Fucosyltransferase 2 induces lung epithelial fucosylation and exacerbates house dust mite–induced airway inflammation

Mice lacking fucosyltransferase 2 show reduced innate allergic inflammation in the airways

“…1 Component diagnosis of peach allergy indicates Pru p 1, Pru p 2, Pru p 3, Pru p 4, Pru p 7, and Pru p 9 are involved. 2,3 Pru p 3 is the dominant allergen responsible for severe allergic reaction, 4 and it is considered to be the primary sensitizer to other LTPs in Mediterranean and Central Europe. 5 The levels of Pru p 3 differ between varieties.…”

Stuck in the MUC: Infinity loop of fucosylation in allergic airway inflammation

“…Secretion of fucosyltransferase is important because human subjects can have a secretor form of FUT2 SeSe and Sese or a nonsecretor sese form of the FUT2 gene. This O-secretor is interesting and highly relevant in the context of the article by Saku et al 2 In the intestine deficient fucosylation leads to development of colitis/inflammatory bowel disease. In this context intestinal epithelial cell fucosylation appears to be a protective mechanism that uses the host's resources to maintain host-microbial interactions during pathogen-induced stress.…”

“…An effect of Fut2 is that bronchial hyperreactivity, measured as airway resistance, is less in Fut2 2/2 mice than in wild-type mice treated with house dust mite. 2 This could be a combination effect of less fucosylated mucins and less stiffness in the mucus in the absence of fucosyltransferase (Fig 1, A). This is of interest because patients with a FUT2 secretor phenotype have more exacerbations.…”

“…If FUT2 is absent from the luminal side of the airways, AAI is reduced. 2 When asthmatic patients had recurrent exacerbations, they were started on additional therapy to combat the exacerbation. It was found that FUT2 asthmatic patients with the secretor SeSe homozygous or Sese heterozygous genotype performed a lot worse than nonsecretor asthmatic patients with the sese genotype.…”

“…3 The article by Saku et al 2 is translational research that applies to the clinical observation of patients with secretor and nonsecretor genotypes. 2 The article is important in that it shows how fucosylation operates and why it is important to genotype asthmatic patients at risk (Fig 1, A). It also explains why disease progression occurs in the O-secretor variant of patients with severe asthma, 3 even when they are started on progressive anti-inflammatory therapy.…”