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PubMed2002

Sequential targeted deficiency of SP-A and -D leads to progressive alveolar lipoproteinosis and emphysema.

Surfactant proteins-A and -D (SP-A and SP-D) are members of the collectin protein family. Mice singly deficient in SP-A and SP-D have distinct phenotypes. Both have altered inflammatory responses to microbial challenges. To further investigate the functions of SP-A and SP-D in vivo, we developed mice deficient in both proteins by sequentially targeting the closely linked genes in embryonic stem cells using graded resistance to G-418. There is a progressive increase in bronchoalveolar lavage phospholipid, protein, and macrophage content through 24 wk of age. The macrophages from doubly deficient mice express high levels of the matrix metalloproteinase MMP-12 and develop intense but patchy lung inflammation. Stereological analysis demonstrates significant air space enlargement and reduction in alveolar septal tissue per unit volume, consistent with emphysema. These changes qualitatively resemble the lung pathology seen in SP-D-deficient mice. These doubly deficient mice will be useful in dissecting the potential overlap in function between SP-A and SP-D in host defense.

Animals↗
PubMedDate not supplied

Immunopathogenesis of Crohn's disease.

This review highlights the huge advances made in the understanding of Crohn's disease in the last 15 years. The pathogenic immune response in the gut wall is a highly polarised T helper cell type 1 response, probably directed against antigens of the commensal flora. There is marked over-expression of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-alpha and increased production of matrix degrading enzymes by fibroblasts and macrophages, which are probably responsible for ulceration and fistula formation. Crohn's disease runs in families and the susceptibility genes identified so far are associated with innate recognition of microbial products (Nod2) or epithelial barrier function (OCTN cation transporter genes and DLG5). Endogenous healing pathways mediated by transforming growth factor (TGF)-beta1 are inhibited because mucosal inflammatory cells express Smad7, the endogenous intracellular inhibitor of TGF-beta signalling. This makes it unlikely that enteral feeds containing TFG-beta are therapeutic by means of direct anti-inflammatory effects, however TGF-beta may still be involved because it is a well known epithelial motogen and may promote mucosal healing, in synergy with changes in mucosal bacterial populations as a result of the change in the diet.

Crohn Disease↗
PubMed2003

A cell-surface molecule selectively expressed on murine natural interferon-producing cells that blocks secretion of interferon-alpha.

Natural interferon (IFN)-producing cells (IPCs) recognize certain viruses and DNA containing deoxycytidylate-phosphatedeoxyguanylate (CpG) motifs through the toll-like receptor (TLR) 9, resulting in secretion of IFN-alpha, interleukin 12 (IL-12), and proinflammatory chemokines. Human IPCs are found mainly in inflamed lymph nodes, where they are presumably recruited from the blood to activate both innate and adaptive responses to microbial infections. Demonstrating IPC recruitment and function in murine infection models has been difficult because multiple antibodies are required to distinguish IPCs from other immune cells and very few IPCs can be recovered from lymph nodes. Here we describe a monoclonal antibody (mAb) that exclusively detects murine IPCs in all lymphoid organs under both normal and inflammatory conditions. Using this antibody, we demonstrate that IPCs are normally present in the T-cell zone of lymph nodes and spleen and that inoculation of peripheral tissues with inflammatory stimuli triggers recruitment of IPC into sentinel lymph nodes, whether the stimuli are able to directly stimulate IPCs through TLR or not. Remarkably, we show that incubation of IPCs with the antibody in vitro or administration of the antibody in vivo dramatically reduce secretion of IFN-alpha in response to CpG DNA without causing IPC depletion. Thus, the antibody identifies an IPC-specific surface molecule that, when engaged, inhibits IFN-alpha secretion.

Animals↗
PubMed1998

Four years' experience of intravenous colomycin in an adult cystic fibrosis unit.

