Background and Objectives: Bronchial asthma (BA) and chronic obstructive pulmonary disease (COPD) are not only common obstructive respiratory conditions but also major causes of morbidity and mortality worldwide. There is, however, a surprising lack of blood-based biomarkers for separating between these pulmonary disorders. The aim of this study was to assess the practical relevance of using serum YKL-40, single or combined, for this purpose. Materials and Methods: Subjects included Romanian patients with BA (n = 24) or COPD (n = 27). YKL-40, fibrinogen, pre-treatment C-reactive protein (CRP), post-treatment CRP, erythrocyte sedimentation rate, interleukin 6 (IL-6), procalcitonin (PCT), absolute neutrophil count, neutrophil percentage, absolute lymphocyte count, lymphocyte percentage, absolute eosinophil count, and eosinophil percentage were measured and compared between these patients. Results: This is the first study investigating the clinical significance of serum YKL-40 in delineating between COPD and BA in Caucasian populations. Only fibrinogen and YKL-40 levels were different between COPD and BA, with the measured values being significantly elevated. These patients exhibited distinct inflammatory profiles. Using the upper quartiles of these variables for the pooled study population (YKL-40: 5100 pg/mL; fibrinogen: 552 mg/dL) as cut-off values, subjects were classified into high or low groups. High YKL-40 adults revealed significantly increased PCT levels. High fibrinogen subjects, by contrast, showed significantly elevated IL-6 concentrations and pre-treatment CRP levels. Low YKL-40 and fibrinogen patients showed the absence of COPD. Conclusions: Combined use of serum YKL-40 and fibrinogen may be useful for identifying the absence of COPD.

Objectives To analyse: (1) the associations between different mannose-binding lectin 2 ( MBL2) genotypes and susceptibility to bronchial asthma (BA) in Romanian children; and (2) the correlations between several patient sociodemographic variables and MBL2 polymorphisms. Methods This prospective observational case–control study included paediatric patients with symptomatic BA and healthy controls. Participants were genotyped for two MBL2 single-nucleotide polymorphisms (SNPs): exon 1 codon 54 A/B variant rs1800450, and -550 promoter H/L variant rs11003125 (GenBank accession). Associations between MBL2 genotypes and susceptibility to BA were determined by calculated odds ratios, and Kendall Tau’s correlations were used to investigate the associations between sociodemographic variables and SNPs. Results Among 59 patients with BA and 65 healthy controls, associations between MBL2 polymorphisms and susceptibility to BA were not found to be statistically significant. Statistically significant weak positive correlations were found between age at diagnosis and A/B genotype, and between the smoking status of biologically male and female parents. A statistically significant weak inverse association was found between male parent smoking status and family history of BA. Conclusion These results may help guide future research into paediatric BA in Romania and Eastern Europe. Due to study limitations, the results require validation in future large-scale studies.

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REzumatIniţierea şi întreţinerea răspunsului inflamator la nivelul căilor respiratorii la pacienţii cu astm bronşic implică interacţiunea între epiteliul respirator, sistemul imunitar înnăscut şi cel adaptiv. Factorii de mediu şi factorii locali induc producţia de mediatori proinflamatori la nivelul epiteliului căilor respiratorii, activând apoi celulele proinflamatorii. Celulele proinflamatorii infiltrează plămânii şi eliberează alţi mediatori, care accentuează răspunsul inflamator la acest nivel, astfel realizând un cerc vicios al inflamaţiei. Acest proces cauzează bronhoconstricţie şi leziuni epiteliale, care determină remodelarea căilor respiratorii.Cuvinte cheie: astm bronşic, copii, inflamaţie cronică, citokine, factori de creştere aBStRaCt The inflammatory response in the airways of patients with asthma involves the interaction between the respiratory epithelium, the innate immune system and the adaptive immunity, which initiates and maintains the chronic inflammatory response. Environmental factors in interaction with local factors induce the production of proinflammatory mediators in the airway epithelium and then activate the proinflammatory cells. The pro-inflammatory cells infiltrate the lungs and release other mediators, which accentuate the inflammatory response at this level, thus achieving a vicious circle of inflammation. This process causes bronchoconstriction and epithelial injury, which results in airway remodeling.