paraaortic lymph nodes; miliary and large-focal generalization in the lungs, parietal and visceral pleura on the left, spleen and liver (acid fast stain; PCR study No. 18-5935 dated 08/13/2018 (Central Research Institute of Tuberculosis) detected DNA of mycobacterium tuberculosis complex). A feature of senile tuberculosis is the course of primary tuberculosis with hematogenic generalization and predominantly exudative-necrotic tissue reaction. Its pathogenesis is mainly due to the phenomenon of "aging immune system" (immunosenescence), as well as inflammaging — features of the inflammatory response in old age. Their main characteristics are the preactivated status of the immune system even before the recognition of the antigen, characterized by a basal level of circulating cytokines, as well as a sharp weakening of the adaptive immune response in the presence of an antigen associated with impaired functioning of the immune system with a large number of memory T cells lacking naive T-cells.

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Wawrocki, Sebastian, and Magdalena Druszczynska. "Inflammasomes inMycobacterium tuberculosis-Driven Immunity." Canadian Journal of Infectious Diseases and Medical Microbiology 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/2309478.

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The development of effective innate and subsequent adaptive host immune responses is highly dependent on the production of proinflammatory cytokines that increase the activity of immune cells. The key role in this process is played by inflammasomes, multimeric protein complexes serving as a platform for caspase-1, an enzyme responsible for proteolytic cleavage of IL-1βand IL-18 precursors. Inflammasome activation, which triggers the multifaceted activity of these two proinflammatory cytokines, is a prerequisite for developing an efficient inflammatory response against pathogenicMycobacterium tuberculosis(M.tb). This review focuses on the role of NLRP3 and AIM2 inflammasomes inM.tb-driven immunity.

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Mvubu, Nontobeko E., and Thamsanqa E. Chiliza. "Exploring the Use of Medicinal Plants and Their Bioactive Derivatives as Alveolar NLRP3 Inflammasome Regulators during Mycobacterium tuberculosis Infection." International Journal of Molecular Sciences 22, no. 17 (August 31, 2021): 9497. http://dx.doi.org/10.3390/ijms22179497.

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Анотація:

Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), is a successful intracellular pathogen that is responsible for the highest mortality rate among diseases caused by bacterial infections. During early interaction with the host innate cells, M. tuberculosis cell surface antigens interact with Toll like receptor 4 (TLR4) to activate the nucleotide-binding domain, leucine-rich-repeat containing family, pyrin domain-containing 3 (NLRP3) canonical, and non-canonical inflammasome pathways. NLRP3 inflammasome activation in the alveoli has been reported to contribute to the early inflammatory response that is needed for an effective anti-TB response through production of pro-inflammatory cytokines, including those of the Interleukin 1 (IL1) family. However, overstimulation of the alveolar NLRP3 inflammasomes can induce excessive inflammation that is pathological to the host. Several studies have explored the use of medicinal plants and/or their active derivatives to inhibit excessive stimulation of the inflammasomes and its associated factors, thus reducing immunopathological response in the host. This review describes the molecular mechanism of the NLRP3 inflammasome activation in the alveoli during M. tuberculosis infection. Furthermore, the mechanisms of inflammasome inhibition using medicinal plant and their derivatives will also be explored, thus offering a novel perspective on the alternative control strategies of M. tuberculosis-induced immunopathology.

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Koff, Alan, and Marwan Mikheal Azar. "Diagnosing peritoneal tuberculosis." BMJ Case Reports 13, no. 2 (February 2020): e233131. http://dx.doi.org/10.1136/bcr-2019-233131.

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Peritoneal tuberculosis (TB) is one of the most challenging forms of extrapulmonary tuberculosis to diagnose. This challenge can be compounded in low incidence regions, and in patients with cirrhosis in whom the presence of ascites alone may not prompt further investigation. A delay in the diagnosis and treatment of peritoneal tuberculosis may lead to worse clinical outcomes. This case describes a 64-year-old Italian male with decompensated cirrhosis being evaluated for liver transplantation, who developed abdominal pain and a persistent inflammatory ascites with peritoneal thickening despite antibiotic therapy. Peritoneal tuberculosis was suspected, although non-invasive and invasive direct mycobacterial testing remained negative. A constellation of positive QuantiFERON-TB Gold In-Tube test, elevated ascitic adenosine deaminase and dramatic symptomatic and radiographic response to empiric anti-tuberculous therapy confirmed the diagnosis of peritoneal tuberculosis. This paper will review the approach to the diagnosis of peritoneal tuberculosis.

