Surfactant proteins A and D in Eustachian tube epithelium

Paananen, Reija; Sormunen, Raija; Glumoff, Virpi; Eijk, Martin van; Hallman, Mikko

doi:10.1152/ajplung.2001.281.3.l660

Cited by 55 publications

(35 citation statements)

References 42 publications

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“…One explanation could be the nature of induced sputum: generally these secretions are derived mainly from the large, more proximal airways and this leads to some problems in the reproducibility of these samples [23,24]. All sputum samples were included because SP-A is mainly expressed in epithelial cells, not only in the distal airways but also in trachea, sinus [46] and even middle ear epithelium [35,47]. The exact quantification of SP-A in the sputum supernatant is also somewhat problematic since sputum is not homogenous and both the induction and isolation process may vary between laboratories.…”

Section: Discussionmentioning

confidence: 99%

Elevation of surfactant protein A in plasma and sputum in cigarette smokers

Mazur¹,

Toljamo²,

Ohlmeier³

et al. 2011

Eur Respir J

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Serum surfactant protein (SP)-A has been postulated to associate with pulmonary fibrosis, but its role in cigarette smoking-related lung diseases is undefined.SP-A levels in plasma and induced sputum in nonsmokers, smokers with respiratory symptoms (cough and/or phlegm) and symptom-free smokers were assessed using a validated EIA method. A total of 474 current smokers without any diseases or medications were enrolled and followed for 2 yrs with 111 of them succeeding in stopping.Plasma SP-A level was detectable in all subjects and elevated in smokers independently of the symptoms compared to nonsmokers (p50.001). After 2 yrs of follow-up, the SP-A level was higher in those who continued smoking compared to the quitters (p,0.001). Plasma SP-A levels were associated with age, smoking history and lung function. Sputum (n5109) SP-A was nondetectable in most nonsmokers, whereas smoking and symptoms increased sputum SP-A highly significantly (p50.001).In conclusion, SP-A may be involved in pathogenesis of cigarette smoking-related lung diseases. Further studies are needed to elucidate the role of SP-A in chronic obstructive pulmonary disease.

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Section: Discussionmentioning

confidence: 99%

Elevation of surfactant protein A in plasma and sputum in cigarette smokers

Mazur¹,

Toljamo²,

Ohlmeier³

et al. 2011

Eur Respir J

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“…SP-D (and MBL) is a member of the collectins, being produced by the alveolar type II cells and nonciliated bronchiolar cells and secreted into the alveolar lining layer, and was originally thought to have only surfactant function in the lungs (17). Interestingly, a recent study showed the presence of SP-D (and SP-A) in the epithelial cells of the porcine Eustachian tube (34), suggesting that they partake in the immune defence during middle ear infections. In view of the grossly increased risk of recurrent middle ear infections in TS patients, this finding could be of special importance.…”

Section: Discussionmentioning

confidence: 99%

The effects of GH and hormone replacement therapy on serum concentrations of mannan-binding lectin, surfactant protein D and vitamin D binding protein in Turner syndrome

