Involvement of the heat-labile serum factor suggests the potential role of the complement for defensin expression. The possible link between the proteins of the complement system and defensin expression may be anticipated since the interaction between the defensins and proteins of the complement system was demonstrated. It was found that HBD2 inhibits the classical pathway of the complement system [37]. Moreover, the interrelationship between the respiratory tract and the complement system was studied in an animal model [38]. The origin of complement proteins present CHIR-99021 solubility dmso in the lining fluid of the respiratory tract

is thought to result mainly from plasma that exudes into the bronchoalveolar space. However, it was shown that human bronchial epithelial cells generate complement protein C3: the modulation

of its expression by proinflammatory cytokines might be an additional regulatory mechanism of local airway defence during infection [39]. Furthermore, the kinetics of the expression of human beta defensins, hBD2 and hBD9, by airway epithelial cells exposed to the deferent morphotypes of A. fumigatus was analysed. Analysis of the kinetics of hBD2 and hBD9 defensin expression by cells exposed to A. fumigatus showed the prompt inducible expression of hBD9, following by delayed hBD2 expression. This could allow us to hypothesize that the host immune system may react against A. fumigatus by using the cascade of newly synthesized defensins that probably possess the different functions. OICR-9429 cell line However, this hypothesis would require further investigation at the protein level. Our Cell Penetrating Peptide data are in agreement with the analysis of kinetics of hBD2 expression by A549 cells exposed to Mycobacterium tuberculosis; infection of A549 cells resulted in hBD2 gene expression as early as 6 hours postinfection, while maximum expression was detected at 18 and 24 hours postinfection [35]. Several lines of evidence eliminated the possibility that observed inducible defensin expression was related to endotoxin contamination of A. fumigatus organisms. First, the addition of Polymixin B (known

for its endotoxin-neutralising activity) to the cells prior to exposure to A. fumigatus organisms did not have any effect on defensin expression. Second, rigorous measures were undertaken to keep endotoxin out of the experimental system, including washing of A. fumigatus organisms with the solution containing Polymixin B during preparation, utilisation of endotoxin-free plasticware and solutions in experiments, and washing of fungal organisms in endotoxin-free PBS prior to use. The expression of hBD2 and hBD9 was found to be higher in A549, 16HBE and primary culture HNT cells exposed to SC compared to RC or HF, as shown by quantitative PCR. During asexual growth, the morphological form of A. fumigatus changes from resting to swollen conidia, which then form germ tubes that continue growing in hyphal form. These transformations are accompanied by the modification of BIBF 1120 surface structures.