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Rothchild, Alissa C., Gregory S. Olson, Johannes Nemeth, Lynn M. Amon, Dat Mai, Elizabeth S. Gold, Alan H. Diercks, and Alan Aderem. "Alveolar macrophages generate a noncanonical NRF2-driven transcriptional response to Mycobacterium tuberculosis in vivo." Science Immunology 4, no. 37 (July 26, 2019): eaaw6693. http://dx.doi.org/10.1126/sciimmunol.aaw6693.

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Alveolar macrophages (AMs) are the first cells to be infected during Mycobacterium tuberculosis (M.tb.) infection. Thus, the AM response to infection is the first of many steps leading to initiation of the adaptive immune response required for efficient control of infection. A hallmark of M.tb. infection is the slow initiation of the adaptive response, yet the mechanisms responsible for this are largely unknown. To study the initial AM response to infection, we developed a system to identify, sort, and analyze M.tb.-infected AMs from the lung within the first 10 days of infection. In contrast to what has been previously described using in vitro systems, M.tb.-infected AMs up-regulate a cell-protective antioxidant transcriptional signature that is dependent on the lung environment but not bacterial virulence. Computational approaches including pathway analysis and transcription factor motif enrichment analysis identify NRF2 as a master regulator of the response. Using knockout mouse models, we demonstrate that NRF2 drives expression of the cell-protective signature in AMs and impairs the control of early bacterial growth. AMs up-regulate a substantial pro-inflammatory response to M.tb. infection only 10 days after infection, yet comparisons with bystander AMs from the same infected animals demonstrate that M.tb.-infected AMs generate a less robust inflammatory response than the uninfected cells around them. Our findings demonstrate that the initial macrophage response to M.tb. in the lung is far less inflammatory than has previously been described by in vitro systems and may impede the overall host response to infection.

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Martens, Gregory W., Meltem Cevik Arikan, Jinhee Lee, Fucheng Ren, Therese Vallerskog, and Hardy Kornfeld. "Hypercholesterolemia Impairs Immunity to Tuberculosis." Infection and Immunity 76, no. 8 (May 27, 2008): 3464–72. http://dx.doi.org/10.1128/iai.00037-08.

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ABSTRACT We demonstrate that apolipoprotein E -deficient (ApoE −/ −) mice are highly susceptible to tuberculosis and that their susceptibility depends on the severity of hypercholesterolemia. Wild-type (WT) mice and ApoE −/ − mice fed a low-cholesterol (LC) or high-cholesterol (HC) diet were infected with ∼50 CFU Mycobacterium tuberculosis Erdman by aerosol. ApoE −/ − LC mice were modestly more susceptible to tuberculosis than WT LC mice. In contrast, ApoE −/ − HC mice were extremely susceptible, as evidenced by 100% mortality after 4 weeks with tuberculosis. The lung pathology of ApoE −/ − HC mice was remarkable for giant abscess-like lesions, massive infiltration by granulocytes, elevated inflammatory cytokine production, and a mean bacterial load ∼2 log units higher than that of WT HC mice. Compared to WT HC mice, the gamma interferon response of splenocytes restimulated ex vivo with M. tuberculosis culture filtrate protein was delayed in ApoE −/ − HC mice, and they failed to control M. tuberculosis growth in the lung. OT-II cells adoptively transferred into uninfected ApoE −/ − HC mice had a weak proliferative response to their antigen, indicating impaired priming of the adaptive immune response. Our studies show that ApoE −/ − deficiency is associated with delayed expression of adaptive immunity to tuberculosis caused by defective priming of the adaptive immune response and that elevated serum cholesterol is responsible for this effect.

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P, Purkait. "Interaction of Inflammatory Molecules in Tuberculosis and Sars Cov-2 Infection." Virology & Immunology Journal 6, no. 1 (February 17, 2022): 1–13. http://dx.doi.org/10.23880/vij-16000286.

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The Hyper-inflammatory immune response is a chief reason for disease severity and mortality in patients. Generally, macrophages and dendritic cells sense and react to microbial or viral invasion by making inflammatory molecules that remove pathogens and help in tissue repair. During tuberculosis infection, alveolar macrophages activate alveolar dendritic cells, which move to lymph nodes. In lymph nodes, the proliferation of CD4+ T cells, CD8+ cells and γδ T cells occur. Mycobacterium tuberculosis (MTB) bacteria further modify the host's immune system for their long survival period. Meanwhile, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infects alveolar macrophages and releases inflammatory cytokine to produce and activate T-cells. MTB and SARS-CoV-2 infections together lead to an increase in the rate of pathogenesis. This type of co-infection in macrophages causes the production of pro- and anti-inflammatory cytokines, which further play an important role in immune-pathogenesis. However, the abnormal or dysregulated response of macrophages leads to harmful effects of the host, as observed in the macrophage activation syndrome induced by severe infections, including the virus SARSCoV-2. Unlike macrophages, dendritic cells (DCs) act as antigen presenting cells. They connect innate and adaptive immunity cells. They are susceptible to cytokine-mediated activation and lead to cytokine production. The cytokine Interleukin-6 (IL6) is an important and unique molecule that can act pro- as well as anti-inflammatory and helps in the development and differentiation of macrophages associated with numerous inflammatory diseases. In this review paper, we have emphasized the vital pathological role of macrophages, dendritic cells and IL-6 in tuberculosis and SARS-CoV-2 infection and prospective therapeutic strategies based upon IL-6 as the main target for preventing the cytokine storm and associated organ failure.

