Mitochondria in Mycobacterium Infection: From the Immune System to Mitochondrial Haplogroups

Souza, Felipe Gouvea de; Cavalcante, Giovanna C.

doi:10.3390/ijms23179511

Cited by 9 publications

(3 citation statements)

References 59 publications

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“…Moreover, additional research will be conducted to comprehend the mechanism of infection-mediated neuroinflammation, with a specific focus on the role of mitochondria dysfunction. Mitochondria dysfunction has been associated with the development of both MS and EAE [39,40], as well as mycobacterial infection [41].…”

Section: Discussionmentioning

confidence: 99%

Mycobacterium avium subsp. paratuberculosis Antigens Elicit a Strong IgG4 Response in Patients with Multiple Sclerosis and Exacerbate Experimental Autoimmune Encephalomyelitis

Cossu

Tomizawa

Yokoyama

et al. 2023

Life

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Neuroinflammation can be triggered by microbial products disrupting immune regulation. In this study, we investigated the levels of IgG1, IgG2, IgG3, and IgG4 subclasses against the heat shock protein (HSP)70533–545 peptide and lipopentapeptide (MAP_Lp5) derived from Mycobacterium avium subsp. paratuberculosis (MAP) in the blood samples of Japanese and Italian individuals with relapsing remitting multiple sclerosis (MS). Additionally, we examined the impact of this peptide on MOG-induced experimental autoimmune encephalomyelitis (EAE). A total of 130 Japanese and 130 Italian subjects were retrospectively analyzed using the indirect ELISA method. Furthermore, a group of C57BL/6J mice received immunization with the MAP_HSP70533–545 peptide two weeks prior to the active induction of MOG35–55 EAE. The results revealed a significantly robust antibody response against MAP_HSP70533–545 in serum of both Japanese and Italian MS patients compared to their respective control groups. Moreover, heightened levels of serum IgG4 antibodies specific to MAP antigens were correlated with the severity of the disease. Additionally, EAE mice that were immunized with MAP_HSP70533–545 peptide exhibited more severe disease symptoms and increased reactivity of MOG35–55-specific T-cell compared to untreated mice. These findings provide evidence suggesting a potential link between MAP and the development or exacerbation of MS, particularly in a subgroup of MS patients with elevated serum IgG4 levels.

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Section: Discussionmentioning

confidence: 99%

Mycobacterium avium subsp. paratuberculosis Antigens Elicit a Strong IgG4 Response in Patients with Multiple Sclerosis and Exacerbate Experimental Autoimmune Encephalomyelitis

Cossu

Tomizawa

Yokoyama

et al. 2023

Life

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“…Neben der Energieproduktion sind Mitochondrien an der Regulation der Apoptose (Zelltod) und der Produktion reaktiver Sauerstoffspezies (ROS) beteiligt. Dadurch sind Mitochondrien Teil von komplexen Zellkommunikationspro-zessen, die zur Homöostase des menschlichen Organismus beitragen können [8].…”

Section: Mitochondriale Dysfunktionunclassified

Mitochondrien und Orthomolekularmedizin: neue Perspektiven in der Behandlung des Fibromyalgie-Syndroms

Bulasikis

2024

Erfahrungsheilkunde

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ZusammenfassungDas Fibromyalgie-Syndrom, eine häufige Schmerzerkrankung mit Symptomen wie Schmerzen, Müdigkeit und kognitiven Störungen, ist eng mit mitochondrialen Dysfunktionen verbunden. Mitochondrien, die für die ATP-Produktion in den Zellen zuständig sind, spielen bei Fibromyalgie eine Schlüsselrolle. Dysfunktionale Mitochondrien führen zu verringerter ATP-Produktion und erhöhter Abhängigkeit vom weniger effizienten anaeroben Stoffwechsel, was die Symptome von Fibromyalgie verstärken kann. Aktuelle Forschungen zeigen eine deutliche Korrelation zwischen mitochondrialen Dysfunktionen und Fibromyalgie, einschließlich Störungen im Muskelenergiestoffwechsel und Anzeichen von oxidativem sowie nitrosativem Stress. Orthomolekularmedizinische Ansätze wie die Supplementierung mit Koenzym Q10, L-Carnitin, B-Vitaminen, D-Ribose und R-Alpha-Liponsäure könnten die mitochondriale Funktion verbessern und bieten neue Behandlungsmöglichkeiten. Diese Methoden zielen darauf ab, die zugrunde liegende Mitochondriopathie zu behandeln, und könnten einen wesentlichen Fortschritt in der Behandlung von Fibromyalgie darstellen. Zusätzlich spielen Lebensstil- und Verhaltensansätze eine wichtige Rolle in der Therapie, indem sie die mitochondriale Biogenese und den Muskelstoffwechsel fördern.

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“…Notably, M. leprae is dependent on the production of energy and nutritional products by the host, resulting from the host–pathogen interaction, undoubtedly involving the main function of mitochondria of energy generation, due to the cellular signaling pathways in which these organelles participate and connect their metabolism to meet their nutrient demands 6 , 7 . Furthermore, due to the decay of the M. leprae genome, which leads to strain uniformity, it is suggested that the genetic background of the host, and not bacterial variability, is a central aspect of susceptibility to leprosy 1 .…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial variants of complex I genes associated with leprosy clinical subtypes

de Souza,

Silva,

de Araújo

et al. 2024

Sci Rep

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Leprosy is a chronic bacterial infection mainly caused by Mycobacterium leprae that primarily affects skin and peripheral nerves. Due to its ability to absorb carbon from the host cell, the bacillus became dependent on energy production, mainly through oxidative phosphorylation. In fact, variations in genes of Complex I of oxidative phosphorylation encoded by mtDNA have been associated with several diseases in humans, including bacterial infections, which are possible influencers in the host response to leprosy. Here, we investigated the presence of variants in the mtDNA genes encoding Complex I regarding leprosy, as well as the analysis of their pathogenicity in the studied cohort. We found an association of 74 mitochondrial variants with either of the polar forms, Pole T (Borderline Tuberculoid) or Pole L (Borderline Lepromatous and Lepromatous) of leprosy. Notably, six variants were exclusively found in both clinical poles of leprosy, including m.4158A>G and m.4248T>C in MT-ND1, m.13650C>A, m.13674T>C, m.12705C>T and m.13263A>G in MT-ND5, of which there are no previous reports in the global literature. Our observations reveal a substantial number of mutations among different groups of leprosy, highlighting a diverse range of consequences associated with mutations in genes across these groups. Furthermore, we suggest that the six specific variants exclusively identified in the case group could potentially play a crucial role in leprosy susceptibility and its clinical differentiation. These variants are believed to contribute to the instability and dysregulation of oxidative phosphorylation during the infection, further emphasizing their significance.

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Mitochondria in Mycobacterium Infection: From the Immune System to Mitochondrial Haplogroups

Cited by 9 publications

References 59 publications

Mycobacterium avium subsp. paratuberculosis Antigens Elicit a Strong IgG4 Response in Patients with Multiple Sclerosis and Exacerbate Experimental Autoimmune Encephalomyelitis

Mycobacterium avium subsp. paratuberculosis Antigens Elicit a Strong IgG4 Response in Patients with Multiple Sclerosis and Exacerbate Experimental Autoimmune Encephalomyelitis

Mitochondrien und Orthomolekularmedizin: neue Perspektiven in der Behandlung des Fibromyalgie-Syndroms

Mitochondrial variants of complex I genes associated with leprosy clinical subtypes

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