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001-es BibID:BIBFORM103836
035-os BibID:(wos)000854410800001 (Scopus)85138156081
Első szerző:Fagyas Miklós (orvos)
Cím:The majority of severe COVID-19 patients develop anti-cardiac autoantibodies / Fagyas Miklós, Nagy Béla, Ráduly Arnold Péter, Mányiné Siket Ivetta, Mártha Lilla, Erdősi Gábor, Sipka Sándor, Enyedi Enikő, Szabó Attila Ádám, Pólik Zsófia, Kappelmayer János, Papp Zoltán, Borbély Attila, Szabó Tamás, Balla József, Balla György, Bai Péter, Bácsi Attila, Tóth Attila
Dátum:2022
ISSN:2509-2715 2509-2723
Megjegyzések:Severe cases of COVID-19 are characterized by an inflammatory burst, which is accompanied by multiorgan failure. The elderly population has higher risk for severe or fatal outcome for COVID-19. Inflammatory mediators facilitate the immune system to combat viral infection by producing antibodies against viral antigens. Several studies reported that the pro-inflammatory state and tissue damage in COVID-19 also promotes autoimmunity by autoantibody generation. We hypothesized that a subset of these autoantibodies targets cardiac antigens. Here we aimed to detect anti-cardiac autoantibodies in severe COVID-19 patients during hospitalization. For this purpose, 104 COVID-19 patients were recruited, while 40 heart failure patients with dilated cardiomyopathy and 20 patients with severe aortic stenosis served as controls. Patients were tested for anti-cardiac autoantibodies, using human heart homogenate as a bait. Follow-up samples were available in 29 COVID-19 patients. Anti-cardiac autoantibodies were detected in 68% (71 out of 104) of severe COVID-19 patients. Overall, 39% of COVID-19 patients had anti-cardiac IgG autoantibodies, while 51% had anti-cardiac autoantibodies of IgM isotype. Both IgG and IgM anti-cardiac autoantibodies were observed in 22% of cases, and multiple cardiac antigens were targeted in 38% of COVID-19 patients. These anti-cardiac autoantibodies targeted a diverse set of myocardial proteins, without apparent selectivity. As controls, heart failure patients (with dilated cardiomyopathy) had similar occurrence of IgG (45%, p = 0.57) autoantibodies, while significantly lower occurrence of IgM autoantibodies (30%, p = 0.03). Patients with advanced aortic stenosis had significantly lower number of both IgG (11%, p = 0.03) and IgM (10%, p < 0.01) type anti-cardiac autoantibodies than that in COVID-19 patients. Furthermore, we detected changes in the anti-cardiac autoantibody profile in 7 COVID-19 patients during hospital treatment. Surprisingly, the presence of these anti-cardiac autoantibodies did not affect the clinical outcome and the prevalence of the autoantibodies did not differ between the elderly (over 65 years) and the patients younger than 65 years of age. Our results demonstrate that the majority of hospitalized COVID-19 patients produce novel anti-cardiac IgM autoantibodies. COVID-19 also reactivates resident IgG autoantibodies. These autoantibodies may promote autoimmune reactions, which can complicate post-COVID recuperation, contributing to post-acute sequelae of COVID-19 (long COVID).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
COVID-19
Anti-cardiac autoantibodies
SARS-CoV-2
Megjelenés:GeroScience. - 44 (2022), p. 2347-2360. -
További szerzők:Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos) Ráduly Arnold Péter (1993-) Mányiné Siket Ivetta (1962-) (laborasszisztens) Mártha Lilla Erdősi Gábor Sipka Sándor ifj. (1980-) (orvos) Enyedi Enikő Edit (1995-) (orvosi laboratóriumi analitikus) Szabó Attila Ádám (1996-) (orvos) Pólik Zsófia Kappelmayer János (1960-) (laboratóriumi szakorvos) Papp Zoltán (1965-) (kardiológus, élettanász) Borbély Attila (1978-) (kardiológus) Szabó Tamás (1968-) (gyermekgyógyász) Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Bai Péter (1976-) (biokémikus) Bácsi Attila (1967-) (immunológus) Tóth Attila (1971-) (biológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00050
GINOP
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2.

001-es BibID:BIBFORM117681
035-os BibID:(WoS)001138525600001 (Scopus)85181969555
Első szerző:Szeőcs Dóra (PhD hallgató)
Cím:Cell-free ascites from ovarian cancer patients induces Warburg metabolism and cell proliferation through TGFbeta-ERK signalling / Szeőcs D., Vida B., Petővári G., Póliska Sz., Janka E., Sipos A., Uray K., Sebestyén A., Krasznai Z., Bai P.