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Nugraha, Jusak. "MYCOBACTERIUM TUBERCULOSIS SISTEM IMUN ALAMIAH TERKAIT PENERIMANYA." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 19, no. 1 (October 14, 2016): 45. http://dx.doi.org/10.24293/ijcpml.v19i1.395.

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Various attemp to investigate immune response towards tuberculosis has been done in order to eradicate or to make vaccination against tuberculosis (TB) effectively. Recently it is known that innate immunity has an important role in immunity to TB despite adaptive immune response, because it was proved that adaptive immune response alone was not sufficient to eradicate this microorganism thoroughly and completely in patient’s body. After Toll-Like Receptor (TLR) was found in the end of the 20th century, many progresses has been obtained in understanding about the activation of this innate immune response. But it is still needed to understand more deeply in the immune response to M. tuberculosis to lead the development of therapy or vaccination that bring into more precise target. The activation through TLR by parts of Mycobacterium induce cytoplasm protein adaptor MyD88 (Myeloid Differentiation factor 88). MyD88 has the function to activate NF- κB and secrete pro-inflammatory cytokine such as TNF-α, IL-6, IL-12. Involvement of MyD88 is not solely dependent of TLR2 receptor and there are another pathways to induce protective function of immunocompetent cells in TB.

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Selvaraj, Paramasivam, Murugesan Harishankar, and Kolloli Afsal. "Vitamin D: Immuno-modulation and tuberculosis treatment." Canadian Journal of Physiology and Pharmacology 93, no. 5 (May 2015): 377–84. http://dx.doi.org/10.1139/cjpp-2014-0386.

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Tuberculosis (TB) is a major global health problem and often coincides with vitamin D deficiency. High doses of vitamin D were widely used to treat TB during the pre-antibiotic era. Vitamin D exerts its action through vitamin D receptor (VDR), and VDR gene polymorphisms are associated with susceptibility or resistance to tuberculosis as well as sputum smear and culture conversion during anti-TB treatment. In-vitro studies have revealed that 1,25-dihydroxyvitamin D3 enhances innate immunity by increased expression of various antimicrobial peptides, including cathelicidin, and induction of autophagy of the infected cells thus restricts the intracellular growth of Mycobacterium tuberculosis in macrophages. On the other hand, vitamin D has been shown to suppress the pro-inflammatory cytokine response and enhance the anti-inflammatory response. Supplementation with vitamin D in concert with treatment for TB may be beneficial with respect to minimizing the excessive tissue damage that occurs during the active stage of tuberculosis disease. Several clinical trials have evaluated vitamin D supplementation as an adjunct therapy in the treatment for tuberculosis. However, results are conflicting, owing to variations in dose regimens and outcomes. Further investigations are needed to find the optimal concentration of vitamin D for supplementation with standard anti-TB drugs to optimize treatment, which could help to effectively manage both drug-sensitive and drug-resistant tuberculosis.

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Collins, Angela, Denise Marciano, Edward Graviss, and Michael Shiloh. "Role of heme oxygenase in the immune response to Mycobacterium tuberculosis in humans (P3095)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 125.21. http://dx.doi.org/10.4049/jimmunol.190.supp.125.21.

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Abstract Mycobacterium tuberculosis, the causative agent of tuberculosis, is the cause of over two million deaths every year. We have previously shown that in mice, Mycobacterium tuberculosis infection induces the production of heme oxygenase, and the subsequent production of carbon monoxide gas is sensed by the bacteria to initiate a dormancy program. Mouse macrophages deficient in heme oxygenase are defective in controlling intracellular Mycobacterium tuberculosis infection and mice deficient in heme oxygenase succumb to disease more readily than wild type mice. While the mechanisms used by mouse macrophages to control intracellular Mycobacterium tuberculosis infection, including nitric oxide synthase, the respiratory burst, acidification and heme oxygenase are well studied; how human macrophages control Mycobacterium tuberculosis infection remains poorly understood. We now show that a polymorphism in the heme oxygenase promoter confers susceptibility to human tuberculosis, that heme oxygenase is induced in human tuberculosis lesions, and that Mycobacterium tuberculosis infection of human macrophages in vitro also induces heme oxygenase. We also show by confocal microscopy that heme oxygenase colocalizes with Mycobacterium tuberculosis in human macrophages, and hee oxygenase enzymatic activity in human macrophages is necessary for inflammatory cytokine production. Thus, we demonstrate an important role for heme oxygenase in controlling Mycobacterium tuberculosis infection.

