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Inflammatory bowel disease is used as a model system to understand these microbial-driven pathologies, but the knowledge gained in this space is extended to less-well-studied intestinal diseases that may also have an important microbial component, including environmental enteropathy and chronic colitis-associated colorectal cancer.
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Pattern recognition receptors (PRRs) are important effectors in the activation of the innate immune responses that recognizes microbial components including nucleic acids1.
The most important pattern recognition receptor family of receptors involved in lupus, namely the Toll-like receptors (TLRs), can recognize a broad range of microbial components, including DNA and RNA.
Recent attention has focused on the depletion of CD4T cells in the gastrointestinal tract, leading to increased microbial translocation and circulation of microbial cellular components, including lipopolysaccharide and bacterial DNA, the levels of which correlate with HIV disease progression.
Understanding how other dietary components, including polyphenols, might modify gut microbial populations and levels of phase I and II enzymes, may yield important information relevant to interindividual variation in chemical metabolism (Kemperman et al. 2010; van Duynhoven et al. 2010).
The microbial exposure associated with health complaints in moldy houses consists of a heterogeneous group of components, including both living and dead bacteria, fungi, and their metabolites and active compounds.
Many major components, including engines, were imported.
Environmental health scientists may need to expand the toxicokinetics of metals and other environmental agents, as well as associated biomarkers, to include the microbial component.
IKK responds to various cellular stimuli, including microbial components, cytokines, growth factors and mitogens, and agents causing stress.
The data presented in this paper are consistent with a model where continuous exposure to microbial material, including components of HIV, creates conditions permissive to the expansion pathologically activated CD4 T cells with the DEM phenotype.
We therefore suggest a model in which the accumulation of DEM CD4 T cells is the result of antigen-driven expansion under conditions when the immune system is exposed to microbial material, including components of HIV, driving innate immune activation.
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