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Although definitive mechanistic evidence is lacking, it has been suggested that these links may be mediated to some degree via both the microbial component and the inflammatory burden that characterize the disease (6– 8).
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Interestingly, the compositional abundance of both the endosymbiotic microbial components and the expressed key gene transcripts for various energy metabolisms vary with the regional geochemical gradient (Sanders et al. 2013).
Lysozyme is produced mainly by macrophages in response to microbial components and many other immune stimulants (Siwicki and Anderson Siwicki and Anderson 1993; Ringø et al. 2012) and it is a preferred marker of the immune response due to its close association with leucocytes (Kiron 2012).
As another PRRs family, Nod-like receptors (NLRs) are intracellular, cytoplasmic sensor for microbial components and danger signals [3], [4].
Incomplete and limited information is available on fluctuations in level and status of serum antibodies directed against microbial components and associated with CD over time.
Several classes of PRRs, including Toll-like receptors, recognize distinct microbial components and directly activate immune cells, including antigen presentation cells such as dendritic cells (DCs).
MiR-146 is also associated with inflammation and innate immune responses where it regulates the response to a variety of microbial components and proinflammatory cytokines [63].
Microbial components and endogenous danger signals trigger the activation of signaling cascades leading to induction of the NF-κB system during sepsis.
Taganov et al. [63] showed that miR-146 regulatory circuit fine-tunes TLR and cytokine signalling, rather than totally abrogating the signal, in response to microbial components and proinflammatory cytokines.
They can also be up-regulated by different microbial components and cytokines [ 4, 5, 18].
Toll-like receptors (TLRs) recognize microbial components and evoke inflammation and immune responses.
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