Aims: Acute lung inflammation, particularly acute respiratory distress syndrome (ARDS), is caused by a variety of pathogens including bacteria and viruses. β-Glucans have been reported to possess both anti-inflammatory and immunomodulatory properties. The current study evaluated the therapeutic effect of β-glucans on polyinosinic:polycytidylic acid (Poly(I:C)) induced lung inflammation in both hamster and mice models.
View Article and Find Full Text PDFHuman lymphatic filariasis, the parasitic disease caused by the filarial nematodes Wuchereria bancrofti, Brugia malayi, and Brugia timori, is ranked as the second most complex clinical condition leading to permanent and long-term disability. The multiple antigen peptide (MAP) approach is an effective method to chemically synthesize and deliver multiple T and B cell epitopes as the constituents of a single immunogen. Here, we report on the design, chemical synthesis, and immunoprophylaxis of three epitopes that have been identified from promising vaccine candidates reported in our previous studies, constructed as MAP on an inert lysine core for human lymphatic filariasis in Jird model.
View Article and Find Full Text PDFBackground: Abundant Larval Transcript (ALT) is one of the major groups of immune-dominant proteins produced by filarial worms during their larval stage. The major B-cell and T-cell epitopic domains of the ALT-2 antigen were mapped to develop a multiple antigenic peptide (MAP) prophylactic antigen against lymphatic filariasis.
Methods And Results: ALT MAP was constructed by solid phase peptide synthesis.
The filarial protein Abundant Larval Transcript-2 (ALT-2) of the filarial parasite Brugia malayi has been shown to produce 74% worm clearance when administered with an adjuvant. In the present study, we show that it not only induces humoral and cell-mediated immunity, but also protection up to 71% in Mastomys coucha, a permissive animal model for filariasis, even without adjuvant. This unique feature of ALT-2 protein is highly restricted to its 21 amino acid N-terminal signal sequence, the absence of which resulted in poor immune response as well as immunoprotection (49%).
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