{'fraction_non_alphanumeric': 0.022054868208714364, 'fraction_numerical': 0.0, 'mean_word_length': 5.480836236933798, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Host/pathogen interactions. Subversion of the mammalian cell cytoskeleton by invasive bacteria.

The high plasticity of the actin cytoskeleton and its dynamics are often exploited by bacterial pathogens, during entry, and in some cases movement and dissemination of these organisms in mammalian cells. Indeed, some bacterial pathogens, including the gram-negative bacteria Salmonella , Shigella , and Yersinia and the gram-positive bacterium Listeria monocytogenes , have the capacity to induce their own uptake into mammalian cells which are normally nonphagocytic. Entry of all of these bacteria requires rearrangement of the host cell actin cytoskeleton, since uptake is impaired by inhibitors of actin polymerization such as cytochalasin D. Exploitation of the cytoskeleton by pathogenic bacteria during entry can be divided, although artificially, into two general strategies, according to the type of morphological changes that occur in the host cell. Entry of Yersinia or Listeria has been described as occurring through a “zipper” type event, while entry of Salmonella or Shigella is often referred to as a “trigger” phenotype. However, even pathogens that share a common strategy appear to target different host proteins to induce uptake. After internalization, invasive bacteria either reside in membrane-bound vacuoles ( Yersinia and Salmonella ), or rapidly lyse such vacuoles and move within the cytoplasm by a process involving continuous polymerization of host actin at the posterior end of the bacterium ( Listeria and Shigella ). This intracytoplasmic movement is a prerequisite for direct cell to cell spreading. While the actin-based motilities of Listeria and Shigella are similar in many aspects, different bacterial proteins are involved, again suggesting that a similar strategy can be accomplished by nonidentical molecular mechanisms.