Dátum:2024
ISSN:2509-2715 2509-2723
Megjegyzések:Ascites plays a key role in supporting the metastatic potential of ovarian cancer cells. Shear stress and carry-over of cancer cells by ascites flow support carcinogenesis and metastasis formation. In addition, soluble factors may participate in the procarcinogenic effects of ascites in ovarian cancer. This study aimed to determine the biological effects of cell-free ascites on carcinogenesis in ovarian cancer cells. Cell-free ascites from ovarian cancer patients (ASC) non-selectively induced cell proliferation in multiple models of ovarian cancer and untransformed primary human dermal fibroblasts. Furthermore, ASC induced a Warburg-type rearrangement of cellular metabolism in A2780 ovarian cancer cells characterized by increases in cellular oxygen consumption and glycolytic flux; increases in glycolytic flux were dominant. ASC induced mitochondrial uncoupling and fundamentally reduced fatty acid oxidation. Ascites-elicited effects were uniform among ascites specimens. ASC-elicited transcriptomic changes in A2780 ovarian cancer cells included induction of the TGF beta-ERK/MEK pathway, which plays a key role in inducing cell proliferation and oncometabolism. ASC-induced gene expression changes, as well as the overexpression of members of the TGF beta signaling system, were associated with poor survival in ovarian cancer patients. We provided evidence that the activation of the autocrine/paracrine of TGF beta signaling system may be present in bladder urothelial carcinoma and stomach adenocarcinoma. Database analysis suggests that the TGF beta system may feed forward bladder urothelial carcinoma and stomach adenocarcinoma. Soluble components of ASC support the progression of ovarian cancer. These results suggest that reducing ascites production may play an essential role in the treatment of ovarian cancer by inhibiting the progression and reducing the severity of the disease.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:GeroScience. - [Epub ahead of print] (2024). -
További szerzők:Vida Beáta (1994-) (szülészet-nőgyógyászat) Petővári Gábor Póliska Szilárd (1978-) (biológus) Janka Eszter Anna (1989-) (bőrgyógyász, népegészségügyi szakember) Sipos Adrienn (1984-) (biológus, biotechnológus) Uray Karen (1964-) (biokémikus) Sebestyén Anna Krasznai Zoárd Tibor (1973-) (szülész-nőgyógyász, gyermeknőgyógyász) Bai Péter (1976-) (biokémikus)
Pályázati támogatás:K142141
NKFIH
FK128387
NKFIH
FK146852
NKFIH
TKP2021-EGA-19
NKFIH
TKP2021-EGA-20
NKFIH
POST-COVID2021-33
Egyéb
NKM2022-30
Egyéb
Internet cím:DOI
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3.

001-es BibID:BIBFORM114386
035-os BibID:(WoS)001060165600001 (Scopus)85169334322
Első szerző:Tóth Emese (biotechnológus)
Cím:Distinct subsets of anti-pulmonary autoantibodies correlate with disease severity and survival in severe COVID-19 patients / Emese Tóth, Miklós Fagyas, Béla Nagy Jr., Ivetta Mányiné Siket, Blanka Szőke, Lilla Mártha, Mohamed Mahdi, Gábor Erdősi, Zsófia Pólik, János Kappelmayer, Zoltán Papp, Attila Borbély, Tamás Szabó, József Balla, György Balla, Attila Bácsi, Zoltán Szekanecz, Péter Bai, Attila Tóth
Dátum:2024
ISSN:2509-2715 2509-2723
Megjegyzések:Autoantibodies targeting the lung tissue were identified in severe COVID-19 patients in this retrospective study. Fifty-three percent of 104 patients developed anti-pulmonary antibodies, the majority of which were IgM class, suggesting that they developed upon infection with SARS-CoV-2. Anti-pulmonary antibodies correlated with worse pulmonary function and a higher risk of multiorgan failure that was further aggravated if 3 or more autoantibody clones were simultaneously present (multi-producers). Multi-producer patients were older than the patients with less or no autoantibodies. One of the identified autoantibodies (targeting a pulmonary protein of ~ 50 kDa) associated with worse clinical outcomes, including mortality. In summary, severe COVID-19 is associated with the development of lung-specific autoantibodies, which may worsen the clinical outcome. Tissue proteome-wide tests, such as the ones applied here, can be used to detect autoimmunity in the post-COVID state to identify the cause of symptoms and to reveal a new target for treatment.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Autoantibody
Clinical outcome
IgG
IgM
Lung
Mortality
Multi-producer
Post-COVID
SARS-CoV-2
Severe COVID-19
Megjelenés:GeroScience. - 46 : 2 (2024), p. 1561-1574. -
További szerzők:Fagyas Miklós (1984-) (orvos) Nagy Béla Jr. (1980-) (labordiagnosztikai szakorvos) Mányiné Siket Ivetta (1962-) (laborasszisztens) Szőke Blanka Mártha Lilla Mahdi, Mohamed (1979-) (orvos, tudományos segédmunkatárs) Erdősi Gábor Pólik Zsófia Kappelmayer János (1960-) (laboratóriumi szakorvos) Papp Zoltán (1965-) (kardiológus, élettanász) Borbély Attila (1978-) (kardiológus) Szabó Tamás Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Bácsi Attila (1967-) (immunológus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Bai Péter (1976-) (biokémikus) Tóth Attila (1971-) (biológus)
Pályázati támogatás:ÚNKP-23-5-DE-482
Egyéb
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DOI
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