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Liu, Min, Zaiguo Wang, Shaolei Ren, and Hongli Zhao. "Exosomes derived from mycobacterium tuberculosis-infected MSCs induce a pro-inflammatory response of macrophages." Aging 13, no. 8 (April 19, 2021): 11595–609. http://dx.doi.org/10.18632/aging.202854.

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Zheng, Ruijuan, Haipeng Liu, Yilong Zhou, Dapeng Yan, Jianxia Chen, Dapeng Ma, Yonghong Feng, et al. "Notch4 Negatively Regulates the Inflammatory Response to Mycobacterium tuberculosis Infection by Inhibiting TAK1 Activation." Journal of Infectious Diseases 218, no. 2 (December 8, 2017): 312–23. http://dx.doi.org/10.1093/infdis/jix636.

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Cervantes, Jorge L., Angel Sanca, and Jose Barragan. "Metformin effect on human macrophage inflammatory response and phagocytosis of Mycobacterium tuberculosis." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 73.9. http://dx.doi.org/10.4049/jimmunol.204.supp.73.9.

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Abstract Metformin (MTF) has a well-documented ability to cfontrol hyperglycemia, which has been shown to have effects on macrophage and lymphocyte functions that are key to controlling tuberculosis (TB) infection. Here, we aimed to better understand the effects of MTF on the phagocytosis of Mycobacterium tuberculosis (Mtb) by human macrophages. PMA-differentiated THP-1 cells with two reporters for nuclear factor-κB (NF-κB), and interferon-regulatory factors (IRFs) were treated with 2mM of MTF for 4 hours, and then inoculated with Mtb from various lineages. Since MTF can also directly inhibit key metabolic processes of Mtb, we controlled this variable by using of gamma-irradiated mycobacteria. Phagocytosis was assessed by immunofluorescent assay. Phagocytosis of Mtb increased in MTF-treated macrophages. NF-κB activation after Mtb stimulation was lower in MTF-treated macrophages. The effect on IRF activation was minimal. Our results indicate that MTF improves phagocytosis of Mtb by macrophages, while it at the same time modulating their inflammatory response. Downregulation of type I IFN pathways, associated with active TB infection, could allow for improved activation of macrophages in the presence of TB infection. These results support the effects of MTF in keys steps TB infection control, and support its use as an additional treatment for TB.

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Bian, Yao, Shaobin Shang, Sharmila Shanmuganad, and Chyung-Ru Wang. "Qa-1b deficiency results in increased inflammatory response in aerogenic Mycobacterium tuberculosis infection (70.14)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 70.14. http://dx.doi.org/10.4049/jimmunol.188.supp.70.14.

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Abstract The murine MHC Ib molecule Qa-1b is known to play roles in both antigen presentation during infection by intracellular pathogens, as well as an immunoregulatory role in autoimmune and viral infection disease models. It has been shown that Qa-1b is able to suppress NK cell and CD8+ T cell activity through the interaction of Qa-1b /self-peptide complexes with inhibitory CD94/NKG2A molecules on activated effector cells. We find that Qa-1b expression is upregulated on a variety of cell types in a mouse model of low-dose, aerogenic infection with Mycobacterium tuberculosis (Mtb). Further, Mtb-infected, Qa-1b -deficient mice demonstrate increased production of INF-γ and IL-17A as compared to wild-type mice, suggesting that Qa-1b primarily plays an immunoregulatory role in Mtb infection. Qa-1b -deficient mice also display increased expression of inhibitory CD94/NKG2A complexes on CD8+ T cells during infection, indicating a potential mechanism by which Qa-1b is able to control immune responses during Mtb infection.

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Chumovatov, N. V., V. E. Eremeev, and A. E. Ergeshov. "Effect of tobacco smoke and nicotine on immune response in tuberculosis infection and other lung diseases." Medical Immunology (Russia) 24, no. 3 (July 13, 2022): 455–62. http://dx.doi.org/10.15789/1563-0625-eot-2484.

