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In the latter form, a uveal component, whether tissue damage or a microbial trigger, stimulates the generation of antigen-specific T cells and/or autoantibodies that are believed to play a pathogenetic role [[3]], hence the term autoimmune uveitis (AU).
The classical activation of macrophages is achieved by stimulation with interferon-γ (INFγ) followed by exposure to a microbial trigger like lipopolysaccharide (LPS) resulting in a pro-inflammatory phenotype [1], [3].
NALP1 and NALP3 evolve in the sensing of endogenous danger signals independent of the microbial trigger.
Endotoxin is the most important microbial trigger in the life-threatening condition sepsis (systemic inflammation due to infection), which kills 4 million people a year worldwide (Cohen, 2002).
The role of infection as a triggering factor is implicated with varying degrees of certainty amongst the SpA subcategories, with ReA having the most clear evidence for a microbial trigger [ 15].
Remarkably, recent findings suggest a dysbalanced microbiom of the nasal cavity rather than a distinct microbial trigger comparable to the dysbiosis in inflammatory bowel diseases like Morbus Crohn [ 18].
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Microbial triggers have been implicated in RA (Zhang et al., 2015).
Chorioamnionitis induced by different microbial triggers results in pulmonary inflammation and subsequent structural simplification in the alveoli and vasculature of the fetal lung [5, 6].
As a response to chronic microbial triggers, innate immune cells, particularly neutrophils, are continuously recruited into CF airways where they combat pathogens but also cause tissue injury through release of oxidants and proteases.
We will also summarize what is known about the microbial triggers and inflammatory consequences of clinically well-known neonatal immune-mediated diseases, such as respiratory distress syndrome (RDS), bronchopulmonary dysplasia (BPD), and necrotizing enterocolitis (NEC).
Inflammatory bowel diseases (IBD), consisting of Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory conditions of the gut believed to occur in genetically predisposed individuals who are exposed to unknown environmental and microbial triggers [1], [2], [3], [4].
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