Characterization of inflorescence-predominant chitinase gene in Metroxylon sagu via differential display

Chitinase is an enzyme that catalyzes the degradation of chitin, commonly induced upon the attack of pathogens and other stresses. A cDNA (MsChi1) was isolated from Metroxylon sagu and expressed predominantly in the inflorescence tissue of M. sagu, suggesting its role in developmental processes. The chitinase cDNA was detected and isolated via differential display and rapid amplification of cDNA ends (RACE). Primers specific to M. saguchitinase were used as probes to amplify the 3′-end and 5′-end regions of chitinase cDNA. Transcript analysis showed that chitinase is expressed in inflorescence and meristem tissues but was not detected in the leaf tissue. Sequence analysis of amplified cDNA fragments of 3′-end and 5′-end regions indicated that the chitinase cDNA was successfully amplified. The M. saguchitinase cDNA isolated was approximately 1,143 bp long and corresponds to 312 predicted amino acids. Alignments of nucleotide and amino acid have grouped this chitinase to family 19 class I chitinase

Acinetobacter baumannii Infection Inhibits Airway Eosinophilia and Lung Pathology in a Mouse Model of Allergic Asthma

Allergic asthma is a dysregulation of the immune system which leads to the development of Th2 responses to innocuous antigens (allergens). Some infections and microbial components can re-direct the immune response toward the Th1 response, or induce regulatory T cells to suppress the Th2 response, thereby inhibiting the development of allergic asthma. Since Acinetobacter baumannii infection can modulate lung cellular and cytokine responses, we studied the effect of A. baumannii in modulating airway eosinophilia in a mouse model of allergic asthma. Ovalbumin (OVA)-sensitized mice were treated with live A. baumannii or phosphate buffered saline (PBS), then intranasally challenged with OVA. Compared to PBS, A. baumannii treatment significantly reduced pulmonary Th2 cytokine and chemokine responses to OVA challenge. More importantly, the airway inflammation in A. baumannii-treated mice was strongly suppressed, as seen by the significant reduction of the proportion and the total number of eosinophils in the bronchoalveolar lavage fluid. In addition, A. baumannii-treated mice diminished lung mucus overproduction and pathology. However, A. baumannii treatment did not significantly alter systemic immune responses to OVA. Serum OVA-specific IgE, IgG1 and IgG2a levels were comparable between A. baumannii- and PBS-treated mice, and tracheobronchial lymph node cells from both treatment groups produced similar levels of Th1 and Th2 cytokines in response to in vitro OVA stimulation. Moreover, it appears that TLR-4 and IFN-γ were not directly involved in the A. baumannii-induced suppression of airway eosinophilia. Our results suggest that A. baumannii inhibits allergic airway inflammation by direct suppression of local pulmonary Th2 cytokine responses to the allergen

Association between cytokines and cerebral MRI changes in the aging brain

The association between cytokines (IL-1β, sIL-4R, IL-6, IL-8, IL-10, IL-12, TNF-α) and subcortical white matter lesions, cortical atrophy and lacunar infarctions of the aging brain was investigated among 268 elderly community participants. Single pro- and anti-inflammatory cytokines were neither associated with WML nor with atrophy and lacunar infarction. An association between atrophy and the chemokine-cytokine factor (containing sIL-4R, IL-6, IL-8) remained significant after adjustment for age, gender, education, depressive symptoms, diabetes mellitus, cardiovascular diseases (stroke, TIA, myocardial infarction, myocardial insufficiency, arrhythmic heart), hypertension, body-mass index, smoking status and aggregation inhibitors as opposed to single cytokines. Atrophy of the parietal, temporal and occipital lobes was associated with the same cytokinechemokine factor for both the whole sample or restricted to those without history of stroke/TIA. The results indicate that a combination of chemokine-cytokines rather than single cytokines may contribute to inflammatory processes associated with cortical atrophy in the aging brain.Bernhard T. Baune, Gerald Ponath, Matthias Rothermundt, Andreas Roesler and Klaus Berge