Specific features of immune complexes in patients with sarcoidosis and pulmonary tuberculosis

Старшинова, Анна; Zinchenko, Ulia; Filatov, M. V.; Denisova, Nina; Istomina, Evgenia; Landa, Sergey; Burdakov, Vladimir; Чурилов, Леонид Павлович; Сапожникова, Н. В.; Pavlova, Maria; Stepanenko, Т.; Mayevskaya, Vera; Yаblonskiy, Petr

doi:10.1007/s12026-018-9052-1

Cited by 18 publications

(20 citation statements)

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“…Another study in a hospital of TB-endemic region reported that a total of 14 out of 70 (20%) "TB patients" with little response to anti-TB treatment received misdiagnosis and were actually lung cancers 13 . Moreover, it was speculated that~15-20% of the patients might be misdiagnosed if using immunological tests for differential diagnosis of TB and sarcoidosis 58 . Thus, lung tissue-based molecular markers might be helpful for differential diagnosis of these lung diseases in certain cases.…”

Section: Discussionmentioning

confidence: 99%

Lung gene expression signatures suggest pathogenic links and molecular markers for pulmonary tuberculosis, adenocarcinoma and sarcoidosis

et al. 2020

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Previous reports have suggested a link between pulmonary tuberculosis (TB), which is caused by Mycobacterium tuberculosis (Mtb), and the development of lung adenocarcinoma (LUAD) and sarcoidosis. Furthermore, these lung diseases share certain clinical similarities that can challenge differential diagnosis in some cases. Here, through comparison of lung transcriptome-derived molecular signatures of TB, LUAD and sarcoidosis patients, we identify certain shared disease-related expression patterns. We also demonstrate that MKI67, an over-expressed gene shared by TB and LUAD, is a key mediator in Mtb-promoted tumor cell proliferation, migration, and invasion. Moreover, we reveal a distinct ossification-related TB lung signature, which may be associated with the activation of the BMP/SMAD/RUNX2 pathway in Mtb-infected macrophages that can restrain mycobacterial survival and promote osteogenic differentiation of mesenchymal stem cells. Taken together, these findings provide novel pathogenic links and potential molecular markers for better understanding and differential diagnosis of pulmonary TB, LUAD and sarcoidosis.

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Section: Discussionmentioning

confidence: 99%

Lung gene expression signatures suggest pathogenic links and molecular markers for pulmonary tuberculosis, adenocarcinoma and sarcoidosis

et al. 2020

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“…Гипотезы о роли экзогенных антропогенных и/ или природных факторов в этиологии саркоидоза и о роли нарушенных аутофагии и поляризации макрофагов в его развитии не противоречат активно развивающимся в последние годы представлениям о его аутоиммунном и/или аутовоспалительном патогенезе [26,40,85].…”

Section: к линико-патофизиологические особенности с аркоидозаunclassified

Comparative aetio-epidemiological analysis of lung tuberculosis versus sarcoidosis: classical and new concepts

et al. 2020

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The review presents data on two similar granulomatous inflammatory diseases: tuberculosis and sarcoidosis of the lungs, which together cover about 5% of all pulmonary pathology, albeit occur with different incidence (20 : 1). Despite the established aetiology of tuberculosis, the disease has not disappeared and nowadays has even acquired a new urgency: It is getting out of control due to growing poverty, the comorbidity with HIV infection, increasing cases of drug resistance of Mycobacteria, insufficient effectiveness and the growing costs of its treatment. Against the background of the expansion of anthropogenic influences and other environmental impacts on the immune system, the incidence of lung sarcoidosis is also increasing, while patients are initially often misdiagnosed with tuberculosis, with resulting unjustified anti-tuberculosis chemotherapy, leading to chronization of the disease with frequent relapses and, accordingly, to an increase in disability and mortality rates. In recent years, clinical manifestations of sarcoidosis due to a variety of trigger aetiological factors with adjuvant-like action (from Mycobacteria to xenobiotics) are considered by a number of authors as a variant of autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA). The article emphasizes the similarity of two granulomatous inflammatory diseases and the concept of two variants of the bodys response to similar or even identical aetiological factors within different human reactivity (possibly on a different mosaic/permissive background). In brief the newest data on experimental models of sarcoidosis are reviewed as well as the role of autophagy disorders and opposite macrophageal polarization in tuberculosis versus sarcoidosis. Authors coined the original hypothesis of the possible therapeutic effectiveness of Rapamycin in sarcoidosis and for the first time posed a question of equivocal character of comorbidity between these granulomatoses and COVID-19 infection.