Gravholt

Leth-Larsen

Lauridsen³

et al. 2004

European Journal of Endocrinology

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Objective: Studies in animals and humans indicate that growth hormone (GH) and insulin-like growth factor-I (IGF-I) modulate immune function. Recently, it was reported that GH therapy increased the level of mannan-binding lectin (MBL) in normal patients, and that treatment of acromegalics with pegvisomant decreased the levels of MBL. The effect on MBL was thought to be due to a specific action of GH, since IGF-I treatment did not affect MBL. Whether it is advantageous or not to have high or low levels of MBL is not known. Likewise, it is not clear how the modifications induced by GH affect immune function. In the present study we examined whether GH or hormone replacement therapy (HRT) in Turner syndrome (TS) influence the serum concentrations of MBL and two other proteins partaking in the innate immune defence, surfactant protein D (SP-D) and vitamin D binding protein (DBP). Design: Study 1: a double-blind crossover study of 12 healthy TS adolescents examined during treatment with either placebo or GH for 2 months, and compared with a control group. Study 2: tripleblind crossover study of 9 healthy TS adolescents randomized to treatment with placebo, GH or GH þ 17b-estradiol. Study 3: 60 adult TS patients (55 received HRT) compared with 59 age-matched controls. Study 4: 27 patients with TS were examined before and during sex hormone replacement with 17b-estradiol and norethisterone and compared with age-matched controls (n ¼ 24). Methods: Measurement of MBL, SP-D, DBP, and other inflammation markers. Results: Study 1: the levels of MBL (P ¼ 0.002) and SP-D (P ¼ 0.012) increased during GH treatment, whereas no changes were observed in comparison with controls. DBP was unchanged by GH, but was significantly higher in TS compared with controls (P ¼ 0.017). Study 2: treatment with GH increased MBL (P ¼ 0.045) and SP-D (P ¼ 0.05) concentrations in TS, while treatment with GH þ 17b-estradiol did not increase levels further. DBP was unchanged by treatment. Study 3: levels of MBL, SP-D, and DBP were similar in adult TS and control subjects. Study 4: DBP levels decreased in response to HRT, while MBL and SPD levels were unchanged. Levels of all three plasma proteins were similar to controls. Conclusion: We show that treatment with GH significantly increases MBL and SP-D concentrations in TS, while HRT marginally decreases DBP. Whether the present findings, suggesting a link between the endocrine and the immune system, have clinical consequences needs to be studied further. European Journal of Endocrinology 150 355-362

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“…Although there are few studies demonstrating surfactant in the upper airways, decreased levels of the various phospholipid components of surfactant have been implicated as playing a role in atrophic rhinitis [3] . Additionally, surfactant has been identifi ed in the porcine Eustachian tube and may contribute to lowering the opening pressure between the nasopharynx and middle ear [4][5][6] . Alterations in surfactant levels may adversely affect Eustachian tube function and contribute to chronic ear infections.…”

Section: Introductionmentioning

confidence: 99%

Presence of Surfactant Lamellar Bodies in Normal and Diseased Sinus Mucosa

Woodworth¹,

Smythe²,

Spicer

et al. 2005

ORL

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Background:Pulmonary surfactant originates from phospholipid lamellar bodies secreted from the type II epithelial cell of the alveolus. In the lower airway, surfactant optimizes surface tension and oxygen exchange, decreases mucus viscosity and aids in mechanical elimination of inhaled pathogens. In addition to the lung, lamellar bodies have been identified in many other cell types throughout the human body. However, no prior studies have identified lamellar bodies in human sinus mucosa. Objectives: We performed ultrastructural studies to assess whether lamellar bodies are present in the human sinus in a variety of diseased and normal epithelium. Methods:We biopsied sinus mucosa from 5 subjects, 1 each with allergic fungal sinusitis, eosinophilic mucin rhinosinusitis, cystic fibrosis, frontal sinus mucocele, and cerebrospinal fluid leak (healthy control). Mouse lung served as a positive control. Specimens were prepared using ferrocyanide-reduced osmium tetroxide and thiocarbohydrazide for fixation (R-OTO method) to avoid extraction of phospholipids during dehydration and were viewed with transmission electron microscopy. Results:We identified lamellar bodies in the sinus mucosa of all patients. Additionally, preservation of mouse lung lamellar bodies confirms that the R-OTO method is a valid technique to preserve these structures. Conclusions:We describe a simpler, faster technique for identification of cellular phospholipid components than those used previously. Definitive identification of these lamellar bodies within ciliated pseudostratified epithelium of the upper airway indicates that surfactant may have a role in sinus function and pathophysiology.

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Surfactant proteins A and D in Eustachian tube epithelium

Cited by 55 publications

References 42 publications

Elevation of surfactant protein A in plasma and sputum in cigarette smokers

Elevation of surfactant protein A in plasma and sputum in cigarette smokers

The effects of GH and hormone replacement therapy on serum concentrations of mannan-binding lectin, surfactant protein D and vitamin D binding protein in Turner syndrome

Presence of Surfactant Lamellar Bodies in Normal and Diseased Sinus Mucosa

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