Nearly all strains of Pseudomonas aeruginosa are sensitive to colomycin sulphomethate, but studies in the 1970s using large doses demonstrated significant renal and neurotoxic side-effects and it is not now commonly used. In this study colomycin (2 megaunits i.v. t.d.s.) has been used extensively in adult cystic fibrosis (CF) patients and its use reviewed to determine its efficacy and safety profile. Fifty-two CF patients (28 male, 24 female; mean age 26 yrs, range 17-39 yrs) received 135 courses (mean two courses each, range 1-7, median length 14 days) of i.v. colomycin (2,414 patient days in total). It was used in combination with one other i.v. antibiotic in 114 courses (85%) and with two others in 18 (13%). In all cases there was significant improvement in spirometry (pretreatment forced expiratory volume in one second (FEV1) % predicted mean 44.4, range 10-101; post-treatment mean 51.3, range 14-108; p<0.0001). No patient had any neurotoxicity but one developed a skin rash and myositis. There was no change in renal function (urea mean pretreatment 4.1 mmol x L(-1) (sD 1.4), mean post-treatment 43 (2.2), p=NS; creatinine mean pretreatment 77.9 mmol x L(-1) (15.3), mean post-treatment 803 (21.6), p=NS). In the authors' experience intravenous colomycin sulphomethate in moderate doses is an effective and safe antipseudomonal antibiotic which is easy to administer. Other clinicians should consider its use in patients with cystic fibrosis.

Adolescent↗
PubMed2002

Screening the fruitfly immune system.

The anti-microbial defense system of Drosophila shows functional similarities with the vertebrate innate immune system. Two recent gene-expression profiling studies of fruitflies challenged with infectious agents have identified key molecular players in the fruitfly's response to bacterial and fungal infection, as well as a large number of immune-regulated genes with unknown immunological function.

Animals↗
PubMed1999

Antimicrobial peptides as mediators of epithelial host defense.

Mammalian epithelial surfaces are remarkable for their ability to provide critical physiologic functions in the face of frequent microbial challenges. The fact that these mucosal surfaces remain infection-free in the normal host suggests that highly effective mechanisms of host defense have evolved to protect these environmentally exposed tissues. Throughout the animal and plant kingdoms, endogenous genetically encoded antimicrobial peptides have been shown to be key elements in the response to epithelial compromise and microbial invasion. In mammals, a variety of such peptides have been identified, including the well-characterized defensins and cathelicidins. A major source of these host defense molecules is circulating phagocytic leukocytes. However, more recently, it has been shown that resident epithelial cells of the skin and respiratory, alimentary, and genitourinary tracts also synthesize and release antimicrobial peptides. Both in vitro and in vivo data support the hypothesis that these molecules are important contributors to intrinsic mucosal immunity. Alterations in their level of expression or biologic activity can predispose the organism to microbial infection. The regulatory and developmental aspects of antimicrobial peptide synthesis are discussed from a perspective that emphasizes the possible relevance to pediatric medicine.

Amino Acid Sequence↗
PubMedDate not supplied

Spatiotemporal variability of wet atmospheric nitrogen deposition to the Neuse River Estuary, North Carolina.

Excessive nitrogen (N) loading to N-sensitive waters such as the Neuse River estuary (North Carolina) has been shown to promote changes in microbial and algal community composition and function (harmful algal blooms), hypoxia and anoxia, and fish kills. Previous studies have estimated that wet atmospheric deposition of nitrogen (WAD-N), as deposition of dissolved inorganic nitrogen (DIN: NO3-, NH3/NH4+) and dissolved organic nitrogen, may contribute at least 15% of the total externally supplied or "new" N flux to the coastal waters of North Carolina. In a 3-yr study from June 1996 to June 1999, we calculated the weekly wet deposition of inorganic and organic N at eleven sites on a northwest-southeast transect in the watershed. The annual mean total (wet DIN + wet organics) WAD-N flux for the Neuse River watershed was calculated to be 956 mg N/m2/yr (15026 Mg N/yr). Seasonally, the spring (March-May) and summer (June-August) months contain the highest total weekly N deposition; this pattern appears to be driven by N concentration in precipitation. There is also spatial variability in WAD-N deposition; in general, the upper portion of the watershed receives the lowest annual deposition and the middle portion of the watershed receives the highest deposition. Based on a range of watershed N retention and in-stream riverine processing values, we estimate that this flux contributes approximately 24% of the total "new" N flux to the estuary.

Agriculture↗
PubMed1994

In vitro determination of ruminal protein degradability using [15N]ammonia to correct for microbial nitrogen uptake.