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The problem of smoking, as well as incidence of tuberculosis, has existed for a long time. The latest WHO data indicate that 1.3 million people die from tuberculosis, and another 7 millions die from smoking every year. Tobacco smoke contains many harmful chemicals, including carbon monoxide, nicotine, nitrogen oxides, and cadmium. A number of studies indicate a high prevalence of smoking among patients with tuberculosis. In most cases, infection with Mycobacterium tuberculosis does not lead to active disease, due to the development of a balanced, homeostatic immune response. The key protective components are inflammatory responses aimed at inhibition of the pathogen growth, its sequestration and final elimination. At the same time, excessive or inadequate immune response may lead to granuloma destruction, tissue damage and, as a result, prolonged duration of treatment due to decreased respiratory function of the lungs. Along with pro-inflammatory mediators, anti-inflammatory mediators are synthesized in the host organism, which can positively or negatively affect the course of disease, depending on the place and time of their production. The balance between pro-and anti-inflammatory mediators in terms of time and expression level plays a crucial role in determining the outcome of infection. In our review, we consider the impact of tobacco smoke on various components of the human immune system, as well as upon the course and outcome of tuberculosis and other lung diseases. In addition, we would like to draw the reader’s attention to the need of adjusting pathogenetic therapy of bronchopulmonary diseases, taking into account the patient’s smoking habits. Tobacco smoking is one of the main causes of the severe course of many infectious and non-infectious diseases of the bronchopulmonary system. The decay products of cigarette smoke disrupt the functioning of the ciliated epithelium of respiratory tract, the production of the mucous component in the bronchi, and reduce the effectiveness of the surfactant system. These negative events interfere with protective mechanisms of the human respiratory system. It is worth of note that tobacco smoke also exerts a systemic effect on the immune system. Data are accumulating on the association between the terms of exposure to tobacco smoke, and a range of adverse tunerculosis manifestations, such as extent of infection, severity of course, reactivation, treatment outcome, and mortality. At the same time, epidemiological studies are able to reveal the associations, but they do not allow us to determine exact causal relationships.

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Saukkonen, Jussi J., Beth Bazydlo, Michael Thomas, Robert M. Strieter, Joseph Keane та Hardy Kornfeld. "β-Chemokines Are Induced by Mycobacterium tuberculosis and Inhibit Its Growth". Infection and Immunity 70, № 4 (квітень 2002): 1684–93. http://dx.doi.org/10.1128/iai.70.4.1684-1693.2002.

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ABSTRACT Chemokines (CK) are potent leukocyte activators and chemoattractants and aid in granuloma formation, functions critical for the immune response to Mycobacterium tuberculosis. We hypothesized that infection of alveolar macrophages (AM) with different strains of M. tuberculosis elicits distinct profiles of CK, which could be altered by human immunodeficiency virus (HIV) infection. RANTES, macrophage inflammatory protein-1α (MIP-1α), and MIP-1β were the major β-CK produced in response to M. tuberculosis infection. Virulent M. tuberculosis (H37Rv) induced significantly less MIP-1α than did the avirulent strain (H37Ra), while MIP-1β and RANTES production was comparable for both strains. MIP-1α and MIP-1β were induced by the membrane, but not cytosolic, fraction of M. tuberculosis. M. tuberculosis-induced CK secretion was partly dependent on tumor necrosis factor alpha (TNF-α). AM from HIV-infected individuals produced less TNF-α and MIP-1β than did normal AM in response to either M. tuberculosis strain. We tested the functional significance of decreased β-CK secretion by examining the ability of β-CK to suppress intracellular growth of M. tuberculosis. MIP-1β and RANTES suppressed intracellular growth of M. tuberculosis two- to threefold, a novel finding. Thus, β-CK contribute to the innate immune response to M. tuberculosis infection, and their diminution may promote the intracellular survival of M. tuberculosis.

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Herrera, María Teresa, Silvia Guzmán-Beltrán, Karen Bobadilla, Teresa Santos-Mendoza, Mario Alberto Flores-Valdez, Luis Horacio Gutiérrez-González, and Yolanda González. "Human Pulmonary Tuberculosis: Understanding the Immune Response in the Bronchoalveolar System." Biomolecules 12, no. 8 (August 20, 2022): 1148. http://dx.doi.org/10.3390/biom12081148.

