<p>Evaluation of plasma antimicrobial peptide LL-37 and nuclear factor-kappaB levels in stable chronic obstructive pulmonary disease</p>

Abstract

BackgroundAntimicrobial peptides are effectors of host defence against infection and inflammation and can encourage wound repair.ObjectivesThe objectives of this study were to investigate the plasma antimicrobial peptide LL-37 and nuclear factor-kappaB (NF-κB) levels in patients with stable COPD compared with a control group and to highlight their importance in immune inflammation.MethodsOne hundred and thirty-eight stable COPD patients and 33 control subjects were enrolled in the study. The COPD patients were classified into four groups based on FEV1 (groups I–IV) and also divided into “low-risk and high-risk” groups (groups A–B [low risk], C–D [high risk]).ResultsPlasma LL-37 levels were significantly lower while plasma NF-κB levels of the COPD patients were significantly higher than those of the control subjects (P<0.001, both). LL-37 levels were significantly lower in group IV than in groups I, II, and III (P<0.01, all). NF-κB levels were significantly higher in groups III and IV than in groups I and II (P<0.05, both). There was a positive correlation between FEV1 and FEV1/FVC in all COPD patients (r=0.742, P<0.001) and in group D (r=0.741, P<0.001). Furthermore, there was an inverse correlation between LL-37 and NF-κB in both the groups C (r=−0.566, P<0.001) and D (r=−0.694, P<0.001) and group C+D combined (r=−0.593, P<0.001). Furthermore, in group C, LL-37 and FEV1 were positively correlated (r=0.633, P<0.001).ConclusionOur study indicated that plasma LL-37 and NF-κB may play an important role in chronic immune inflammation. Decreased LL-37 levels may be particularly high risk for patients in stage IV disease. The role of LL-37 as a target for treatment of the immune system and COPD must be widely evaluated.

Effects of cigarette smoke on barrier function and tight junction proteins in the bronchial epithelium: protective role of cathelicidin LL-37

“…These findings suggest that there may be cell type-specific gene regulation of TJ proteins by LL-37. There is growing evidence of an association between LL-37 and the pathogenesis of COPD [18–21]. High sputum LL-37 levels in stable COPD were associated with increased risk of exacerbations, non-typeable Haemophilus influenzae colonization, and high levels of inflammatory markers [20].…”

“…High sputum LL-37 levels in stable COPD were associated with increased risk of exacerbations, non-typeable Haemophilus influenzae colonization, and high levels of inflammatory markers [20]. Meanwhile, plasma LL-37 levels in patients with COPD were lower than those in control subjects, and LL-37 level and FEV 1 were positively correlated in the severe COPD group [21]. The LL-37 levels in bronchoalveolar lavage fluid were elevated in patients with COPD at GOLD I–II stage, but reduced in patients with advanced COPD at GOLD III–IV stage [19].…”

“…Among the AMPs, LL-37 is the only member of the cathelicidin family found in humans and was reported to upregulate the levels of TJ proteins and increase human epidermal keratinocyte barrier function [16, 17]. There is also growing evidence that LL-37 is involved in the pathogenesis of COPD [18–21]. A previous study showed that LL-37 levels in sputum were elevated in patients with COPD compared with control subjects, but decreased in asthmatic patients [22].…”

Expression and Function of Host Defense Peptides at Inflammation Sites

“…However, if their production is out of the physiological range, they may contribute to an undesirable inflammation in response to local (e.g., periodontal, respiratory, intestinal, and skin) and systemic (e.g., sepsis) infections. They might also function as pathophysiological events of inflammatory diseases, cancers, and even psychiatric disorders (Table 1) [17][18][19][20][21][22][23]. In addition, HDPs have been indicated as potential biomarkers in numerous infectious and non-infectious diseases [24].…”

Discovery of Selenocysteine as a Potential Nanomedicine Promotes Cartilage Regeneration With Enhanced Immune Response by Text Mining and Biomedical Databases

“…Eight HUB Genes with scores of >0.900 (maximum confidence) were chosen to create the PPI networks: CAMP and TOLLIP, DEFA3, HLA-DQA2, SLC38A6, SLC3A1, FAM20A and ANO8 ( Figure 5). CAMP translates the set of an antimicrobial peptide family, characterized by chemoattractant, immune mediator induction, and immunoreaction regulation (Snoussi et al, 2018;Uysal et al, 2019). Toll interacting protein (TOLLIP) encodes a ubiquitin-binding protein that regulates inflammatory signalling (Diao et al, 2016;Shah et al, 2017).…”