Toll-like receptor 2 (TLR2), a member of the Toll-like receptor family, plays an important role in recognition of, and subsequent immune response activation against, mycobacteria. The genetic polymorphism of TLR2 (arginine to glutamine substitution at residue 753 (Arg753Gln)) has been associated with a negative influence on TLR2 function, which may, in turn, determine the innate host response to mycobacteria. The aim of the present study was to investigate the Arg753Gln single nucleotide polymorphism of the TLR2 gene in tuberculosis (TB) patients compared to healthy controls.A retrospective case/control study was carried out. The Arg753Gln polymorphism of the TLR2 gene was studied in 151 TB patients compared to 116 ethnically and agematched healthy control subjects.The TLR2 polymorphism (adenine (A) allele) was observed in 17.9 and 7.7% of TB patients and controls, respectively. When the ratios of the three genotypes were compared between the two groups, the AA genotype was found to be more significantly associated with TB. Allele frequencies for guanine (G) and A were found to be 0.95 and 0.05 in the control group and 0.86 and 0.14 in the TB patient group, respectively. The risk of developing TB disease was increased 6.04-and 1.60-fold for carriers of the AA and GA genotypes, respectively.In conclusion, the present data suggest that the arginine to glutamine substitution at residue 753 polymorphism of the Toll-like receptor 2 gene influences the risk of developing tuberculosis.

The allergens implicated in this report reflect previous data from similar patient groups in North America. Asthmatic children suffer more severe reactions than non-asthmatic children. It appears that British adults need better access to expert care of their allergies. Even when it is prescribed and available self-injectable adrenaline appears under-used in severe reactions. The incidence of severe but non-fatal allergic reactions in the UK may have been underestimated in the past.

No abstract

Mannose-binding lectin (mbl), one of the important components of innate immunity, can activate the lectin pathway of the complement system. After binding mannose containing carbohydrate structures of foreign antigen, mbl initiates and regulates the inflammatory responses. Asthma is a complex inflammatory disease of the lung involving many components of the immune system. Our objective was to investigate the serum mbl levels of asthmatic children in comparison with healthy controls. Serum mbl levels were determined by nephelometric assay in 72 asthmatic children (5-15 yr old) and 30 healthy age-matched controls. Mbl levels of asthmatic children were measured both during acute attack and after complete remission. There was no significant difference between the mbl levels during acute attack (median 4.1 mg/l) or quiescence of symptoms (median 3.6 mg/l). Serum mbl levels both during acute attack or quiescence of symptoms was significantly higher in asthmatic children than in the healthy controls (median 2.8 mg/l, p < 0.0001 for each). Furthermore, mbl levels of asthmatic children positively correlated with peripheral blood eosinophils (r = 0.377, p < 0.001), which is a systemic component of airway inflammation in asthma. Our findings indicate that mbl may be implicated in the pathogenesis of asthma by contributing to airway inflammation or by increasing the risk of developing asthma.

Recurrent wheezing in infancy may be associated with many environmental and genetic factors. It is possible that allergen avoidance merely delays rather than prevents the development of allergic disorders.