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Mycobacterium tuberculosis, the causal agent of one of the most devastating infectious diseases worldwide, can evade or modulate the host immune response and remain dormant for many years. In this review, we focus on identifying the local immune response induced in vivo by M. tuberculosis in the lungs of patients with active tuberculosis by analyzing data from untouched cells from bronchoalveolar lavage fluid (BALF) or exhaled breath condensate (EBC) samples. The most abundant resident cells in patients with active tuberculosis are macrophages and lymphocytes, which facilitate the recruitment of neutrophils. The cellular response is characterized by an inflammatory state and oxidative stress produced mainly by macrophages and T lymphocytes. In the alveolar microenvironment, the levels of cytokines such as interleukins (IL), chemokines, and matrix metalloproteinases (MMP) are increased compared with healthy patients. The production of cytokines such as interferon (IFN)-γ and IL-17 and specific immunoglobulin (Ig) A and G against M. tuberculosis indicate that the adaptive immune response is induced despite the presence of a chronic infection. The role of epithelial cells, the processing and presentation of antigens by macrophages and dendritic cells, as well as the role of tissue-resident memory T cells (Trm) for in situ vaccination remains to be understood.

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Saelee, Chutiphon, Jariya Hanthamrongwit, Phyu Thwe Soe, Prasong Khaenam, Naharuthai Inthasin, Pattama Ekpo, Patchanee Chootong, and Chaniya Leepiyasakulchai. "Toll-like receptor-mediated innate immune responses by recognition of the recombinant dormancy-associated Mycobacterium tuberculosis proteins Rv2659c and Rv1738." PLOS ONE 17, no. 9 (September 1, 2022): e0273517. http://dx.doi.org/10.1371/journal.pone.0273517.

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Tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb) poses a major threat to the global public health. Importantly, latent tuberculosis infection (LTBI) still impedes the elimination of TB incidence since it has a substantial risk to develop active disease. A multi-stage subunit vaccine comprising active and latency antigens of Mtb has been raised as the promising vaccine to trigger immune protection against all stages of TB. Therefore, the discovery of new antigens that could trigger broad immune response is essential. While current development of TB vaccine mainly focuses on protective immunity mediated by adaptive immune response, the knowledge on triggering the innate immune response by antigens is still limited. We showed that recombinant dormancy-associated Mtb proteins Rv2659c and Rv1738 were recognized by human innate immune recognition molecules, Toll-like receptors (TLRs) 2 and 4 by using HEK-Blue™ hTLR2/hTLR4 systems. We further demonstrated that these two proteins activated phosphorylated NF-κB p65 (Ser536) in the human CD14+ blood cells. We also investigated that these two proteins significantly induced level of pro- and anti-inflammatory cytokines (IL-1β, IL-6, IL-8, IL-10 and TNF-α) which were mediated through TLR2 and TLR4 pathways in human peripheral blood mononuclear cells (hPBMCs). These findings suggest that proteins Rv2659c and Rv1738 stimulated innate immune response targeting TLR2 and TLR4 to produce inflammatory cytokines, and their benefits would be valuable for the development of an effective prophylactic tuberculosis vaccine.

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Kinsella, Rachel L., Jacqueline M. Kimmey, Asya Smirnov, Reilly Woodson, Margaret R. Gaggioli, Sthefany M. Chavez, Darren Kreamalmeyer, and Christina L. Stallings. "Autophagy prevents early proinflammatory responses and neutrophil recruitment during Mycobacterium tuberculosis infection without affecting pathogen burden in macrophages." PLOS Biology 21, no. 6 (June 15, 2023): e3002159. http://dx.doi.org/10.1371/journal.pbio.3002159.

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The immune response to Mycobacterium tuberculosis infection determines tuberculosis disease outcomes, yet we have an incomplete understanding of what immune factors contribute to a protective immune response. Neutrophilic inflammation has been associated with poor disease prognosis in humans and in animal models during M. tuberculosis infection and, therefore, must be tightly regulated. ATG5 is an essential autophagy protein that is required in innate immune cells to control neutrophil-dominated inflammation and promote survival during M. tuberculosis infection; however, the mechanistic basis for how ATG5 regulates neutrophil recruitment is unknown. To interrogate what innate immune cells require ATG5 to control neutrophil recruitment during M. tuberculosis infection, we used different mouse strains that conditionally delete Atg5 in specific cell types. We found that ATG5 is required in CD11c+ cells (lung macrophages and dendritic cells) to control the production of proinflammatory cytokines and chemokines during M. tuberculosis infection, which would otherwise promote neutrophil recruitment. This role for ATG5 is autophagy dependent, but independent of mitophagy, LC3-associated phagocytosis, and inflammasome activation, which are the most well-characterized ways that autophagy proteins regulate inflammation. In addition to the increased proinflammatory cytokine production from macrophages during M. tuberculosis infection, loss of ATG5 in innate immune cells also results in an early induction of TH17 responses. Despite prior published in vitro cell culture experiments supporting a role for autophagy in controlling M. tuberculosis replication in macrophages, the effects of autophagy on inflammatory responses occur without changes in M. tuberculosis burden in macrophages. These findings reveal new roles for autophagy proteins in lung resident macrophages and dendritic cells that are required to suppress inflammatory responses that are associated with poor control of M. tuberculosis infection.

