disrupt bacterial replication in infected macrophages. This cumulative evidence indicates the methylation effect of Legionella effector Lpg2936 on the host autophagy-related molecules Atg7 and LC3B and subsequent reduction in the expression levels of autophagy effectors during intracellular replication of L. pneumophila.

Helicobacter pylori (H. pylori) is a Gram-negative, spiraling, microaerophilic bacteria that normally infect the stomach of human and produces stomach inflammation which can develop to gastric ulcers of the stomach or the upper part of the small intestine. Several cellular signaling pathways such as mitogen activated protein kinases (MAPKs) and RNA activating factor 1 (RAF-1) signaling cascade may be involved in H. Pylori infection. MAPKs are a type of extracellular communication that consists of a chain of proteins that extends from cell receptors to nuclear DNA. MAPK signaling is usually triggered by cell receptors attaching to epidermal growth factors (EGF), also known as the growth factor pathway or extracellular signal-regulated kinase (ERK). By administering HeLa cells with Sorafenib (SOR), a systemic medication for malignant malignancies, we studied the possibility of inhibiting H. pylori replication. In pretreated and infected cells, the expression of RAF-1 and autophagy related 5 (Atg5) was monitored to see if targeting these factors can disrupt H. Pylori intracellular replication. Surprisingly, the relative expression of bacterial 16s ribosomal RNA in SOR-treated cells revealed a competitive suppression of bacterial replication (16srRNA). Furthermore, SOR therapy successfully controlled the expression of the Raf-1 and Atg5 genes without causing any toxicity. In addition, SOR therapy lowered the production of tumor necrosis factor (TNF-) in a dose and time-dependent manner. These data suggest that SOR can disrupt H. Pylori replication in HeLa cells by suppressing MAPK and autophagy signaling, with minimal TNF-generation from treated cells.