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“…The development of SFN is considered to be the result of a cytokine-mediated in ammation, which is typical for various autoimmune diseases, including sarcoidosis (5)(6)(7)(8). Small nerve ber damage is also observed in systemic lupus erythematosus, Sjogren's syndrome, and bromyalgia (9,10).…”

Section: Introductionmentioning

confidence: 99%

Small Fiber Neuropathy in Pulmonary Sarcoidosis and Tuberculosis: Clinical and Histological Correlates

Старшинова

Basantsova

Zinchenko

et al. 2020

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Sarcoidosis (SC) is the granulomatous disease of an unknown origin, where the differential diagnosis with tuberculosis (TB) is challenging and vital for patients’ prognosis. The common neurological complication in SC is a small fiber neuropathy (SFN), that is considered to be the result of the chronic inflammation, and remains significantly understudied. There is no reliable data, whether such complication is observed in TB patients, where the systemic inflammation is also described. Aim: To identify the clinical and histological correlates of the small fiber neuropathy in sarcoidosis and tuberculosis patients.Materials and methods. A study was performed in 2018 – 2019 years and included 71 patients with pulmonary sarcoidosis (n=25), pulmonary tuberculosis (n=21), and healthy subjects (n=25). For the clinical verification of the SFN, the “Small fiber neuropathy screening list” (SFN-SL) was used. A punch biopsy of the skin was performed followed by the enzyme immunoassay analysis with PGP 9.5 antibodies.Results of the study: Up to 60% of sarcoidosis patients and 19% tuberculosis patients report the presence of at least one complaint, which may be associated with SFN. The most frequent complaints included dysfunctions of the cardiovascular, musculoskeletal system and gastrointestinal tract. A negative, statistically significant correlation between the intraepidermal nerve fiber density (IEND) and SFN-SL score was revealed in both groups (Spearman coefficient, r = -0.3508, p = 0.0102, and r = -0.7382, p = 0.0064, respectively). Wherein, the density of small nerve fibers in the patients with pulmonary sarcoidosis was lower, compared to the patients with tuberculosis (Mann-Whitney test, p = 0.0047). Conclusion: In patients with pulmonary sarcoidosis, small fiber neuropathy may develop as a result of systemic immune-mediated inflammation. The most common symptoms of this complication were dysautonomia and mild sensory dysfunction. Wherein, in tuberculosis patients clinical and histological symptoms of the small fiber neuropathy were subsequently less prominent, which may represent the difference between the autoimmune and bacterial inflammation. The validated questionnaires and histologic verification of the diagnosis help to establish the severity of neuropathy of small fibers, to determine the prognosis, to plan the treatment strategн, and also may allude the possibility for the additional criteria of differential diagnosis between two diseases.

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Specific features of immune complexes in patients with sarcoidosis and pulmonary tuberculosis

Cited by 18 publications

References 12 publications

Lung gene expression signatures suggest pathogenic links and molecular markers for pulmonary tuberculosis, adenocarcinoma and sarcoidosis

Lung gene expression signatures suggest pathogenic links and molecular markers for pulmonary tuberculosis, adenocarcinoma and sarcoidosis

Comparative aetio-epidemiological analysis of lung tuberculosis versus sarcoidosis: classical and new concepts

Small Fiber Neuropathy in Pulmonary Sarcoidosis and Tuberculosis: Clinical and Histological Correlates

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