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Chakravarty, Soumya D., Guofeng Zhu, Ming C. Tsai, Vellore P. Mohan, Simeone Marino, Denise E. Kirschner, Luqi Huang, JoAnne Flynn, and John Chan. "Tumor Necrosis Factor Blockade in Chronic Murine Tuberculosis Enhances Granulomatous Inflammation and Disorganizes Granulomas in the Lungs." Infection and Immunity 76, no. 3 (January 22, 2008): 916–26. http://dx.doi.org/10.1128/iai.01011-07.

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ABSTRACT Tumor necrosis factor (TNF) is a prototypic proinflammatory cytokine that contributes significantly to the development of immunopathology in various disease states. A complication of TNF blockade therapy, which is used increasingly for the treatment of chronic inflammatory diseases, is the reactivation of latent tuberculosis. This study used a low-dose aerogenic model of murine tuberculosis to analyze the effect of TNF neutralization on disease progression in mice with chronic tuberculous infections. Histological, immunohistochemical, and flow cytometric analyses of Mycobacterium tuberculosis-infected lung tissues revealed that the neutralization of TNF results in marked disorganization of the tuberculous granuloma, as demonstrated by the dissolution of the previously described B-cell-macrophage unit in granulomatous tissues as well as by increased inflammatory cell infiltration. Quantitative gene expression studies using laser capture microdissected granulomatous lung tissues revealed that TNF blockade in mice chronically infected with M. tuberculosis leads to the enhanced expression of specific proinflammatory molecules. Collectively, these studies have provided evidence suggesting that in the chronic phase of M. tuberculosis infection, TNF is essential for maintaining the structure of the tuberculous granuloma and may regulate the granulomatous response by exerting an anti-inflammatory effect through modulation of the expression of proinflammatory mediators.

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Mazahery, Claire, Steven Chirieleison, Supriya Shukla, Sophia Onwuzulike, Mukesh Jain, W. Henry Boom, Derek W. Abbott, and Clifford V. Harding. "Macrophage Krüppel-like factor 4 regulates response to Mycobacterium tuberculosis infection." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 148.22. http://dx.doi.org/10.4049/jimmunol.198.supp.148.22.

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Abstract Krüppel-like factor 4 (KLF4) is a transcription factor that polarizes macrophages towards an anti-inflammatory (M2) phenotype, which suggests that it may regulate immune responses to Mycobacterium tuberculosis (Mtb), as immune evasion by Mtb may be due to an overabundance of anti-inflammatory mediators in response to infection. We hypothesize that myeloid KLF4 is permissive of immune evasion by Mtb, causing decreased control of Mtb infection. There are no prior in vivo data on the role of KLF4 in infection. Using mice with myeloid-specific knockout of KLF4 (LysMCre/CreKLF4fl/fl, abbreviated Mye-KO) we observed decreased Mtb CFU in macrophage cultures in vitro and in lungs of Mye-KO mice early in infection (day 14) relative to wild-type controls. However, these experiments also revealed complexities to the KLF4-Mtb relationship. Despite their improved control of early infection, at later time points Mye-KO mice developed worsened clinical disease features, such as wasting, which suggests that the loss of KLF4 results in pathologic immune state. In addition, we found discrepancy between KLF4 RNA and protein expression during Mtb infection, suggesting that KLF4 is regulated at a posttranslational level during infection. We are designing an in vitro system in which to study the molecular mechanisms of KLF4 regulation and activity in macrophages. Our data indicate that KLF4 plays an important role is regulating immune responses to Mtb with the potential to both diminish host defense mechanisms and repress host-damaging immune mechanisms.

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Mishra, Bibhuti B., and Christopher Sassetti. "Neutrophilic inflammation promotes bacterial growth during Tuberculosis." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 63.3. http://dx.doi.org/10.4049/jimmunol.196.supp.63.3.

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Abstract Nitric oxide is generally assumed to protect from tuberculosis by inhibiting the growth of Mycobacterium tuberculosis (Mtb), thereby preventing tissue damage. In contrast, we report that nitric oxide protects the host by repressing a neutrophil recruitment cascade that requires IL-1, CXCR2 and 12-lipoxygenase (12-LOX)-derived eicosanoids. Inhibition of the neutrophil recruitment alone enables the susceptible NOS2 KO mice to control Mtb growth, suggesting that neutrophilic inflammation, not an intrinsic anti-bacterial defect, drives susceptibility. By using a library of bacterial transposon mutants as reporters of host derived stress conditions, we show that granulocytic inflammation generates a nutrient-replete growth-permissive environment for Mtb which obviates the need for essential virulence factors, including the siderophore, mycobactin, and the virulence-related lipid, phthiocerol dimycocerosate, that are otherwise indispensable for establishing infection. A similar inflammatory pathway promotes TB in humans, as human genetic polymorphism that increases 12-LOX expression is associated with TB risk. The concentration of 12-LOX products correlates with neutrophil numbers and bacterial burden in the bronchoalveolar lavage of patients with pulmonary tuberculosis. We propose that Mtb exploits the inflammatory response to preferentially replicate at sites of tissue damage that promote contagion.

