Endotoxin markers in bronchoalveolar lavage fluid of patients with interstitial lung diseases

Szponar, Bogumiła; Larsson, Lennart; Domagała‐Kulawik, Joanna

doi:10.1186/2049-6958-7-54

Cited by 2 publications

(4 citation statements)

References 29 publications

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“…The route of exposure to mold and bacterial by-products most likely results from the inhalation of respirable (diameter 5 micron) aerosolized particulates and bioaerosols that are deposited on the nasal mucosa and deep into small airways and alveoli of adults and children where diffusion of toxins into the brain and systemic circulation occurs [38-40 42-45]. Thus, the symptoms and health complaints of the parents in this study are consistent with those reported by others regarding health, moisture and exposure to microbial growth [5,20,21,26,31,[67][68][69][70][71][72][73][74][75][76][77].…”

Section: Discussionsupporting

confidence: 80%

“…It is appropriate to address a few other issues regarding the complexity of the indoor environment resulting from water intrusion leading to amplification of fungi, bacteria and their biological products as follows: 1) Inhalation of 1,3--D-glucans from cell walls of mold can lead to inflammation of the lungs and the production of pro-inflammatory cytokines. In addition, sarcoidosis in occupants of water-damaged homes related to exposure to molds has been successfully treated with antifungal therapy [68][69][70][71]; 2) Endotoxins released by Gram negative bacteria are associated with acute and chronic inflammatory responses in the lungs of rodents and humans [72][73][74][75][76][77]; 3) The Actinobacteria (Streptomyces and Mycobacterium spp) have been identified in damp indoor environments, witch can cause lung infections as well as skin and tissue actinomycetoma [79][80][81][82][83][84]. Toxic metabolites (valinomycin, monactin, nonactin and staurosporin produced by Streptomyces spp in dust co-occurring with fungal secondary metabolites opens the possibility of interactions between bacterial and fungal toxins on the health of occupants of water-damaged homes and buildings [31][32][33][34][35][36][37][38][39][40][41].…”

Section: Discussionmentioning

confidence: 99%

“…Toxic metabolites (valinomycin, monactin, nonactin and staurosporin produced by Streptomyces spp in dust co-occurring with fungal secondary metabolites opens the possibility of interactions between bacterial and fungal toxins on the health of occupants of water-damaged homes and buildings [31][32][33][34][35][36][37][38][39][40][41]. With respect to nontuberculin Mycobacterium several species are known to cause Mycobacterium Avium Complex (MAC) and while some species are known to produce the cytopathic toxins, mycolactone [72][73][74][75][76][77][78][79][80][81][82][83][84].…”

Section: Discussionmentioning

confidence: 99%

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A Case of Reye’s-Like Syndrome in a 68-Day Old Infant: Water Damaged Home, Mold, Bacteria and Aflatoxins.

Gray¹,

Thrasher²,

Hooper³

et al. 2015

Int. J. Clin. Toxicol.

