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Neutrophilic airway inflammation represents a pathologically distinct form of asthma and frequently appears in symptomatic adulthood asthmatics. However, clinical impacts and mechanisms of the neutrophilic inflammation have not been thoroughly evaluated up to date. Areas covered: Currently, distinct clinical manifestations, triggers, and molecular mechanisms of the neutrophilic inflammation (namely Toll-like receptor, Th1, Th17, inflammasome) are under investigation in asthma. Furthermore, possible role of the neutrophilic inflammation is being investigated in respect to the airway remodeling. We searched the related literatures published during the past 10 years on the website of Pub Med under the title of asthma and neutrophilic inflammation in human. Expert commentary: Epidemiologic and experimental studies have revealed that the neutrophilic airway inflammation is induced by a wide variety of stimuli including ozone, particulate matters, cigarette smoke, occupational irritants, endotoxins, microbial infection and colonization, and aeroallergens. These triggers provoke diverse immune and inflammatory responses leading to progressive and sometimes irreversible airway obstruction. Clinically, neutrophilic airway inflammation is frequently associated with severe asthma and poor response to glucocorticoid therapy, indicating the need for other treatment strategies. Accordingly, therapeutics will be targeted against the main mediators behind the underlying molecular mechanisms of the neutrophilic inflammation.

The authors devised a novel biphasic scaffold combining hyaluronic acid and atelocollagen for the chondral phase and combining hydroxyapatite (HA) and beta-tricalcium phosphate (beta-TCP) for the osseous phase. The biphasic scaffold was fabricated by placing the freeze-dried chondral phase over the HA/beta-TCP scaffold prewetted with hyaluronate/atelocollagen solution. Chondrocytes were isolated in 28 rabbits, expanded, injected inside the chondral phase of the biphasic scaffold, and then cultured in chondrogenic medium. After 2 weeks of in vitro culture, chondrocytes had evenly infiltrated inside the chondral phase and produced extracellular matrix. For in vivo study, a large osteochondral defect was made on the patellar groove of the right distal femur and managed using one of the following methods: filling with cell-biphasic scaffold composite (group I); implanting only biphasic scaffold (group II); placing the removed osteochondral fragments back into the defect (group III, positive control); leaving empty (group IV, negative control). Seven rabbits were allocated to each group. After 12 weeks, the International Cartilage Repair Society Macroscopic Score was highest in group III, followed by group I, group II, and lastly group IV. Depression of the defect was greatest in group IV. There were three rabbits (two in group I and one in group II) that were completely denuded of the chondral phase. The junction to adjacent native cartilage was distinct in rabbits of all groups. The International Cartilage Repair Society Visual Histological Score was highest in group III, followed by groups II and I, and lastly group IV. In conclusion, our results suggest that a biphasic osteochondral composite using a chondral phase consisting of hyaluronate and atelocollagen and an osseous phase consisting of HA and beta-TCP holds the promise for repair of osteochondral defects.

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