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DiNardo, Andrew R., Anna M. Mandalakas, Gugu Maphalala, Godwin Mtetwa, Temhlanga Mndzebele, Piluca Ustero, Makhosazana Hlatshwayo, Emily M. Mace, Jordan S. Orange, and George Makedonas. "HIV Progression Perturbs the Balance of the Cell-Mediated and Anti-Inflammatory Adaptive and Innate Mycobacterial Immune Response." Mediators of Inflammation 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/1478340.

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Introduction. Our objective is to understand how HIV infection increases the risk of progression from latent tuberculosis (TB) to active disease. We understand now that immunity is a balance of competing immune responses by multiple cell types. Since T-lymphocyte production of interferon-gamma (IFN-γ) in response toMycobacterium tuberculosis (Mtb) antigens fails to differentiate disease from latent infection, we applied a comprehensive profiling methodology to define immune biomarkers that reliably predict a patient’s TB risk.Methods. We established a cohort of HIV-infected adults with TB disease from Swaziland. Multiparametric flow cytometry was used to quantify the mycobacterial-specific anti-inflammatory (IL-4 and IL-10) and proinflammatory (IFN-γ) immune response.Results. From 12 HIV-infected Swaziland patients with TB disease, the CD4+, CD8+, Double Negative, and CD56+CD3−lymphocytes increase their IL-4 : IFN-γratio as HIV disease worsens (Spearmanrof −0.59; −0.59; −0.60; and −0.59, resp.;p<0.05). Similarly, HIV severity is associated with an increased IL-10 : IFN-γratio (Spearmanrof −0.76;p=0.01).Conclusion. As HIV disease progresses, both the adaptive and innate branches skew away from an inflammatory and towards anti-inflammatory phenotype.

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Аbdullаev, R. Yu, O. G. Komissаrovа, and O. R. Terentievа. "Specific parameters of iron metabolism in tuberculosis." Tuberculosis and Lung Diseases 99, no. 3 (April 6, 2021): 58–66. http://dx.doi.org/10.21292/2075-1230-2021-99-3-58-66.

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The review presents data from 55 publications about specific parameters of iron metabolism in the human body including those ill with tuberculosis. It describes processes aimed at isolating iron from pathogens and promoting the acquisition of iron by pathogens from the host. A decrease in the level of iron circulating in the blood serum in the case of tuberculosis is primarily a component of the systemic inflammatory response and belongs to the mechanisms of innate immunity that limit the reproduction of an infectious agent in the human body. However, its true deficiency can be involved in the decrease in the level of circulating iron.

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D'Souza, C. D., A. M. Cooper, A. A. Frank, R. J. Mazzaccaro, B. R. Bloom, and I. M. Orme. "An anti-inflammatory role for gamma delta T lymphocytes in acquired immunity to Mycobacterium tuberculosis." Journal of Immunology 158, no. 3 (February 1, 1997): 1217–21. http://dx.doi.org/10.4049/jimmunol.158.3.1217.

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Abstract Although a role for gammadelta receptor-bearing T cells in the acquired immune response to infection with Mycobacterium tuberculosis is suggested by several lines of evidence, the only data indicating a possible role in specific protective immunity have been provided by very high dose i.v. infection models. In the current study, more modest low dose inocula delivered by the aerosol route grew identically in wild-type controls and in mutant mice in which the Cdelta gene of the gammadelta TCR has been disrupted by homologous recombination. This situation did not change if the inoculum size was increased or if an aerosol challenge with an M. tuberculosis strain of higher virulence was given. However, while the control and containment of these infections was similar, the mutant mice exhibited a substantial pyogenic form of the granulomatous response compared with the lymphocytic response seen in control animals, a finding that may well explain mortality in the former group if high i.v. doses are given. These data indicate that gammadelta T cells do not directly contribute to protection against tuberculosis or that they do so only when bacterial loads are very high. Instead, the data suggest that gammadelta T cells perhaps play an important role by influencing local cellular traffic, promoting the influx of lymphocytes and monocytes, and limiting the access of inflammatory cells that do not contribute to protection but may cause tissue damage.

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