A review of alcohol–pathogen interactions: New insights into combined disease pathomechanisms

Osna, Natalia A.; New-Aaron, Moses; Dagur, Raghubendra Singh; Thomes, Paul; Simon, Liz; Levitt, Danielle E.; McTernan, Patrick M.; Molina, Patricia E.; Choi, Hye Yeon; Machida, Keigo; Sherman, Kenneth E.; Riva, Antonio; Phillips, S M; Chokshi, Shilpa; Kharbanda, Kusum K.; Weinman, Steven A.; Ganesan, Murali

doi:10.1111/acer.14777

Cited by 9 publications

(4 citation statements)

References 80 publications

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“…The reason for this is both ultrastructural changes of myocytes and their atrophy, and changes in electrolyte homeostasis and bioelectric activity in general [ 44 ]. During the development of alcoholic myopathy, first of all, there is a hypergeneration of free radicals in dysfunctional mitochondria [ 45 , 46 ], which causes the destruction of the membrane structures of myocytes and functional disorders of their enzyme systems [ 47 ]: a decrease in the activity of Na + /K + -ATPase and an increase in ‒ Ca 2+ -ATPase. The miotic disorders cause an imbalance in the correction of the joints positioning and progressive muscle weakness, which leads to the degradation of muscle strength with 3, 6 and 9 months of alcoholization.…”

Section: Resultsmentioning

confidence: 99%

The effect of C60 fullerene on the mechanokinetics of muscle gastrocnemius contraction in chronically alcoholized rats

Motuziuk,

Nozdrenko,

Prylutska

et al. 2023

Heliyon

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Section: Resultsmentioning

confidence: 99%

The effect of C60 fullerene on the mechanokinetics of muscle gastrocnemius contraction in chronically alcoholized rats

Motuziuk,

Nozdrenko,

Prylutska

et al. 2023

Heliyon

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“…Viral hepatitis and NASH are important causes of liver cancer development. Liver fibrosis due to viral hepatitis and NASH has been shown to be a risk factor for the development of hepatocellular carcinoma 49 – 51 . It has been suggested that ADAM12 is significantly associated with liver fibrosis 52 .…”

Section: Discussionmentioning

confidence: 99%

ADAM12 is an independent predictor of poor prognosis in liver cancer

Sun

Wang

et al. 2022

Sci Rep

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Disintegrin and metalloproteinase 12 (ADAM12) is thought to trigger the occurrence and development of numerous tumours, including colorectal, breast, and pancreatic cancers. On the basis of The Cancer Genome Atlas (TCGA) datasets, in this study, the relationship between ADAM12 gene expression and hepatocellular carcinoma (HCC), the prognostic value of this relationship, and the potential mechanisms influencing HCC development were evaluated. The results showed that the ADAM12 gene was significantly and highly expressed in liver cancer tissue. The high expression of the ADAM12 gene in liver cancer tissue significantly and positively correlated with T stage, pathological stage, and residual tumour. Kaplan–Meier and Cox regression analyses revealed that ADAM12 gene expression is an independent risk factor influencing the prognosis of patients with liver cancer. Pathway analyses of ADAM12 in HCC revealed ADAM12-correlated signalling pathways, and the expression level of ADAM12 was associated with immune cell infiltration. In vitro experiments demonstrated that the expression level of ADAM12 in Huh-7 and Hep3B cells was significantly higher than that in other HCC cells. ShRNA transfection experiments confirmed that the expression levels of TGF-β and Notch pathway-related proteins were significantly decreased. An EdU cell proliferation assay showed that a low level of ADAM12 gene expression significantly inhibited the proliferative activity of HCC cells. Cell cycle experiments showed that low ADAM12 expression blocked the G1/S phase transition. Overall, this research revealed that high ADAM12 gene expression implies a poor prognosis for patients with primary liver cancer. In addition, it is a potential indicator for the diagnosis of liver cancer.

