Secretory IgA from submucosal glands does not compensate for its airway surface deficiency in chronic obstructive pulmonary disease

Du, Rui-Hong; Richmond, Bradley W.; Blackwell, Timothy S.; Cates, Justin M.; Massion, Pierre P.; Ware, Lorraine B.; Lee, Jae Woo; Кононов, А. В.; Lawson, William; Polosukhin, Vasiliy V.

doi:10.1007/s00428-015-1854-0

Cited by 16 publications

(26 citation statements)

References 36 publications

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“…In 2001, Pilette and coworkers (13) reported that secretory component expression is reduced in airways of patients with COPD. Subsequently, we showed that pIgR expression is down-regulated in COPD and that airway surface SIgA deficiency is widespread in COPD and correlates with severity of airflow obstruction (14,15). Consistent with these observations, cultured airway epithelial cells from patients with COPD were reported to express lower levels of pIgR than airway epithelial cells from healthy control subjects (16).…”

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confidence: 52%

Secretory IgA Deficiency in Individual Small Airways Is Associated with Persistent Inflammation and Remodeling

Polosukhin

Richmond

et al. 2017

Am J Respir Crit Care Med

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Rationale: Maintenance of a surface immune barrier is important for homeostasis in organs with mucosal surfaces that interface with the external environment; however, the role of the mucosal immune system in chronic lung diseases is incompletely understood.Objectives: We examined the relationship between secretory IgA (SIgA) on the mucosal surface of small airways and parameters of inflammation and airway wall remodeling in chronic obstructive pulmonary disease (COPD).Methods: We studied 1,104 small airways (,2 mm in diameter) from 50 former smokers with COPD and 39 control subjects. Small airways were identified on serial tissue sections and examined for epithelial morphology, SIgA, bacterial DNA, nuclear factor-kB activation, neutrophil and macrophage infiltration, and airway wall thickness.Measurements and Main Results: Morphometric evaluation of small airways revealed increased mean airway wall thickness and inflammatory cell counts in lungs from patients with COPD compared with control subjects, whereas SIgA level on the mucosal surface was decreased. However, when small airways were classified as SIgA intact or SIgA deficient, we found that pathologic changes were localized almost exclusively to SIgAdeficient airways, regardless of study group. SIgA-deficient airways were characterized by (1) abnormal epithelial morphology, (2) invasion of bacteria across the apical epithelial barrier, (3) nuclear factor-kB activation, (4) accumulation of macrophages and neutrophils, and (5) fibrotic remodeling of the airway wall.Conclusions: Our findings support the concept that localized, acquired SIgA deficiency in individual small airways of patients with COPD allows colonizing bacteria to cross the epithelial barrier and drive persistent inflammation and airway wall remodeling, even after smoking cessation.

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confidence: 52%

Secretory IgA Deficiency in Individual Small Airways Is Associated with Persistent Inflammation and Remodeling

Polosukhin

Richmond

et al. 2017

Am J Respir Crit Care Med

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“…1,3 Roy and colleagues showed that Muc5b, but not Muc5ac, was required for airway defense and that the decrease of Muc5b could hamper mucus clearance. 19 Additionally, publications have stated that the levels of MUC5B in BALF and sputum were increased in COPD patients, [32][33][34] while carbocisteine could balance fucosylated and sialylated sugar chains, 13 normalize the viscous property of mucus 12 and reduce MUC5AC expression. We speculated that the decrease of Muc5b might have played an important role in COPD pathogenesis and carbocisteine might reduce the expression of Muc5b in COPD mice model.…”

Section: Discussionmentioning

confidence: 99%

CARBOCISTEINE INHIBITS THE EXPRESSION OF Muc5b IN COPD MOUSE MODEL

2017

Respirology

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could predict poor outcomes in exacerbation of COPD including serum albumin, hemoglobin, white blood cell count, serum sodium on the first day of admission and previous history of exacerbation. Binary logistic regression was used to identify factors associated with respiratory failure.Results: A total of 349 admission records were reviewed. The subjects' mean AE SD age was 74.2AE11.6 years, and 274 (78.5%) were male.During the admission, a total of 87 patients (24.9%) had respiratory failure and required ventilatory supports. In-hospital mortality rate was 8.0%. The only factor that associated with respiratory failure was low serum albumin level on the first admission day, 3.40AE0.62 g/dL (in respiratory failure group) compare to 3.67AE0.57 (in non-respiratory failure group), P=0.003.The other factors such as hemoglobin level, white blood cell count, serum sodium and history of previous exacerbation were not significantly associated with respiratory failure.Conclusions: Serum albumin on the first day of admission could predict respiratory failure in COPD patients with acute exacerbation.

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“…In 2001, Pilette et al reported that SC expression was reduced in airways of COPD (11). Subsequently, researchers found that patients with COPD had reduced SIgA in bronchoalveolar lavage (12). Polosukhin et al have shown that pIgR expression is down-regulated in COPD and that SIgA deficiency is correlated with severity of airflow obstruction(13).…”

Section: Introductionmentioning

confidence: 99%

Effect of hydrogen inhalation on IL-40 and SIgA in a Rat Model of Pulmonary Mucosal Immunity

Sun

Zhu

et al. 2020

Preprint

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AbstractBackgroundRecently, some researchers have reported that PIgR expression is down-regulated in Chronic Obstructive Pulmonary Disease (COPD) and SIgA deficiency correlates with severity of airflow obstruction. What’ s more, some studies have demonstrated that 2 percent of hydrogen or hydrogen water is effective in treating and preventing various diseases.ObjectivesThe aim of this study was to observe the effect of hydrogen on the expression of SIgA, PIgR, IL-4, IL-5, TGF-β1 and IL-40 in lung tissue of COPD rats, to study the relationship between lung pathology parameter and SIgA, PIgR, therefore we can understand the effect of hydrogen on the development of COPD by changing SIgA expression of airway mucosal in COPD rats.MethodsA rat model of COPD was established by cigarette smoke exposure, and different concentrations of hydrogen were inhaled as intervention measures. After 4 months of cigarette smoke exposure, pathologic changes and airway wall remodeling of the lung were assessed by optical microscope. The protein expressions of SIgA, PIgR, IL-4, IL-5, TGF-β1 as well as IL-40 in the lung tissues were observed by immunohistochemistry or Western blot. The correlation between lung pathology parameter and the expression of SIgA, PIgR was analyzed. The correlation between SIgA and the expression of IL-4, IL-5, TGF-β1 and IL-40 was analyzed.ResultsThe results showed that hydrogen inhalation significantly ameliorated lung pathology and airway wall remodeling, increased the protein expression of SIgA, PIgR, IL-4, IL-5, and IL-40, and reduced the protein expression of TGF-β1.ConclusionsInhalation of 22% and 41.6% hydrogen showed a better effect than inhalation of 2% hydrogen. Hydrogen inhalation can significantly improve the expression of SIgA on the mucosal surface of COPD rats, which may be one of the mechanisms which hydrogen works on COPD pathogenesis.

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Secretory IgA from submucosal glands does not compensate for its airway surface deficiency in chronic obstructive pulmonary disease

Cited by 16 publications

References 36 publications

Secretory IgA Deficiency in Individual Small Airways Is Associated with Persistent Inflammation and Remodeling

Secretory IgA Deficiency in Individual Small Airways Is Associated with Persistent Inflammation and Remodeling

CARBOCISTEINE INHIBITS THE EXPRESSION OF Muc5b IN COPD MOUSE MODEL

Effect of hydrogen inhalation on IL-40 and SIgA in a Rat Model of Pulmonary Mucosal Immunity

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