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Autophagy, a lysosome-dependent protein degradation mechanism, is a highly conserved catabolic process seen in all eukaryotes. This cell protection system, which is present in all tissues and functions at a basic level, can be up- or downregulated in response to various stresses. A disruption in the natural route of the autophagy process is frequently followed by an interruption in the inherent operation of the body’s cells and organs. Probiotics are live bacteria that protect the host through various mechanisms. One of the processes through which probiotics exert their beneficial effects on various cells and tissues is autophagy. Autophagy can assist in maintaining host homeostasis by stimulating the immune system and affecting numerous physiological and pathological responses. In this review, we particularly focus on autophagy impairments occurring in several human illnesses and investigate how probiotics affect the autophagy process under various circumstances.Abbreviation: AD: Alzheimer disease; AKT: AKT serine/threonine kinase; AMPK: 5′AMP-activated protein kinase; ATG: autophagy related; CCl4: carbon tetrachloride; CFS: cell-free supernatant; CMA: chaperone-mediated autophagy; CRC: colorectal cancer; EPS: L. plantarum H31 exopolysaccharide; HD: Huntington disease; HFD: high-fat diet; HPV: human papillomavirus; IFNG/IFN-γ: interferon gamma; IL6: interleukin 6; LGG: L. rhamnosus GG; LPS: lipopolysaccharide; MTOR: mechanistic target of rapamycin kinase; MTORC1: MTOR complex 1; NAFLD: non-alcoholic fatty liver disease; NASH: non-alcoholic steatohepatitis; PD: Parkinson disease; Pg3G: pelargonidin-3-O-glucoside; PI3K: phosphoinositide 3-kinase; PolyQ: polyglutamine; ROS: reactive oxygen species; SCFAs: short-chain fatty acids; SLAB51: a novel formulation of lactic acid bacteria and bifidobacteria; Slp: surface layer protein (of acidophilus NCFM); SNCA: synuclein alpha; ULK1: unc-51 like autophagy-activating kinase 1; YB: B. longum subsp. infantis YB0411; YFP: yeast fermentate prebiotic. [ABSTRACT FROM AUTHOR]

Helicobacter pylori as a class I carcinogen is correlated with a variety of severe gastroduodenal diseases; therefore, H. pylori eradication has become a priority to prevent gastric carcinogenesis. However, due to the emergence and spread of multidrug and single drug resistance mechanisms in H. pylori, as well as serious side effects of currently used antibiotic interventions, achieving successful H. pylori eradication has become exceedingly difficult. Recent studies expressed the intention of seeking novel strategies to improve H. pylori management and reduce the risk of H. pylori-associated intestinal and extragastrointestinal disorders. For which, vitamin supplementation has been demonstrated in many studies to have a tight interaction with H. pylori infection, either directly through the regulation of the host inflammatory pathways or indirectly by promoting the host immune response. On the other hand, H. pylori infection is reported to result in micronutrient malabsorption or deficiency. Furthermore, serum levels of particular micronutrients, especially vitamin D, are inversely correlated to the risk of H. pylori infection and eradication failure. Accordingly, vitamin supplementation might increase the efficiency of H. pylori eradication and reduce the risk of drug-related adverse effects. Therefore, this review aims at highlighting the regulatory role of micronutrients in H. pylori-induced host immune response and their potential capacity, as intrinsic antioxidants, for reducing oxidative stress and inflammation. We also discuss the uncovered mechanisms underlying the molecular and serological interactions between micronutrients and H. pylori infection to present a perspective for innovative in vitro investigations, as well as novel clinical implications. [ABSTRACT FROM AUTHOR]