The influence of antibiotic exposure in the early postnatal period on the development of intestinal microbiota was monitored in 26 infants including five antibiotic-treated (AT) subjects orally administered a broad-spectrum antibiotic for the first 4 days of life and three caesarean-delivered (CD) subjects whose mothers were intravenously injected by the similar type of antibiotics in the same period. The faecal bacterial composition was analysed daily for the first 5 days and monthly for the first 2 months. Terminal restriction fragment length polymorphisms in the AT subjects showed less diversity with the attenuation of the colonization of some bacterial groups, especially in Bifidobacterium and unusual colonization of Enterococcus in the first week than the control antibiotic-free infants (AF, n = 18). Quantitative real-time PCR showed overgrowth of enterococci (day 3, P = 0.01; day 5, P = 0.003; month 1, P = 0.01) and arrested growth of Bifidobacterium (day 3, P = 0.03) in the AT group. Furthermore, after 1 month, the Enterobacteriaceae population was markedly higher in the AT group than in the AF group (month 1, P = 0.02; month 2, P = 0.02). CD infants sustained similar, although relatively weaker, alteration in the developing microbiota. These results indicate that antibiotic exposure at the beginning of life greatly influences the development of neonatal intestinal microbiota.

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We investigated the correlation between fecal bacteria composition in early infancy and the prevalence of allergic diseases in late infancy. The fecal microbiota in the first 2 months was profiled using the 16S rRNA V6 short-tag sequences in the community and statistically compared between two groups of subjects who did and did not show allergic symptoms in the first 2 years (n = 11 vs. 11). In the allergic group, genus Bacteroides at 1 month and genera Propionibacterium and Klebsiella at 2 months were more abundant, and genera Acinetobacter and Clostridium at 1 month were less abundant than in the nonallergic group. Allergic infants who showed high colonization of Bacteroides and/or Klebsiella showed less colonization of Clostridium perfringens/butyricum, suggesting antagonism between these bacterial groups in the gastrointestinal tract. It was also remarkable that the relative abundance of total Proteobacteria, excluding genus Klebsiella, was significantly lower in the allergic than in the nonallergic group at the age of 1 month. These results indicate that pyrosequence-based 16S rRNA gene profiling is valid to find the intestinal microbiotal disorder that correlates with allergy development in later life.

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E En nd do ot th he el li in n--1 1 a an nd d i in nt te er rl le eu uk ki in n--8 8 i in n h hi ig gh h a al lt ti it tu ud deABSTRACT: We present a case of high altitude pulmonary oedema (HAPE) with pulmonary hypertension and polymorphoneuclear leucocyte (PMN) accumulation in bronchoalveolar lavage fluid (BALF), which occurred in a 21 year old man. Plasma endothelin-1 (ET-1) and interleukin-8 (IL-8) concentration in BALF were elevated on admission, and returned to normal level at recovery, when the pulmonary artery pressure and the PMN counts in BALF were normal. In addition, E-selectin and intercellular adhesion molecule-1 (ICAM-1) in BALF were also slightly increased on admission.These findings suggest that endothelin-1 is a vasoconstrictor which contributes to the pulmonary hypertension in high altitude pulmonary oedema, and that some of the inflammatory mediators play an important role in chemotaxis and accumulation of polymorphonuclear leucocytes in the development of high altitude pulmonary oedema. Eur Respir J., 1996Respir J., , 9, 1947Respir J., -1949. High altitude pulmonary oedema (HAPE) is a severe type of acute mountain sickness. It is a serious, sometimes fatal illness related to rapid exposure to altitude. Although the pathophysiological mechanism of HAPE remains unclear, it has long been suggested that pulmonary vasoconstriction and increased pulmonary vascular permeability are important contributory factors [1,2]. Recent studies have suggested that endothelin is related to pulmonary vasoconstriction [3][4][5], and that the increased pulmonary vascular permeability is probably caused by inflammatory mediators [6][7][8][9][10]. However, no studies have been conducted on the role of endothelin and cytokines in patients with HAPE. We report a case of HAPE, documenting the possible role of endothelin-1 (ET-1), and polymorphoneuclear leucocyte (PMN) chemotactic mediators, such as interleukin-8 (IL-8). Case reportA Japanese male university student, aged 21 yrs, who was healthy before climbing, arrived at the foot of the Japan Alps at 1,000 m above sea level. The next morning, he started climbing to a snowy valley about 2,000 m above sea level and still felt well. On the third day, whilst climbing to Mt Yari (3,180 m), he developed general fatigue, followed by headache, cough, sputum, poor appetite and fever (38˚C). After staying all day to rest at 3,000 m, his condition progressively deteriorated. On the fifth day, he was lethargic, comatose, cyanotic, and had a cough with foamy sputum. He was rescued, transported by helicopter, and admitted to our Shinshu University Hospital (660 m).On admission, he had cyanosis and was unconscious. His temperature was 38˚C, pulse rate 140 beats·min -1 , respiration rate 26 breaths·min -1 , and his blood pressure 140/90 mmHg. Coarse crackles were audible over both sides of the lung. He showed decerebrate rigidity. An examination of the ocular fundi showed papilloedema and multiple flame-shaped and blot haemorrhages in both fundi. A chest roentgenogram revealed patc...