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“…Известно, что на этапе прогрессирования хронических фиброзирующих процессов в печени ведущая патогенетическая роль принадлежит уже не этиологическим факторам [2,3], которые способны лишь усиливать и ускорять процесс необратимого повреждения печени, а развитию глубоких структурных и функциональных нарушений иммунной системы. Иммунная система, являясь одной из важнейших регуляторных систем организма (наряду с нервной и гуморальной), ответственна не только за поддержание иммунного гомеостаза, но и за регуляцию восстановительных регенераторных процессов [4−6], а также за реализацию защитно-приспособительных реакций организма, не связанных с иммунным ответом [7].…”

Section: Reviewunclassified

Progressive dysfunction of the immune system as a factor preventing recoverable regeneration of the liver in chronic fibrosing diseases

Онищенко,

Никольская,

Шагидулин

2023

Zhurnal «Patologicheskaia Fiziologiia I Eksperimental`naia Terapiia»

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С целью выявления критериев прогнозирования тяжести повреждения печени и эффективности корригирующей терапии в обзоре обсуждаются особенности прогрессирования дисфункции иммунитета при хронических фиброзирующих заболеваниях печени. Несмотря на различия в этиопатогенезе хронических заболеваний печени, развитие фиброза и цирроза печени происходит на фоне однотипно прогрессирующих проявлений дисфункции компонентов врождённого и адаптивного иммунитета, а также изменений костного мозга – центрального органа иммуногенеза. Наблюдаемые сдвиги формируются как следствие хронического воздействия на организм интоксикации, транслокации бактерий из кишечника, нарушенного метаболизма и прогрессирующего системного воспаления. Уже на раннем этапе активации процессов фиброзирования печени клетки врождённого и адаптивного иммунитета становятся длительно гиперактивированными, появляются субпопуляции с профиброгенными иммуносупрессирующими свойствами (стадия субкомпенсации). По мере прогрессирования деструктивных процессов в печени (переход фиброза в цирроз) в состоянии иммунных клеток появляются признаки истощения функции, выраженного цитокинового дисбаланса и стойкой иммуносупрессии (стадия декомпенсации или «иммунного паралича»). Иммуносупрессия при этом становится фактором повышенной восприимчивости организма к бактериальным инфекциям и септическим осложнениям, а также фактором глубокого торможения регуляции восстановительных процессов (второй важнейшей функции иммунитета) и развития необратимости повреждения печени. Стадийность развития иммунного дисбаланса при прогрессировании фиброза в цирроз может быть выявлена с помощью маркеров врожденного и адаптивного иммунитета, а также по содержанию в крови CD34+ клеток костного мозга. Обсуждается значение выявления стадий иммунного дисбаланса для прогнозирования тяжести (обратимости) повреждения печени и эффективности применения корригирующей терапии. This review discusses features of progressive immune dysfunction in chronic fibrosing liver diseases to identify criteria for predicting the severity of liver (L) damage and the effectiveness of corrective therapy. Despite differences in the etiopathogenesis of chronic L disease, the development of L fibrosis and cirrhosis is associated with similarly progressing manifestations of dysfunction of innate and adaptive immunity components, as well as changes in the bone marrow, the central organ of immunogenesis. These changes result from chronic intoxication, bacterial translocation from the gut, impaired metabolism, and progressive systemic inflammation. Already at the early stage of L fibrosis activation, innate and adaptive immune cells become chronically hyperactivated, and subpopulations with profibrogenic immunosuppressive properties emerge (subcompensation stage). With the progression of hepatic destructive processes (evolution of fibrosis to cirrhosis), the immune cells display signs of functional exhaustion, pronounced cytokine imbalance, and persistent immunosuppression (decompensation stage or “immune paralysis”). In this case, immunosuppression becomes a factor of increased susceptibility of the body to bacterial infections and septic complications, as well as a factor of deep inhibition of the regenerative process (the second most important immunity function) and the development of irreversible L damage. The staging of the immune imbalance during the progression of L fibrosis to cirrhosis can be detected with markers of innate and adaptive immunity and by the blood content of CD34+ bone marrow cells. The authors discussed the importance of identifying the stages of immune imbalance for predicting the severity (reversibility) of L damage and the effectiveness of corrective therapy.

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A review of alcohol–pathogen interactions: New insights into combined disease pathomechanisms

Cited by 9 publications

References 80 publications

The effect of C60 fullerene on the mechanokinetics of muscle gastrocnemius contraction in chronically alcoholized rats

The effect of C60 fullerene on the mechanokinetics of muscle gastrocnemius contraction in chronically alcoholized rats

ADAM12 is an independent predictor of poor prognosis in liver cancer

Progressive dysfunction of the immune system as a factor preventing recoverable regeneration of the liver in chronic fibrosing diseases

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