By William Shafer
Microbes are in our midst quickly after delivery. fortunately, the variety of innocuous (and frequently worthwhile) microbes a long way outnumber those who may do us damage. Our skill to ward-off pathogens in our surroundings, together with those who can colonize our external and/or inside surfaces, is determined by the integrative motion of the innate and adaptive immunity platforms. This quantity of CTMI, entitled Antimicrobial Peptides and Human ailment, is devoted to the function of antimicrobial peptides (AMPs) within the innate host safeguard procedure of homo sapiens.
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Extra info for Antimicrobial Peptides and Human Disease (Current Topics in Microbiology and Immunology)
This peptide is more basic, has a broader spectrum and stronger bactericidal activity against Gram-positive and Gram-negative bacteria, as well as yeast, and is salt-insensitive at concentrations less than 200 mM Na+ ions (Harder et al. 2001). Most biological ﬂuids, including sputum (Halmerbauer et al. 2000), airway surface liquid (Baconnais et al. 1999) and serum/plasma (Hoshino et al. 2003) contain Mg2+ and Ca2+ at free concentrations between 1 and 2 mM, and the presence of these ions is generally more detrimental to antimicrobial activity than Na+ alone.
For example, adenovirus transfer of LL-37/hCAP18 into the lungs of mice that were subsequently challenged with Pseudomonas aeruginosa led to a reduction in both the bacterial load and in production of the pro-inﬂammatory cytokine, TNF-α (Bals et al. 1999), and intriguingly, similar gene therapy decreased susceptibility to sepsis induced by LPS in the complete absence of bacterial infection. In other models, the simultaneous instillation into the mouse lung of P. aeruginosa and either of HBD2 or a LL37 derivative led to reduced lung damage and pro-inﬂammatory cytokine production, but did not affect bacterial counts (Sawa et al.
HBD2 is inducible during the course of inﬂammation and infection in the gastrointestinal system, as observed at both the mRNA and protein levels. HBD2 expression in intestinal and colonic epithelial cell lines is increased upon stimulation with IL-1α, ﬂagellin or bacteria, in an NF-κB-dependent manner (O’Neil et al. 1999; Ogushi et al. 2001), and by either lipopolysaccharide (LPS) or lipoteichoic acid (LTA) in a TLR4 and TLR2-dependent manner (Vora et al. 2004). Interestingly, other inﬂammatory Immunomodulatory Properties of Defensins and Cathelicidins 33 mediators such as TNF-α and LPS do not induce HBD2 up-regulation (O’Neil et al.
Antimicrobial Peptides and Human Disease (Current Topics in Microbiology and Immunology) by William Shafer