Arterial endothelin-1 level in pulmonary emphysema and interstitial lung disease. Relation with pulmonary hypertension during exercise. T. Yamakami, O. Taguchi, E.C. Gabazza, M. Yoshida, T. Kobayashi, H. Kobayashi, H. Yasui, H. Ibata, Y Adachi. ERS Journals Ltd 1997. ABSTRACT: This study was undertaken to assess the arterial plasma levels of endothelin-1 (ET-1) and their relationship with pulmonary haemodynamic and gas exchange variables during exercise in patients with emphysema and interstitial lung disease (ILD).Incremental cycle ergometry was performed in all patients up to maximal capacity. At rest, arterial ET-1 levels were higher in emphysema (1.86±0.35 pg·mL -1 ; p<0.02) and ILD (1.75±0.25 pg·mL -1 ; p<0.03) patients than in controls (1.35±0.18 pg·mL -1 ). Emphysema (2.08±0.26 versus 1.70±0.40 pg·mL -1 ) and ILD (1.98±0.21 versus 1.67±0.02 pg·mL -1 ) patients with pulmonary hypertension (PH) presented significantly (p<0.05) higher arterial ET-1 levels than those without. At rest, arterial ET-1 levels were significantly correlated with mean pulmonary arterial pressure (Ppa) in both ILD (r=0.8, p=0.01) and emphysema (r=0.5, p=0.03) patients. During exercise, the arterial ET-1 levels were significantly correlated with arterial oxygen (Pa,O 2 ) (r=-0.6, p=0.04), alveolar-arterial oxygen difference (r=0.8, p=0.01), and Ppa (r=0.6, p=0.04) in ILD patients, but not in those with emphysema.In brief, the results of this study suggest that arterial endothelin-1 is markedly increased in interstitial lung disease and emphysema patients, and that, it is related to the exercise-induced exacerbation of pulmonary hypertension in patients with interstitial lung disease, but not in those with emphysema. Eur Respir J 1997; 10: 2055-2060. Pulmonary artery hypertension is the major cardiovascular complication of emphysema and advanced interstitial lung disease (ILD) [1]. Pulmonary hypertension (PH) is important, not only because it is associated with right ventricular hypertrophy (or cor pulmonale) but also because it adversely affects prognosis in these patients [2]. The mechanisms responsible for PH include thrombotic obstruction of pulmonary blood vessels, reduced distensibility of the pulmonary vascular bed, pulmonary vascular obstruction produced by medial hypertrophy or intimal proliferation, and pulmonary vasoconstriction elicited by acute or chronic alveolar hypoxia [3,4]. Of these, hypoxic vasoconstriction has been considered one of the major factors involved in the pathogenesis of sustained PH or in the development of acute exacerbation of PH in patients with emphysema or advanced ILD [5]. However, the precise mechanism by which hypoxia induces pulmonary vasoconstriction and the structural changes that ensue from chronic hypoxia have not been fully elucidated. Endothelin-1 (ET-1), a vasoconstricting peptide originally isolated from cultured human endothelial cells, may play a relevant role in the pathogenesis of PH during hypoxia [6][7][8]. This assumption is supported by previous findings that showed that the e...

Objective

Objective Diabetic nephropathy (DN) is a common cause of end