An in vitro procedure was developed to estimate rate and extent of ruminal protein degradation using [15N]H3 to quantify uptake of protein degradation products for microbial protein synthesis. Incubations were conducted for 6 h in stirrer flasks with ruminal inoculum plus buffer, reducing solution, pectin, soluble carbohydrates, and added (15NH4)2SO4. Seven protein concentrates were tested in the system. Samples of media were analyzed for 15N enrichment of NH3, microbial N, and total solids N. Degradation rate was computed from net (i.e., protein-added minus blank) release of NH3 N plus net synthesis of microbial protein N; escape was estimated assuming ruminal passage rate = .06/h. Over the course of the incubations, pH was stable at 6.6, protozoal numbers increased slightly, and microbial protein content increased by more than 200%. Free AA had not accumulated at the end of the incubations. Microbial protein synthesis was a linear function (P < .001; r2 = .780) of extent of degradation. Mean degradation rates and ruminal escapes determined were, respectively, .569/h and 10% (casein), .148/h and 29% (solvent soybean meal), .036/h and 63% (expeller soybean meal), .026/h and 70% (low solubles fish meal), .063/h and 49% (high solubles fish meal), .034/h and 64% (corn gluten meal), and .050/h and 55% (roasted soybeans). Overall, degradation rates averaged 28% greater than those previously estimated using an inhibitor in vitro system; however, rates obtained for the fish meals using the 15N method were slower.

Ammonia↗
PubMed2026

[Intestinal microbiota alterations after digestive tract reconstruction surgery and their impacts on host physiology].

The gut microbiota, acknowledged as the human body's 'second genome', plays a pivotal role in maintaining health. Digestive tract reconstruction surgery profoundly alters the anatomical structure and physiological environment of the gastrointestinal tract, thereby inducing significant shifts in the intestinal microbiota. These microbial changes subsequently influence host physiological functions through metabolic, immune, neuroendocrine, and other pathways. For instance, Roux-en-Y gastric bypass surgery enriches short-chain fatty acid(SCFA)-producing Bacteroides, improving systemic insulin sensitivity. Conversely, pancreaticoduodenectomy leads to a marked enrichment of potential pathobionts such as Klebsiella and Clostridium, which may elevate the risk of infections and tumor recurrence. This review comprehensively summarizes the characteristic changes in the gut microbiota following various digestive tract reconstruction procedures and discusses their multifaceted impacts on host physiology, aiming to provide insights for future experimental research and clinical practice.

Humans↗
PubMed2005

A dual role for TGF-beta1 in the control and persistence of fungal pneumonia.

TGF-beta1 (TGF) has been implicated in the pathogenesis of several chronic infections and is thought to promote microbial persistence by interfering with macrophage function. In rats with experimental pulmonary cryptococcosis, increased lung levels of TGF were present at 12 mo of infection. Within the lung, expression of TGF localized to epithelioid cells and foamy macrophages in areas of inflammation. Increased TGF expression was also observed in the lungs of experimentally infected mice and a patient with pulmonary cryptococcosis. TGF reduced Ab and serum-mediated phagocytosis of Cryptococcus neoformans by rat alveolar macrophages (AM) and peripheral blood monocytes, and this was associated with decreased chemokine production and oxidative burst. Interestingly, TGF-treated rat AM limited both intracellular and extracellular growth of C. neoformans. Control of C. neoformans growth by TGF-treated rat AM was due to increased secretion of lysozyme, a protein with potent antifungal activity. The effects of TGF on the course of infection were dependent on the timing of TGF administration relative to the time of infection. TGF treatment of chronically infected rats resulted in reduced lung fungal burden, while treatment early in the course of infection resulted in increased fungal burden. In summary, our studies suggest a dual role for TGF in persistent fungal pneumonia whereby it contributes to the local control of infection by enhancing macrophage antifungal efficacy through increased lysozyme secretion, while limiting inflammation by inhibiting macrophage/monocyte phagocytosis and reducing associated chemokine production and oxidative burst.

Animals↗
PubMed2006

Nucleotide-binding oligomerization domain-like receptors: intracellular pattern recognition molecules for pathogen detection and host defense.

