Spiral bound mct mp4 download - accept. opinion
Lack of airway submucosal glands impairs respiratory host defenses.
Discussion
These results indicate that airway SMGs protect the lung by contributing to two critical respiratory host defenses, bacterial killing by ASL and production of strands of mucus. As a result, when challenged with S. aureus, EDA-KO lungs were compromised in their ability to eradicate bacteria, especially in regions normally populated by SMGs. Results from many previous studies underlie the assumption that SMGs play a critical role in host defense. Our findings provide direct evidence for that hypothesis, both in vivo and ex vivo.
Surface airway epithelia can also produce antimicrobials and mucins that facilitate bacterial killing and MCT (Widdicombe and Wine, ; Ganz, ; Bartlett et al., ; Fischer et al., ). What then is the evolutionary benefit of having SMGs in humans and pigs? One potential advantage is that SMGs markedly expand the number of epithelial cells available to produce antimicrobials and mucus and deliver them onto the airway surface (Widdicombe and Wine, ; Choi et al., ; Reid, ). In addition, innervation of SMGs by vagal cholinergic efferents enables them to rapidly secrete SMG products on demand (Wine, ; Widdicombe, ; Ballard and Spadafora, ). The ability to quickly deliver copious amounts of antimicrobials, mucins, and other mucus products could be critically important for responding to acute challenges such as aspiration, irritants, and pathogens.
Another potential advantage of having SMGs is that the mucus they produce emerges onto the airway surface in the form of strands (Hoegger et al., ; Ermund et al., ; Ostedgaard et al., ; Ermund et al., ; Fischer et al., ; Tipirneni et al., ; Trillo-Muyo et al., ; Xie et al., ). Our ex vivo and in vivo data and earlier reports indicate that strands of mucus bind to large particles and transmit forces from beating cilia, thereby initiating and sustaining particle transport up the airways and out of the lung (Hoegger et al., ; Fischer et al., ). Consistent with these findings, disrupting mucus strands by breaking disulfide cross links between mucin molecules impairs MCT (Fischer et al.,
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