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Introduction: Reye's Syndrome is characterized by acute encephalopathy, hepatic injury accompanied with elevated serum ammonia, serum fatty acids, amino acids and triglycerides; hypoglycemia, prolonged prothrombin time, fatty infiltration of the liver, and mitochondrial pathology. We present an infant that died at 68 days of age with Reye 's syndrome. The infant and parents were exposed to airborne fungi, bacteria and toxic bioaerosols resulting from water intrusion in the home. The purpose of this study was to investigate and, if possible, to determine the cause of death of the infant with respect to the fungi, bacteria and their toxins present in the families water-damaged home. Materials and Methods: Health and genetic history was done on the family (father, mother and two siblings). Environmental evaluation was carried out to identify airborne fungi and bacteria in the home. Clinical testing of the baby while in the hospital provided data on blood chemistry and EEG results. Mitochondrial studies on skin fibroblasts and skeletal muscle were carried out testing for functions of Complexes I-IV and mitochondrial DNA mutations. Light and E.M. microscopy were done on liver biopsy material. Immunoaffinity column and fluorometry were used to detect aflatoxins (B1, B2, G1 and G2) in liver autopsy material. The mother's breast milk and urine was tested for mycotoxins: trichothecenes, aflatoxins and ochratoxin. Results: Medical and genetic history were negative for familial diseases similar to Reye's syndrome and for mitochondrial DNA mutations. Aortic and pulmonic valve abnormalities were observed. Environmental testing revealed the presence of elevated levels of several species of fungi and bacteria in the infant's bedroom and other rooms of the home. Clinical diagnostic tests of the infant revealed metabolic acidosis, elevated serum ammonia, triglycerides, pyruvic and lactic acids, serum alanine, and beta-hydroxybutyrate. Mitochondrial studies showed decreased function of complexes I-IV and the absence of known mutations associated with mitochondrial diseases. Microscopy (light and E.M.) of biopsies demonstrated the accumulation of glycogen in muscle and fatty droplets in the liver. Aflatoxins were detected in the infant's liver (2.1 ppb), and the mother's breast milk (15 ppb), while maternal urine was positive for trichothecenes (4.76 ppb) and ochratoxin (3.4 ppb). Conclusions: After a review of the peer reviewed literature, we conclude that the infant died of a Reye's-Like Syndrome at the age of 68 days (all 22 cited criteria were met). Clinical and autopsy findings were consistent with this disease process. The valvular abnormalities found are associated with actinomycetes exposure. The medical and genetic histories were negative for any familial diseases of a similar nature. The infant had mitochondrial dysfunction of complexes I-IV, suggesting mitochondrial disease consistent with alflatoxin toxicity. The presence of aflatoxins in the liver supports the causal role of this mycotoxin in the illness of this infant...

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

A Case of Reye’s-Like Syndrome in a 68-Day Old Infant: Water Damaged Home, Mold, Bacteria and Aflatoxins.

Gray¹,

Thrasher²,

Hooper³

et al. 2015

Int. J. Clin. Toxicol.

View full text Add to dashboard Cite

show abstract

“…Quantitation of 3-hydroxy fatty acids also has been useful in clinical studies of infection: bronchial lavage fluid of patients with lung diseases (201); salivary 3-hydroxy fatty acids in periodontitis (202); and serum 3-hydroxy fatty acids in cardiac patients with endotoxemia (203). Importantly, the 3-hydroxy fatty acids in LPS appear to be active in stimulating the immune system (204, 205).…”

Section: Biomarkers Of Systemic Bacterial Exposuresmentioning

confidence: 99%

Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

Djurić

2017

Translational Research

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Obesity increases the risks of many cancers. One important mechanism behind this association is the obesity-associated pro-inflammatory state. Although the composition of the intestinal microbiome undoubtedly can contribute to the pro-inflammatory state, perhaps the most important aspect of host-microbiome interactions is host exposure to components of intestinal bacteria that stimulate the inflammatory reactions. Systemic exposures to intestinal bacteria can be modulated by dietary factors by altering both the composition of the intestinal microbiota as well as absorption of bacterial products from the intestinal lumen. In particular, high fat and high energy diets have been shown to facilitate absorption of bacterial lipopolysaccharide (LPS) from intestinal bacteria. Biomarkers of bacterial exposures that have been measured in blood include LPS-binding protein, sCD14, fatty acids characteristic of intestinal bacteria and immunoglobulins specific for bacterial LPS and flagellin. The optimal strategies to reduce these pro-inflammatory exposures, whether by altering diet composition, avoiding a positive energy balance or reducing adipose stores, likely differ in each individual. Biomarkers that assess systemic bacterial exposures therefore should be useful to optimize and personalize preventive approaches for individuals and groups with specific characteristics, and to gain insight into the possible mechanisms involved with different preventive approaches.

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Endotoxin markers in bronchoalveolar lavage fluid of patients with interstitial lung diseases

Cited by 2 publications

References 29 publications

A Case of Reye’s-Like Syndrome in a 68-Day Old Infant: Water Damaged Home, Mold, Bacteria and Aflatoxins.

A Case of Reye’s-Like Syndrome in a 68-Day Old Infant: Water Damaged Home, Mold, Bacteria and Aflatoxins.

Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

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