The nucleotide binding oligomerization domain-like receptor (NLR) family of pattern recognition molecules is involved in a diverse array of processes required for host immune responses against invading pathogens. Unlike TLRs that mediate extracellular recognition of microbes, several NLRs sense pathogens in the cytosol and upon activation induce host defense signaling pathways. Although TLRs and NLRs differ in their mode of pathogen recognition and function, they share similar domains for microbial sensing and cooperate to elicit immune responses against the pathogen. Genetic variation in several NLR genes is associated with the development of inflammatory disorders or increased susceptibility to microbial infection. Further understanding of NLRs should provide critical insight into the mechanisms of host defense and the pathogenesis of inflammatory diseases.

Adaptor Proteins, Signal Transducing↗
PubMed1975

[Transmissivity of the various R factors found among E. coli cultures circulating under natural conditions].

Transmissivity of drug resistance in wild strains of E. coli was shown to be determined not only by the presence of the transmissive factor and r-determinants in the microbial cell, but also by the functional activity of the R-factor. The capacity of the R-factor for transmission depended to a certain extent on the number of the r-determinants in the R-factor and the presence of various r-determinants in the R-factor.

Ampicillin↗
PubMedDate not supplied

The biochemistry of collagen.

Collagen synthesis and subsequent extracellular stabilization and turnover are multi-step processes. The sequence of events in these processes is reviewed and correlated with collagen pathologies.

Animals↗
PubMed1976

Hepatic fibrosis.

Explore the source record for details and available documents.

Amino Acids↗
PubMed1986

Association of defective monocyte chemotaxis with recurrent acute exacerbations in chronic obstructive lung disease.

Since mononuclear phagocytes are crucial in resisting microbial challenge in the lung, selected functions of blood monocytes were studied in 27 patients with chronic bronchitis (19 with hypersecretory symptoms and many acute infectious exacerbations and eight with obstructive symptoms without recurrent infections), and compared with 82 healthy controls. While monocytes from patients with solely obstructive symptoms had a normal migratory function, both spontaneous and chemotactic migration were depressed in the patients with hypersecretory symptoms. Phagocytic activity of the blood monocytes was equally depressed in both subgroups. Intracellular killing of Candida albicans was normal in all patients when compared with smoking control subjects. Chemotactic responsiveness was thus decreased only in patients with hypersecretory symptoms, suggesting that a defect in monocyte migration in these patients might contribute to the high incidence of acute bronchial exacerbations.

Aged↗
PubMed1986

Immunomodulating effect of autohaemotherapy (a literature review).

An analysis is presented of experimental and clinical data from different authors on the stimulating effect of autohaemotherapy with regard to the immunological reactivity of humans and animals as well as in vitro experiments with lymphocytes. Erythrolysate has been found to exert a more powerful effect than intact erythrocytes. The stimulating effect of autohaemotherapy on both irradiated and non-irradiated animals manifests itself in an increase in resistance to infection (increased LD50 in experimental infection), enhanced production of antibodies to microbial and tissue antigens and activated functioning of cell-mediated immune defence mechanisms. The favourable influences on radioresistance and the antitumour effect of authohaemotherapy are described. Induced desensitization plays an important part in the mechanism of action of autohaemotherapy. The administration of large doses of erythrocytes or of erythrolysate results in immunosuppression. Autohaemotherapy does not cause side effects and is feasible both on an in-and out-patient basis.

Animals↗
PubMed1987

[Detection of a system of microsomal monooxygenases in the rodent malaria parasite Plasmodium berghei].

A microsomal fraction from the cells of the malaria parasite of rodent Plasmodium berghei was obtained. The spectral properties of microsomal preparations suggest that P. berghei microsomes contain cytochromes b5 and P-420. Electrophoretic separation of microsomal proteins revealed the presence of proteins whose molecular mass corresponds to NADPH-cytochrome c reductase, cytochrome P-450 and epoxide hydratase. The activities of NADPH-cytochrome c reductase and benzpyrene hydroxylase were determined. The spectral parameters, electrophoretic data and enzymatic activities of microsomal proteins indicate that P. berghei cells contain a cytochrome P-450 monooxygenase system. The interrelationship between the activity of the microsomal monooxygenase system and the resistance of P. berghei cells to the antimalaria preparation chloroquine is discussed.

Animals↗